The DOI matches its Crossref record; 102 of the 102 references it cites were found in a registry or an index; 8 of the 233 sources its claims cite were checked for support.
Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation
Open accessAbstract
Recent laboratory findings suggest that it might be possible to promote cerebral plasticity and neurological recovery after stroke by use of exogenous pharmacological or cell-based treatments. Brain microvasculature and glial cells respond in concert to ischaemic stressors and treatment, creating an environment in which successful recovery can ensue. Neurons remote from and adjacent to the ischaemic lesion are enabled to sprout, and neural precursor cells that accumulate with cerebral microvessels in the perilesional tissue further stimulate brain plasticity and neurological recovery. These factors interact in a highly dynamic way, facilitating temporally and spatially orchestrated responses of brain networks. In view of the complexity of the systems involved, stroke treatments that stimulate and amplify these endogenous restorative mechanisms might also provoke unwanted side-effects. In experimental studies, adverse effects have been identified when neurorestorative treatments were administered to animals with severe associated illnesses, after thrombolysis with alteplase, and when therapies were initiated outside appropriate time windows. Balancing the opportunities and possible risks, we provide suggestions for the translation of restorative therapies from the laboratory to the clinic.
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110 Not checked yet · 26 Own interpretation · 14 No basis given · 3 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In rodents, beneficial effects were reported even when treatments were initiated days, weeks, or months after stroke.14–20”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
What the sources say
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Partly supportedcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain sourceExperimental — accuracy not yet measured
The Materials and methods section reports transplantation in rats 7 days after stroke, and the Results report significantly improved functional recovery compared with vehicle controls. This supports treatment initiated days after stroke, but the paper does not report beneficial treatment initiated weeks or months afterward; its references to weeks describe follow-up and recovery, not treatment initiation. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Not checked yetcites [16] Zhang, 2002, Sildenafil induces neurogenesis and promotes functional recovery after stroke in rats, Stroke source
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [18] Shen, 2007, Therapeutic benefit of bone marrow stromal cells administered 1 month after stroke, J Cereb Blood Flow Metab source
- Partly supportedcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain sourceExperimental — accuracy not yet measured
The study summary (p. 2) reports improved motor recovery in mice given erythropoietin starting three days after stroke, supporting the days-later part of the claim. The paper does not report beneficial treatment initiated weeks or months after stroke; its four-week treatment period began at 72 hours (Animal groups, p. 3). (LLM, conf=0.88)
- Supportedcites [20] Tsai, 2011, Delayed anti-Nogo-A therapy improves function after chronic stroke in adult rats, Stroke source
The Discussion (page not supplied) reports improved function with anti-Nogo-A treatment begun 24 hours or 1 week after stroke and significant improvement when treatment began 9 weeks after stroke—approximately two months. These findings support the cited statement about beneficial effects in rodents at delays spanning days, weeks, and months. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Contralesional plasticity as a basis for neurological recovery occurs in several species (eg, in rats,11,15,17 mice,12,19,24 and macaques32).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Partly supportedcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain sourceExperimental — accuracy not yet measured
This source is cited for the rat example, not the mouse or macaque examples. The Results report contralesional axonal sprouting and functional recovery in treated rats, but the Discussion says the importance of contralesional dendritic plasticity for recovery remains to be determined. It therefore does not establish contralesional plasticity as a basis for recovery. (LLM, conf=0.88)
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Supportedcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
This source is cited as an example for rats, not for the separately cited mice and macaques. The Abstract (Background and Purpose; Conclusions) describes contralesional corticospinal remodeling in rats after stroke and says it may contribute to functional recovery. (LLM, conf=0.93)
- Supportedcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
The citation is attached to the mice portion of the species list, not the rat or macaque examples. The Discussion (p. 14) reports that erythropoietin increased projections from the contralesional motor cortex in mice, and the Discussion (p. 15) links this shift in plasticity to beneficial functional recovery. (LLM, conf=0.92)
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [32] Freund, 2006, Nogo-A-specific antibody treatment enhances sprouting and functional recovery after cervical lesion in adult primates, Nat Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Subsequently, axonal fibre tracts reorganise along the infarct rim.21,23”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In view of the long therapeutic time window and the fact that tissue reperfusion is not a requirement, neuro restorative therapies can potentially benefit all stroke patients.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
hedgedconditional- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Brain microvasculature and glial cells respond in concert to ischaemic stressors and treatment, creating an environment in which successful recovery can ensue.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Instead, homologous fibres originating from the contralesional motor cortex grow out across the midline to reach denervated neurons in target structures of the lesioned pyramidal tract (figure 1).10–12,15,17,19,24”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [10] Papadopoulos, 2002, Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat, Ann Neurol source
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“In addition to the sprouting of pyramidal tract fibres, remodelling of transcallosal projections connecting the two motor cortices occurs.14,25”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Not checked yetcites [25] Liu, 2010, Bone marrow stromal cells enhance inter- and intracortical axonal connections after ischemic stroke in adult rats, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Importantly, neurorestorative treatments do not necessarily promote the growth of terminal axons distal to the site of injury, as was shown after delivery of the growth factors erythropoietin and vascular endothelial growth factor (VEGF).19,24”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Profound neurorestorative processes are induced in brain tissue in response to focal cerebral ischaemia.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, a comparably extended time window exists in which brain remodelling could be therapeutically modulated.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
hedged- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Neurons remote from and adjacent to the ischaemic lesion are enabled to sprout, and neural precursor cells that accumulate with cerebral microvessels in the perilesional tissue further stimulate brain plasticity and neurological recovery.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Recent laboratory findings suggest that it might be possible to promote cerebral plasticity and neurological recovery after stroke by use of exogenous pharmacological or cell-based treatments.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“Thus, the injured brain exhibits a re-emergence of childhood organisational patterns, reminiscent of an ontogenetic state.5”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
What the sources say
- Not checked yetcites [5] Cramer, 2000, Recovery recapitulates ontogeny, Trends Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Surviving pyramidal tract axons distal to the site of ischaemic injury sprout.19”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Clearly, this endogenous remodelling of the CNS is not sufficient to restore neurological function, and our goal is to capitalise on these recovery events to further stimulate and amplify endogenous restorative mechanisms by means of pharmacological or cell-based methods.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
boosted- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Terminal axonal sprouting is enhanced in both the ipsilesional19,24 and the contra lesional12,19 pyramidal tract system.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Post-ischaemic endogenous plasticity partly compensates for the loss of axons in target structures of damaged fibre bundles at various levels of the brain (eg, red nucleus and facial nucleus) and spinal cord.12,19,24”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In rodents, the survival of ischaemic pyramidal tract axons can be improved by pharmacological and cell-based treatments.26–28”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
- Not checked yetcites [27] Ding, 2008, Magnetic resonance imaging investigation of axonal remodeling and angiogenesis after embolic stroke in sildenafil-treated rats, J Cereb Blood Flow Metab source
- Not checked yetcites [28] Cui, 2010, Niacin treatment of stroke increases synaptic plasticity and axon growth in rats, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In view of the complexity of the systems involved, stroke treatments that stimulate and amplify these endogenous restorative mechanisms might also provoke unwanted side-effects.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“By sharp contrast with neuroprotection, the efficacy of neuro restorative therapies does not depend on the successful reperfusion of ischaemic brain tissue.11,12,15,17,21”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
What the sources say
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [21] Li, 2009, MRI identification of white matter reorganization enhanced by erythropoietin treatment in a rat model of focal ischemia, Stroke source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“After stroke, many patients, even elderly patients, show substantial neurological improvement.6”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
What the sources say
- Not checked yetcites [6] Dimyan, 2011, Neuroplasticity in the context of motor rehabilitation after stroke, Nat Rev Neurol source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Importantly, axonal growth responses are relatively uniform for different types of treatment: contralesional sprouting was evident after delivery of growth factors,19,24 neutralising antibodies directed against the axonal growth inhibitor NogoA,11,17 neurostimulants (eg, amphetamine), 29 and cell-based therapeutics, namely bone-marrow-derived stromal cells12,30 or neural pre cursor cells.15”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [29] Papadopoulos, 2009, Motor recovery and axonal plasticity with short-term amphetamine after stroke, Stroke source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Unfortunately, the studies of neural precursor cell ablation focused on structural tissue preservation in the first 24 h after stroke.43”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [43] Jin, 2010, Transgenic ablation of doublecortin-expressing cells suppresses adult neurogenesis and worsens stroke outcome in mice, Proc Natl Acad Sci USA source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Contralesional sprouting after treatment with growth factors is associated with profound alterations of gene expression, including the downregulation of axonal growth inhibitors19,24 and inflammatory signals19,31 in the vicinity of the contralesional pyramidal tract.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [31] Herz, 2011, Intracerebroventricularly delivered VEGF promotes contralesional corticorubral plasticity after focal cerebral ischemia via mechanisms involving anti-inflammatory actions, Neurobiol Dis source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Enhanced plasticity and neurological recovery after stroke were evident not only in young but also in older animals.17,26,33”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
- Not checked yetcites [33] Zhang, 2006, Delayed treatment with sildenafil enhances neurogenesis and improves functional recovery in aged rats after focal cerebral ischemia, J Neurosci Res source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“After stroke, angiogenic factors are expressed by neurons and astrocytes, which induce microvascular growth.4,47–50”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [4] Hermann, 2009, Implications of vascular endothelial growth factor for postischemic neurovascular remodeling, J Cereb Blood Flow Metab source
- Not checked yetcites [47] Forsythe, 1996, Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1, Mol Cell Biol source
- Not checked yetcites [48] Marti, 2000, Hypoxia-induced vascular endothelial growth factor expression precedes neovascularization after cerebral ischemia, Am J Pathol source
- Not checked yetcites [49] Wang, 2005, VEGF overexpression induces post-ischaemic neuroprotection, but facilitates haemodynamic steal phenomena, Brain source
- Not checked yetcites [50] Kilic, 2006, The phosphatidylinositol-3 kinase/Akt pathway mediates VEGF's neuroprotective activity and induces blood brain barrier permeability after focal cerebral ischemia, FASEB J source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This fact raises doubts about the contribution of neuronal cell replacement to neurological recovery.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, evidence for axonal remodelling in response to stroke that is amplified by restorative therapy is robust in the laboratory setting.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
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In the paper
“Neurogenesis is sustained in the germinal niches in the subventricular zone of the lateral ventricle and the subgranular layer of the dentate gyrus, which host neural precursor cells even during adulthood.34,35”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [34] Zhang, 2001, Proliferation and differentiation of progenitor cells in the cortex and the subventricular zone in the adult rat after focal cerebral ischemia, Neuroscience source
- Not checked yetcites [35] Arvidsson, 2002, Neuronal replacement from endogenous precursors in the adult brain after stroke, Nat Med source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The finding that neural precursor cells prevent ischaemic injury and promote neurological recovery could be attributed to bystander effects related to the interaction of neuroblasts with the microvasculature in the vicinity of the ischaemic lesion, which creates an environment that promotes brain remodelling (figure 2).14,15,37,45”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
- Not checked yetcites [37] Thored, 2007, Long-term neuroblast migration along blood vessels in an area with transient angiogenesis and increased vascularization after stroke, Stroke source
- Not checked yetcites [45] Teng, 2008, Coupling of angiogenesis and neurogenesis in cultured endothelial cells and neural progenitor cells after stroke, J Cereb Blood Flow Metab source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“After treatment with bone-marrow-derived stromal cells, structural effects on the preservation of corticospinal axons persisted for up to 1 year.26”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Meanwhile, evidence that neuro genesis contributes to functional neurological recovery has been obtained in studies with transgenic ablation of neural precursor cells expressing the marker doublecortin43 and in studies with exogenous delivery of adult neural precursor cells,14,15,44 which reported impaired or enhanced neurological recovery, respectively.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [43] Jin, 2010, Transgenic ablation of doublecortin-expressing cells suppresses adult neurogenesis and worsens stroke outcome in mice, Proc Natl Acad Sci USA source
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
- Not checked yetcites [44] Bliss, 2007, Cell transplantation therapy for stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This lateral inhibition, which is a key process underlying structural development during ontogeny, is recapitulated after ischaemia.53–55”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [53] Al Haj Zen, 2010, Inhibition of delta-like-4-mediated signaling impairs reparative angiogenesis after ischemia, Circ Res source
- Not checked yetcites [54] Takeshita, 2007, Critical role of endothelial Notch1 signaling in postnatal angiogenesis, Circ Res source
- Not checked yetcites [55] Zacharek, 2009, Simvastatin increases notch signaling activity and promotes arteriogenesis after stroke, Stroke source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Importantly, neuroblasts also reinforce angiogenesis via release of VEGF.45”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [45] Teng, 2008, Coupling of angiogenesis and neurogenesis in cultured endothelial cells and neural progenitor cells after stroke, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In healthy tissue, chondroitin sulphate proteoglycans are secreted by both astrocytes and oligodendrocytes to create a growth-repulsive microenvironment for axons and dendrites.1,63”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The spatial orientation and distribution of fibres were shown to be controlled by leucine-rich repeat and IgG domain containing protein 1 (Lingo1) and Nogo receptor 1, which directed the newly formed axons to cortical areas that were otherwise not targeted.72”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Therapeutic inter ventions promoting axonal plasticity, such as delivery of VEGF or bone-marrow-derived stromal cells, further decrease proteoglycan levels.24,65”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [65] Shen, 2008, Downregulation of neurocan expression in reactive astrocytes promotes axonal regeneration and facilitates the neurorestorative effects of bone marrow stromal cells in the ischemic rat brain, Glia source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The interactions between endothelial cells and neuroblasts are especially strong during the first month after stroke.57,58”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [57] Chen, 2005, Endothelial nitric oxide synthase regulates brain-derived neurotrophic factor expression and neurogenesis after stroke in mice, J Neurosci source
- Not checked yetcites [58] Wang, 2006, Matrix metalloproteinase 2 (MMP2) and MMP9 secreted by erythropoietin-activated endothelial cells promote neural progenitor cell migration, J Neurosci source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Reduced neurogenesis in old animals could be related to lower expression of VEGFR2 on the surface of neural precursor cells, as reported in 2-year-old mice compared with 3-month-old or 12-month-old mice.79”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [79] Gao, 2009, Attenuation of brain response to vascular endothelial growth factor-mediated angiogenesis and neurogenesis in aged mice, Stroke source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Neuronal growth responses include sets of signals that have to be activated synergistically so that axonal outgrowth can occur.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The tumour suppressor phosphatase and tensin homolog (PTEN) and its downstream target mammalian target of rapamycin (mTOR), for example, were shown to induce the sprouting of apical but not basal dendrites of mouse cortical layer 2/3 pyramidal neurons.71”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [71] Chow, 2009, Laminar and compartmental regulation of dendritic growth in mature cortex, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, insulin-like growth factor 1 was localised mainly to astrocytes in the periinfarct cortex of 2-month-old rats, but exhibited predominantly neuronal labelling in 2-year-old rats.72”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition to these cell-specific actions, astrocytes and oligodendrocytes release proteins and proteoglycans into the extracellular space that directly modulate neuronal plasticity and growth.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In the case of treatment with bone-marrow-derived stromal cells, neurological improvements persisted in middle-aged rats (12 months of age) for at least 1 year.26”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As such, microvascular sprouting and neurogenesis bidirectionally promote each other (figure 2).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“By contrast with the astrocytic and oligodendroglial proteoglycans, neuronal growth signals have a high degree of specificity for some but not other neuronal populations and for defined plasticity processes (figure 3).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The numbers of proliferating neural pre cursor cells in the subventricular zone and subgranular layer were lower in the brain tissue of 15-month-old rats than in that of 3-month-old rats, both under normal physiological and ischaemic conditions.78”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [78] Darsalia, 2005, Stroke-induced neurogenesis in aged brain, Stroke source
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In the paper
“In the peri-infarct tissue, newly formed vessels create a milieu for the migration, homing, and neuronal differentiation of neuroblasts via release of stromal derived factor 1, VEGF, and matrix metalloproteinases 2 and 9, which attract neuroblasts.58,59”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [58] Wang, 2006, Matrix metalloproteinase 2 (MMP2) and MMP9 secreted by erythropoietin-activated endothelial cells promote neural progenitor cell migration, J Neurosci source
- Not checked yetcites [59] Chopp, 2007, Neurogenesis, angiogenesis, and MRI indices of functional recovery from stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“PTEN and mTOR were not involved in induction of dendritic plasticity in layer 5 pyramidal neurons.71”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [71] Chow, 2009, Laminar and compartmental regulation of dendritic growth in mature cortex, Nat Neurosci source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In response to focal cerebral ischaemia, these proteoglycans are downregulated in areas exhibiting axonal growth over a period of 2–3 weeks after stroke.64”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
- Not checked yetcites [64] Carmichael, 2005, Growth-associated gene expression after stroke: evidence for a growth-promoting region in peri-infarct cortex, Exp Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The dynamic responses of neurons after stroke require efficient mechanisms to prevent uncontrolled axonal or dendritic growth, thus ensuring that maladaptive sprouting does not occur.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Newly formed microvessels exert trophic influences on the brain parenchyma via release of growth factors, such as BDNF.57”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [57] Chen, 2005, Endothelial nitric oxide synthase regulates brain-derived neurotrophic factor expression and neurogenesis after stroke in mice, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Glutamatergic AMPA receptors contribute to learning-induced motor plasticity.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Lingo1 immuno staining, by contrast, was stronger in neurons of old rats (2 years of age) than in young rats (2 months of age).72”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Indeed, the expression of plasticity-related proteins in neurons differs between young and old animals.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Axonal sprouting of cortical neurons contralateral to the stroke has specific electrophysiological accompaniments characterised by low-frequency synchronised neuronal activity in the range of 0·2–2·0 Hz on day 1 and of 0·1–0·4 Hz on days 2–3.73”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [73] Carmichael, 2002, Synchronous neuronal activity is a signal for axonal sprouting after cortical lesions in the adult, J Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In patients, a close relation exists between blood flow and neurological improvement after stroke.56”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [56] Arkuszewski, 2009, Perfusion computed tomography in prediction of functional outcome in patients with acute ischaemic stroke, Nucl Med Rev Cent East Eur
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The continuous rehearsal of activation patterns provides the basis for temporally and spatially organised axonal growth (figure 3), an understanding of which could allow the development of rehabilitation strategies to reinforce the effects of neurorestorative therapies.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This enhanced perfusion directly provides for the metabolic needs of the tissue.4”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [4] Hermann, 2009, Implications of vascular endothelial growth factor for postischemic neurovascular remodeling, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Subsequent to ischaemic stroke, AMPA receptor activation by pharmacological allosteric modulators evokes the release of BDNF in the peri-infarct cortex, thus enhancing motor recovery.75”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [75] Clarkson, 2011, AMPA receptor-induced local brain-derived neurotrophic factor signaling mediates motor recovery after stroke, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Although evidence is limited, recent studies suggest that impaired angiogenesis in patients with hypercholesterolaemia parallels disturbances in synaptic plasticity.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [86] Chang, 2009, Age-related influence of the HDL receptor SR-BI on synaptic plasticity and cognition, Neurobiol Aging source
- Not checked yetcites [87] Hwang, 2010, Sex differences in high-fat diet-induced obesity, metabolic alterations and learning, and synaptic plasticity deficits in mice, Obesity source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: The effects of hypertension and hypercholesterolaemia on brain remodelling are not fully known.
None of the sources cited for this claim have been checked yet.
In the paper
“Similar findings about the importance of timing for administration of a neurorestorative therapy for stroke have been reported for VEGF94 and modulators of matrix metallo proteinases.95”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“NogoA deactivation initiated by genetic knockout or by intracerebral ventricular delivery of neutralising antibodies decreased neuronal survival and delayed neuronal recovery when the deactivation was constitutive or initiated 24 h before the stroke.93”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [93] Kilic, 2010, Role of Nogo-A in neuronal survival in the reperfused ischemic brain, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In view of the high prevalence of hypercholesterolaemia in stroke patients, blood lipids might be a suitable target for neurorestorative therapies.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: The effects of hypertension and hypercholesterolaemia on brain remodelling are not fully known.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In view of several discoveries showing the potential of neurons, brain microvascular cells, and glial cells to respond to pharmacological or cell-based restorative treatments under conditions of focal cerebral ischaemia, we are poised to promote stroke recovery in human beings.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The relevance of associated diseases for the efficacy of plasticity-promoting therapies was recently shown in rats with streptozotocin-induced diabetes.80”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Experiments in animals that are otherwise healthy poorly represent comorbidities.
In the paper
“The possibility of unfavourable effects of specific neurorestorative treatments when given at an inappropriate timepoint was suggested in a recent study of the effects of NogoA deactivation after transient focal cerebral ischaemia in mice.93”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [93] Kilic, 2010, Role of Nogo-A in neuronal survival in the reperfused ischemic brain, J Cereb Blood Flow Metab source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Crosslinks between neuronal plasticity and death have also been described for CD95 (Apo1/Fas).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [96] Reich, 2008, Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?, Trends Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Although evidence is limited to a rather small number of studies, the preserved neurological recovery in old animals argues against specific age limits for neurorestorative treatments.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Stroke occurs mainly in later life.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The need for primate studies relates to the organisation of neuronal networks, which is far more complex in human beings than in rodents.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Most current knowledge comes from laboratory animals, chiefly rodents.
None of the sources cited for this claim have been checked yet.
In the paper
“This preserved response to NogoA antibodies suggests that the growth factor abnormalities might not be clinically relevant.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [82] Hennigan, 2009, Deficits in LTP and recognition memory in the genetically hypertensive rat are associated with decreased expression of neurotrophic factors and their receptors in the dentate gyrus, Behav Brain Res source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“These vascular changes are driven by many factors, including reduced endothelial NO synthase (eNOS) activity, excessive lipid peroxidation, and overactivation of matrix metalloproteinases 2 and 9, calpain 1 and 2, and the small RhoGTPase RhoA.83,84”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [83] Duan, 2000, Hypercholesterolemia inhibits angiogenesis in response to hindlimb ischemia: nitric oxide-dependent mechanism, Circulation
- Not checked yetcites [84] ElAli, 2011, Increased blood–brain barrier permeability and brain edema after focal cerebral ischemia induced by hyperlipidemia: role of lipid peroxidation and calpain–1/2, matrix metalloproteinase–2/9, and rhoA overactivation, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In spontaneously hypertensive rats, subtle abnormalities in the expression of neuro trophic factors and their receptors, namely reduced levels of BDNF, neutrophins 3 and 4, TrkA, and TrkB, have been described in the dentate gyrus.82”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [82] Hennigan, 2009, Deficits in LTP and recognition memory in the genetically hypertensive rat are associated with decreased expression of neurotrophic factors and their receptors in the dentate gyrus, Behav Brain Res source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: The effects of hypertension and hypercholesterolaemia on brain remodelling are not fully known.
In the paper
“In mice receiving a high-fat diet, contextual fear conditioning and passive avoidance deficits were associated with reduced CA1 long-term potentiation and long-term depression.87”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [87] Hwang, 2010, Sex differences in high-fat diet-induced obesity, metabolic alterations and learning, and synaptic plasticity deficits in mice, Obesity source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These abnormalities were attributed to increased angiogenin expression in the brain and brain-supplying arteries of rats with diabetes.80”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The thrombolytic drug alteplase might compromise restorative stroke treatments, as shown in the recent German multicentre erythropoietin trial,90”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Drug interactions with the thrombolytic drug alteplase
What the sources say
- Not checked yetcites [90] Ehrenreich, 2009, Recombinant human erythropoietin in the treatment for acute ischemic stroke, Stroke source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In neurons and neural precursor cells, CD95 is not a death receptor.96”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [96] Reich, 2008, Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?, Trends Neurosci source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The promotion of brain remodelling and plasticity is not limited to a sharp and well defined therapeutic window.1–3”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [1] Carmichael, 2006, Cellular and molecular mechanisms of neural repair after stroke: making waves, Ann Neurol source
- Not checked yetcites [2] Murphy, 2009, Plasticity during stroke recovery: from synapse to behaviour, Nat Rev Neurosci source
- Not checked yetcites [3] Zhang, 2009, Neurorestorative therapies for stroke: underlying mechanisms and translation to the clinic, Lancet Neurol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Importantly, no effect on neuronal survival was reported when anti-NogoA antibodies were delivered after focal cerebral ischaemia.93”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [93] Kilic, 2010, Role of Nogo-A in neuronal survival in the reperfused ischemic brain, J Cereb Blood Flow Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Yet, because of the neurovascular remodelling processes activated in response to stroke, a time interval of a few days to months after stroke exists in which neurological recovery presumably is most promising.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In hypercholesterolaemic mice lacking scavenger receptor class B type I, age-related deficits of spatial memory have been described that were accompanied by impaired long-term potentiation of hippocampal CA1 neurons.86”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [86] Chang, 2009, Age-related influence of the HDL receptor SR-BI on synaptic plasticity and cognition, Neurobiol Aging source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Solid evidence exists for a contribution of pyramidal tract remodelling to functional recovery in stroke patients.101,102”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [101] Cramer, 1997, A functional MRI study of subjects recovered from hemiparetic stroke, Stroke source
- Not checked yetcites [102] Gerloff, 2006, Multimodal imaging of brain reorganization in motor areas of the contralesional hemisphere of well recovered patients after capsular stroke, Brain source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Genetic influences on corticospinal plasticity have recently been shown in human beings by using transcranial magnetic stimulation techniques, whereby healthy patients carrying the Val66Met polymorphism in the BDNF gene exhibited significantly smaller training-induced increases in the amplitude of motor evoked potentials.103”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [103] Kleim, 2006, BDNF val66met polymorphism is associated with modified experience-dependent plasticity in human motor cortex, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Stroke patients vary substantially in age and genetic background, as well as in the aetiology, localisation, and size of brain infarcts (panel 1).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites panel 1
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This finding paves the way for neurorestorative therapies far into the rehabilitation phase.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Since sprouting axons need to cover larger distances in human beings than in rodents, the contribution of axonal plasticity to neurological recovery might be diminished.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An important species difference relates to the anatomical size of the brain, which is about an order of magnitude larger (in terms of length measures) in human beings than in rodents (panel 1).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites panel 1
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In each of these cases, the thera peutic intervention was associated with a deterioration of neurological state and structural brain damage (panel 2).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites panel 2
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“In view of the Janus-like role of brain-repair signals for neuronal injury,5,100 the initiation of neurorestorative therapies in the very acute phase of stroke would probably induce more undesirable effects than would treatment in the very late (chronic) phase.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Animal studies have identified medical conditions that specifically undermine neurorestorative therapies by making the brain prone to detrimental responses.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
- Not checked yetcites [91] Zechariah, 2010, Combination of tissue-plasminogen activator with erythropoietin induces blood–brain barrier permeability, extracellular matrix disaggregation and DNA fragmentation after focal cerebral ischemia in mice, Stroke source
- Not checked yetcites [92] Jia, 2010, Erythropoietin in combination with tissue plasminogen activator exacerbates brain hemorrhage when treatment is initiated 6 hours after stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Heterogeneous patient populations could be a reason for the failure of therapeutic interventions because they might dilute the benefits of treatment.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 54
- Probably not a substantial claim. 9
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Despite the robust evidence for specific time windows in which neuronal plasticity and angiogenesis are most active,64,66,67 neurorestorative treatments were still successful in animals once brain remodelling was induced months after the stroke.18,20”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [64] Carmichael, 2005, Growth-associated gene expression after stroke: evidence for a growth-promoting region in peri-infarct cortex, Exp Neurol source
- Partly supportedcites [66] Shen, 2010, Astrocytic endogenous glial cell derived neurotrophic factor production is enhanced by bone marrow stromal cell transplantation in the ischemic boundary zone after stroke in adult rats, Glia sourceExperimental — accuracy not yet measured
The Introduction reports that bone marrow stromal cell transplantation ameliorates functional deficits in rodent stroke models. But this paper administered cells 24 hours after ischemia and assessed the animals eight days after stroke (Materials and Methods; Discussion), not months later. A one-month treatment appears only in a cited study’s title in the References; the paper does not establish the claimed months-later timing or sequence of brain remodelling. (LLM, conf=0.88)
- Partly supportedcites [67] Zacharek, 2007, Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke, J Cereb Blood Flow Metab sourceExperimental — accuracy not yet measured
The study reports that MSC treatment promoted angiogenesis and vascular stabilization in rats after stroke. But the Methods passage (indexed as Abstract; page unavailable) says MSCs were given 24 hours after stroke, with measurements at 4 and 14 days. It does not support successful treatment initiated months after stroke. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Additionally, brain capillaries sprout, and glial cells are activated to create a favourable cerebral environment for neuronal growth and plasticity.3,4”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
What the sources say
- Not checked yetcites [3] Zhang, 2009, Neurorestorative therapies for stroke: underlying mechanisms and translation to the clinic, Lancet Neurol source
- Not checked yetcites [4] Hermann, 2009, Implications of vascular endothelial growth factor for postischemic neurovascular remodeling, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These factors interact in a highly dynamic way, facilitating temporally and spatially orchestrated responses of brain networks.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Neuroprotective agents must be delivered to the site of ischaemic injury, which by definition includes tissue that is highly underperfused. Neurorestorative therapies target viable tissue with adequate and intact perfusion.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Many endogenous restorative responses, including neuronal plasticity, neurogenesis, and angiogenesis, can be targeted with pharmacological or cell-based treatments to stimulate neurological recovery after stroke.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“By contrast with neuroprotection, which requires an acute intervention, treatments promoting neurological recovery by remodelling of brain tissue can be instituted during the stroke recovery phase.10–15”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Benefits of neurorestorative therapies
What the sources say
- Not checked yetcites [10] Papadopoulos, 2002, Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat, Ann Neurol source
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
- Not checked yetcites [13] Kilic, 2008, Delayed melatonin administration promotes neuronal survival, neurogenesis and motor recovery, and attenuates hyperactivity and anxiety after mild focal cerebral ischemia in mice, J Pineal Res source
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While neuronal plasticity is actively inhibited during adulthood, a crucial time window opens in the post-acute ischaemic phase that is characterised by intense neuronal sprouting.1,2”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Introduction
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In experimental studies, adverse effects have been identified when neurorestorative treatments were administered to animals with severe associated illnesses, after thrombolysis with alteplase, and when therapies were initiated outside appropriate time windows.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Stroke induces anterograde Wallerian degeneration of pyramidal tract axons, the degree of which depends on the severity of the ischaemic insult (figure 1).19,21,22”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [21] Li, 2009, MRI identification of white matter reorganization enhanced by erythropoietin treatment in a rat model of focal ischemia, Stroke source
- Not checked yetcites [22] Liu, 2009, Remodeling of the corticospinal innervation and spontaneous behavioral recovery after ischemic stroke in adult mice, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Neurons remote from and adjacent to the ischaemic lesion are enabled to sprout, and neural precursor cells that accumulate with cerebral microvessels in the perilesional tissue further stimulate brain plasticity and neurological recovery.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Neurogenesis is stimulated in response to stroke and is substantially amplified by therapeutic interventions that promote functional recovery.33–36”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [33] Zhang, 2006, Delayed treatment with sildenafil enhances neurogenesis and improves functional recovery in aged rats after focal cerebral ischemia, J Neurosci Res source
- Not checked yetcites [34] Zhang, 2001, Proliferation and differentiation of progenitor cells in the cortex and the subventricular zone in the adult rat after focal cerebral ischemia, Neuroscience source
- Not checked yetcites [35] Arvidsson, 2002, Neuronal replacement from endogenous precursors in the adult brain after stroke, Nat Med source
- Not checked yetcites [36] Chen, 2003, Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke, Ann Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Microvessels and neuroblasts mutually support each other via release of trophic factors, resulting in a tight interplay that stimulates brain remodelling processes, reducing delayed neuronal degeneration,14,45 promoting neuronal plasticity,15 modulating glial responses,14,46 and attenuating brain inflammation14,46 (figure 2).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [14] Bacigaluppi, 2009, Delayed post-ischaemic neuroprotection following systemic neural stem cell transplantation involves multiple mechanisms, Brain source
- Not checked yetcites [45] Teng, 2008, Coupling of angiogenesis and neurogenesis in cultured endothelial cells and neural progenitor cells after stroke, J Cereb Blood Flow Metab source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
- Not checked yetcites [46] Lee, 2008, Antiinflammatory mechanism of intravascular neural stem cell transplantation in haemorrhagic stroke, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The survival rate of adult neural precursor cells in the brain parenchyma is poor and only a small percentage of the cells differentiate into neurons.35,39–42”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [35] Arvidsson, 2002, Neuronal replacement from endogenous precursors in the adult brain after stroke, Nat Med source
- Not checked yetcites [39] Zhang, 2004, Stroke transiently increases subventricular zone cell division from asymmetric to symmetric and increases neuronal differentiation in the adult rat, J Neurosci source
- Not checked yetcites [40] Bacigaluppi, 2008, Neural stem/precursor cells for the treatment of ischemic stroke, J Neurol Sci source
- Not checked yetcites [41] Zhang, 2011, Ascl1 lineage cells contribute to ischemia-induced neurogenesis and oligodendrogenesis, J Cereb Blood Flow Metab source
- Not checked yetcites [42] Doeppner, 2011, Acute hepatocyte growth factor treatment induces long-term neuroprotection and stroke recovery via mechanisms involving neural precursor cell proliferation and differentiation, J Cereb Blood Flow Metab source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“Acting through VEGF receptor 2 (VEGFR2), which is localised at high concentrations at the tip of newly formed capillaries, VEGF induces endothelial proliferation,4,47–49 and concur rently upregulates the transmembrane ligand delta-like ligand 4, which signals to microvascular cells in the capillary stalk, to downregulate VEGFR2 via interaction with its receptor Notch 1, thus pre venting uncontroll”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [4] Hermann, 2009, Implications of vascular endothelial growth factor for postischemic neurovascular remodeling, J Cereb Blood Flow Metab source
- Not checked yetcites [47] Forsythe, 1996, Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1, Mol Cell Biol source
- Not checked yetcites [48] Marti, 2000, Hypoxia-induced vascular endothelial growth factor expression precedes neovascularization after cerebral ischemia, Am J Pathol source
- Not checked yetcites [49] Wang, 2005, VEGF overexpression induces post-ischaemic neuroprotection, but facilitates haemodynamic steal phenomena, Brain source
- Not checked yetcites [51] Ridgway, 2006, Inhibition of Dll4 signalling inhibits tumour growth by deregulating angiogenesis, Nature source
- Not checked yetcites [52] Hellström, 2007, Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“When a stroke occurs, these cells proliferate and migrate in the direction of the ischaemic lesion, propagating in chains along blood vessels.37,38”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neurogenesis
What the sources say
- Not checked yetcites [37] Thored, 2007, Long-term neuroblast migration along blood vessels in an area with transient angiogenesis and increased vascularization after stroke, Stroke source
- Not checked yetcites [38] Zhang, 2009, Patterns and dynamics of subventricular zone neuroblast migration in the ischemic striatum of the adult mouse, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This lesion-remote plasticity involves the midline crossing of fibres from the contralesional to the ipsilesional hemisphere at the level of the red nucleus10,17,19,24 and the re-entry of fibres into the contralesional hemicord at the level of the cervical spinal cord (figure 1).11,12,15”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Neuronal plasticity
What the sources say
- Not checked yetcites [10] Papadopoulos, 2002, Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat, Ann Neurol source
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [19] Reitmeir, 2011, Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract plasticity, Brain source
- Not checked yetcites [24] Reitmeir, 2012, Vascular endothelial growth factor induces contralesional corticobulbar plasticity and functional neurological recovery in the ischemic brain, Acta Neuropathol source
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
- Not checked yetcites [12] Liu, 2008, Contralesional axonal remodeling of the corticospinal system in adult rats after stroke and bone marrow stromal cell treatment, Stroke source
- Not checked yetcites [15] Andres, 2011, Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain, Brain source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“AMPA receptor antagonists impair neurological outcome, as does blockade of BDNF by TrkB-Fc-impregnated hydrogel.75”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [75] Clarkson, 2011, AMPA receptor-induced local brain-derived neurotrophic factor signaling mediates motor recovery after stroke, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In the peri-infarct cortex of the lesioned hemisphere, tonic inhibition of layer 2/3 pyramidal neurons was present from 3–14 days after stroke and was mediated by extrasynaptic GABAA receptors.74”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [74] Clarkson, 2010, Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Subsequent to focal cerebral ischaemia, and in parallel to the downregulation of growth-repulsive proteoglycans, astrocytes de novo express neurotrophic factors, such as glial-cell-line-derived neurotrophic factor (GDNF)66 and VEGF,67 and serine proteases, namely tissue plasminogen activator (tPA).68”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
- Not checked yetcites [66] Shen, 2010, Astrocytic endogenous glial cell derived neurotrophic factor production is enhanced by bone marrow stromal cell transplantation in the ischemic boundary zone after stroke in adult rats, Glia source
- Not checked yetcites [67] Zacharek, 2007, Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke, J Cereb Blood Flow Metab source
- Not checked yetcites [68] Xin, 2010, Increasing tPA activity in astrocytes induced by multipotent mesenchymal stromal cells facilitate neurite outgrowth after stroke in the mouse, PLoS One source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“From a systems biological perspective, an intervention that modulates endogenous restorative responses, such as axonal growth, neurogenesis, and angiogenesis, will probably alter tissue homoeostasis and could lead to adverse side-effects.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The continuous rehearsal of activation patterns provides the basis for temporally and spatially organised axonal growth (figure 3), an understanding of which could allow the development of rehabilitation strategies to reinforce the effects of neurorestorative therapies.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
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Probably not a substantial claim. It may be too vague to check against evidence.
In the paper
“Astrocytes also remove excitatory neurotransmitters (eg, glutamate) and electrolytes (eg, potassium) from the extracellular space, thus controlling neuronal excitability and enabling synaptic plasticity.62”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
- Not checked yetcites [62] Pannasch, 2011, Astroglial networks scale synaptic activity and plasticity, Proc Natl Acad Sci USA source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Delivery of bone-marrow-derived stromal cells or mesenchymal stromal cells was shown to further increase levels of GDNF66 and tPA68,69 and reduce levels of the tPA inhibitor plasminogen activator inhibitor 1.70”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
What the sources say
- Not checked yetcites [66] Shen, 2010, Astrocytic endogenous glial cell derived neurotrophic factor production is enhanced by bone marrow stromal cell transplantation in the ischemic boundary zone after stroke in adult rats, Glia source
- Not checked yetcites [68] Xin, 2010, Increasing tPA activity in astrocytes induced by multipotent mesenchymal stromal cells facilitate neurite outgrowth after stroke in the mouse, PLoS One source
- Not checked yetcites [69] Shen, 2011, Endogenous tissue plasminogen activator mediates bone marrow stromal cell-induced neurite remodeling after stroke in mice, Stroke source
- Not checked yetcites [70] Xin, 2011, Multipotent mesenchymal stromal cells increase tPA expression and concomitantly decrease PAI-1 expression in astrocytes through the sonic hedgehog signaling pathway after stroke (in vitro study), J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Glial cells, especially astrocytes, control brain homoeostasis and create a microenvironment for successful brain remodelling.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Neuronal activity induces temporally and spatially tuned responses in the brain (figure 3).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An effect of age was not only seen for neuronal sprouting, but also for neurogenesis and angiogenesis.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Astrocytes and oligodendrocytes provide basic trophic support that is independent of brain region or surrounding neuronal populations, thus setting the stage for brain plasticity processes (figure 3).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Glial cells in brain remodelling and plasticity
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“A pharmacological antagonist of the GABAA receptor α5 subunit prevented the excessive inhibition, as did genetic deletion of the GABAA receptor α5 or δ subunits, and improved stroke recovery.74”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [74] Clarkson, 2010, Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Aged rats respond to plasticity-promoting therapies, but age might have an effect on some of the processes targeted by neurorestorative interventions.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
- Not checked yetcites [76] Zhang, 2005, Functional recovery in aged and young rats after embolic stroke: treatment with a phosphodiesterase type 5 inhibitor, Stroke source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Stroke occurs mainly in later life.
None of the sources cited for this claim have been checked yet.
In the paper
“Improved neurological recovery associated with preservation of pyramidal tract axons ipsilateral to the stroke and enhanced pyramidal tract sprouting contralateral to the stroke was identified in 25-month-old or 12-month-old rats with ischaemia treated with neutralising anti-NogoA antibodies,17 pharmacological compounds, 76 or bone-marrow-derived stromal cells.26”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [76] Zhang, 2005, Functional recovery in aged and young rats after embolic stroke: treatment with a phosphodiesterase type 5 inhibitor, Stroke source
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Although the de novo generation of neurons in the ischaemic striatum was very similar in both groups, neurogenesis was decreased in the dentate gyrus of 15-month-old rats when exposed to focal cerebral ischemia.78”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [78] Darsalia, 2005, Stroke-induced neurogenesis in aged brain, Stroke source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Studies on angiogenesis suggest that new vessel formation has roles in ischaemic brain remodelling after stroke that are independent of blood flow, and that angiogenesis contributes to stroke recovery in a substantive way.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Although neurological recovery was successful, dendritic and synaptic plasticity of hippocampal CA3 and CA1 pyramidal and dentate gyrus granule cells was not influenced by anti-NogoA antibodies in old rats (24 months of age), yet improvements in spatial memory were reported.77”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [77] Gillani, 2010, Cognitive recovery in the aged rat after stroke and anti-Nogo-A immunotherapy, Behav Brain Res source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In the rat somatosensory whisker barrel field, the ATP-dependent DNA-modifying enzyme α-thalassaemia/mental retardation syndrome X-linked (ATRX) protein, which controls neuronal survival and migration during brain development, contributes to the formation of axonal growth cones, which are stabilised by insulin-like growth factor 1.72”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Signals controlling axonal and dendritic sprouting
What the sources say
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The serine protease activated protein C enhances this neurovascular interplay, stimulating endothelial proliferation and tube formation60 and inducing proliferation and migration of neural precursor cells61 via protease-activated receptor 1.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Biological substrates for neurological recovery > Angiogenesis
What the sources say
- Not checked yetcites [60] Uchiba, 2004, Activated protein C induces endothelial cell proliferation by mitogen-activated protein kinase activation in vitro and angiogenesis in vivo, Circ Res source
- Not checked yetcites [61] Thiyagarajan, 2008, Activated protein C promotes neovascularization and neurogenesis in postischemic brain via protease–activated receptor 1, J Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In histo chemical studies, neointima formation and arteriole narrowing were exacerbated by bone-marrow-derived stromal cells in rats with diabetes, as was macrophage accumulation in blood vessels.80”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Instead, CD95 activation was shown to promote survival and differentiation of neural precursor cells, resulting in enhanced recovery of working memory in mice with global cerebral ischaemia.97”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [97] Corsini, 2009, The death receptor CD95 activates adult neural stem cells for working memory formation and brain repair, Cell Stem Cell source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“In cerebral endothelial cell culture, the effects of vitamin B3 on capillary tube formation were reduced after eNOS inhibition or Tie2 knockdown,85 showing a role for eNOS and angiopoietin 1 in the beneficial effects of the high-density lipoprotein elevation.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [85] Chen, 2007, Niaspan increases angiogenesis and improves functional recovery after stroke, Ann Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Neurons, cerebral microvascular cells, and glial cells respond synergistically to therapeutic interventions, creating an environment in which successful recovery can take place.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“In rats with cerebral ischaemia, vitamin B3 administration, which elevates high-density lipoprotein and thereby reduces serum cholesterol, increased angiogenesis, the expression of VEGF and angiopoietin 1, and enhanced the phosphorylation (ie, activation) of eNOS and the angiopoietin-1 receptor Tie2, thus improving neurological recovery.85”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [85] Chen, 2007, Niaspan increases angiogenesis and improves functional recovery after stroke, Ann Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“After focal cerebral ischaemia in rats, vitamin B3 was used to increase high-density lipoprotein concentrations, which enhanced white matter remodelling in the peri-infarct tissue, increased BDNF and TrkB levels, and down regulated Nogo-receptor levels.88”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [88] Cui, 2010, Niacin treatment of stroke increases synaptic plasticity and axon growth in rats, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Hypercholesterolaemia reduces angiogenesis83 and promotes blood–brain barrier permeability.84”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [83] Duan, 2000, Hypercholesterolemia inhibits angiogenesis in response to hindlimb ischemia: nitric oxide-dependent mechanism, Circulation
- Not checked yetcites [84] ElAli, 2011, Increased blood–brain barrier permeability and brain edema after focal cerebral ischemia induced by hyperlipidemia: role of lipid peroxidation and calpain–1/2, matrix metalloproteinase–2/9, and rhoA overactivation, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The effects of hypertension and hypercholesterolaemia on brain remodelling are not fully known.
None of the sources cited for this claim have been checked yet.
In the paper
“Although restorative treat ments can promote neurological recovery in old ani mals,17,26,72,76–79 specific findings in ageing animals72,77–79 and in animals with vascular risk factors80,82,86,87 suggest that the efficacy of new therapeutics might be compromised in elderly patients with risk factors.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [17] Markus, 2005, Recovery and brain reorganization after stroke in adult and aged rats, Ann Neurol source
- Not checked yetcites [26] Shen, 2007, One-year follow-up after bone marrow stromal cell treatment in middle-aged female rats with stroke, Stroke source
- Not checked yetcites [72] Li, 2010, An age-related sprouting transcriptome provides molecular control of axonal sprouting after stroke, Nat Neurosci source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Experiments in animals that are otherwise healthy poorly represent comorbidities.
In the paper
“In focal cerebral ischaemia, spontaneously hypertensive rats had preserved contralesional pyramidal tract sprouting in response to treatment with neutralising antibodies directed against NogoA, which was consistent with functional neurological improvements that were very similar to those in non-hypertensive rats.11”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [11] Wiessner, 2003, Anti-Nogo-A antibody infusion 24 hours after experimental stroke improved behavioral outcome and corticospinal plasticity in normotensive and spontaneously hypertensive rats, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Enhanced neurogenesis is associated with enhanced neuronal survival in most but not all conditions: in a recent study examining effects of ephrin-B3 deficiency, enhanced proliferation and survival of endogenous neural precursor cells but exacerbation of ischaemic injury were reported.99”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [99] Doeppner, 2011, Enhancement of endogenous neurogenesis in ephrin-B3 deficient mice after transient focal cerebral ischemia, Acta Neuropathol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Unexpectedly, erythropoietin did not improve clinical outcome in stroke patients but increased the risk of serious complications, namely death, bleeding, oedema, and thromboembolic events in patients who received alteplase.90”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Drug interactions with the thrombolytic drug alteplase
What the sources say
- Not checked yetcites [90] Ehrenreich, 2009, Recombinant human erythropoietin in the treatment for acute ischemic stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Neural surface receptors integrate signals with diverse functions, such as neuronal injury and repair,96 which depending on the pathophysiological context could have Janus-like roles in the ischaemic brain.5,100”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [96] Reich, 2008, Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?, Trends Neurosci source
- Not checked yetcites [5] Cramer, 2000, Recovery recapitulates ontogeny, Trends Neurosci source
- Not checked yetcites [100] Lo, 2008, A new penumbra: transitioning from injury into repair after stroke, Nat Med source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“With respect to clinical translation, these studies have two important limitations: the predominance of studies in young, otherwise healthy animals and the scarcity of studies in non-human primates.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Experiments in animals that are otherwise healthy poorly represent comorbidities.
- Rests on an assumption: Most current knowledge comes from laboratory animals, chiefly rodents.
None of the sources cited for this claim have been checked yet.
In the paper
“Subsequent experimental studies have shown that erythropoietin activated matrix metalloproteinases 2 and 9 after focal cerebral ischaemia, an effect that was potentiated by alteplase, thus provoking blood–brain barrier leakage, brain oedema, and haemorrhagic transformation of brain infarcts.91,92”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Drug interactions with the thrombolytic drug alteplase
What the sources say
- Not checked yetcites [91] Zechariah, 2010, Combination of tissue-plasminogen activator with erythropoietin induces blood–brain barrier permeability, extracellular matrix disaggregation and DNA fragmentation after focal cerebral ischemia in mice, Stroke source
- Not checked yetcites [92] Jia, 2010, Erythropoietin in combination with tissue plasminogen activator exacerbates brain hemorrhage when treatment is initiated 6 hours after stroke, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Para doxically, treatment with bone-marrow-derived stromal cells did not improve neurological recovery in rats with diabetes, but increased mortality, blood–brain barrier leakage, and brain haemorrhage.80”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In embryonic hippocampal and cortical neurons, activation of CD95 stimulated neurite branching, which occurred in a caspase-independent and death-domain-dependent manner and was paralleled by an increase in non-phosphorylated Tau.98”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Timing of treatment and crosslinks between neuronal plasticity and death
What the sources say
- Not checked yetcites [98] Zuliani, 2006, Control of neuronal branching by the death receptor CD95 (Fas/Apo-1), Cell Death Differ source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Fibre bundles are frequently affected by strokes, in human beings, because of the large contribution of white matter to the whole brain volume (panel 1) and the common manifestation of strokes in deep brain structures.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites panel 1
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“After delivery of an adeno-associated viral VEGF vector, both proliferation of neural precursor cells and formation of brain capillaries were compromised in old mice (24 months).79”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with age
What the sources say
- Not checked yetcites [79] Gao, 2009, Attenuation of brain response to vascular endothelial growth factor-mediated angiogenesis and neurogenesis in aged mice, Stroke source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“in which 522 patients were randomly assigned to receive placebo or erythropoietin within 6 h after ischaemic stroke. 331 (63%) patients in this study received alteplase treatment.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Drug interactions with the thrombolytic drug alteplase
What the sources say
- Not checked yetcites [90] Ehrenreich, 2009, Recombinant human erythropoietin in the treatment for acute ischemic stroke, Stroke source
plainn = 522- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Statins also have neurorestorative properties (ie, promotion of neuronal survival, angiogenesis, and neurogenesis).36,89”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Potential limitations of neurorestorative therapies > Compromised brain remodelling and plasticity associated with vascular risk factors
What the sources say
- Not checked yetcites [36] Chen, 2003, Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke, Ann Neurol source
- Not checked yetcites [89] Kilic, 2005, Post-ischemic delivery of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin protects against focal cerebral ischemia in mice via inhibition of extracellular-regulated kinase-1/-2, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Such findings have been reported for severe associated systemic diseases (ie, diabetic vasculopathy),80 subsequent to systemic thrombolysis,91,92 and when restorative treat ments were initiated at inappropriate timepoints (ie, before stroke;93 table).”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [80] Chen, 2011, Adverse effects of bone marrow stromal cell treatment of stroke in diabetic rats, Stroke source
- Not checked yetcites [91] Zechariah, 2010, Combination of tissue-plasminogen activator with erythropoietin induces blood–brain barrier permeability, extracellular matrix disaggregation and DNA fragmentation after focal cerebral ischemia in mice, Stroke source
- Not checked yetcites [92] Jia, 2010, Erythropoietin in combination with tissue plasminogen activator exacerbates brain hemorrhage when treatment is initiated 6 hours after stroke, Stroke source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, this evidence results from indirect outcome measures, such as MRI101 and electroencephalography,102 which provide infor mation about the macroscopic (ie, tissue), but not microscopic (ie, cellular or even subcellular) level.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
What the sources say
- Not checked yetcites [101] Cramer, 1997, A functional MRI study of subjects recovered from hemiparetic stroke, Stroke source
- Not checked yetcites [102] Gerloff, 2006, Multimodal imaging of brain reorganization in motor areas of the contralesional hemisphere of well recovered patients after capsular stroke, Brain source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“With these therapies, we can essentially treat all patients, and we are not hampered by reduced tissue perfusion, which restricts delivery of neuroprotective agents, nor by the requirement of rapid intervention, within hours after stroke.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A robust biological substrate to drive functional improvements is present in many stroke patients, even in elderly people.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Conclusions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although neurorestoration after stroke in animals seems relevant to human beings, testing restorative therapy in people is far more complex than in laboratory animals.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Most current knowledge comes from laboratory animals, chiefly rodents.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The benefits of restorative therapy are evident.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Conclusions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although experimental studies make use of defined pathophysiological states, to assess comparably uniform stroke lesions with defined topography in homogeneous, often genetically inbred, animals, the clinical setting is much more diverse and complex than are laboratory conditions.”
§ Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation > Consequences for clinical translation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Most current knowledge comes from laboratory animals, chiefly rodents.
The paper relies on this without support.
The restorative mechanisms observed in animal models are sufficiently similar to those in humans that therapies targeting them could promote human recovery.
“Promising results from experimental studies have subsequently led to clinical trials,3,7–9 the results of which are eagerly awaited.”
The paper relies on this without support.
Adverse effects seen in experimental animals under specific conditions predict potential adverse effects in human patients.
“In experimental studies, adverse effects have been identified when neurorestorative treatments were administered to animals with severe associated illnesses, after thrombolysis with alteplase, and when therapies were initiated outside appropriate time windows.”
The paper relies on this without support.
Stroke occurs mainly in later life.
“Stroke affects human beings mainly in the later stages of life.”
The paper relies on this without support.
Experiments in animals that are otherwise healthy poorly represent comorbidities.
“Experimental studies poorly mimic comorbidities, because experiments are done mainly in animals that are otherwise healthy.”
The paper relies on this without support.
The effects of hypertension and hypercholesterolaemia on brain remodelling are not fully known.
“The consequences of both risk factors for brain remodelling are not completely understood.”
The paper relies on this without support.
Most current knowledge comes from laboratory animals, chiefly rodents.
“Our current knowledge derives largely from laboratory animals, mainly rodents.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“This theory suggests that high frequency repetition should strengthen neural networks and minimize independent neuronal activation, potentially reducing maladaptive behaviors.2,12”
From A randomized control trial of intensive aphasia therapy after acute stroke: The Very Early Rehabilitation for SpEech (VERSE) study (2021) · cites this paper as [2]
In the citing paper
“Evidence from human motor and animal stroke recovery models suggests the first 90 days post stroke is the ‘window of opportunity’ 2 where the greatest potential to harness spontaneous recovery exists. 12”
From A randomized control trial of intensive aphasia therapy after acute stroke: The Very Early Rehabilitation for SpEech (VERSE) study (2021) · cites this paper as [2]
Citations
Cites
Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1
Forsythe, J. A., Jiang, B.-H., Iyer, N. V., Agani, F., Leung, S. W., Koos, R. D., & Semenza, G. L. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.9.4604 · Cited by 3,981
Neuronal replacement from endogenous precursors in the adult brain after stroke
Arvidsson, A., Collin, T., Kirik, D., Kokaia, Z., & Lindvall, O. (2002) · Nature Medicine · doi:10.1038/nm747 · Cited by 2,799
Plasticity during stroke recovery: from synapse to behaviour
Murphy, T. H., & Corbett, D. (2009) · Nature Reviews Neuroscience · doi:10.1038/nrn2735 · Cited by 1,938
Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis
Hellström, M., Phng, L.-K., Hofmann, J. J., Wallgard, E., Coultas, L., Lindblom, P., Alva, J., Nilsson, A.-K., Karlsson, L., Gaiano, N., et al. (2007) · Nature · doi:10.1038/nature05571 · Cited by 1,775
VEGF enhances angiogenesis and promotes blood–brain barrier leakage in the ischemic brain
Zhang, Z. G., Zhang, L., Jiang, Q., Zhang, R., Davies, K., Powers, C., Bruggen, N. V., & Chopp, M. (2000) · Journal of Clinical Investigation · doi:10.1172/jci9369 · Cited by 1,296
Self-citationA functional MRI study of subjects recovered from hemiparetic stroke
Cramer, S. C., Nelles, G., Benson, R. R., Kaplan, J. D., Parker, R. A., Kwong, K. K., Kennedy, D. N., Finklestein, S. P., & Rosen, B. R. (1997) · Stroke · doi:10.1161/01.str.28.12.2518 · Cited by 1,019
Inhibition of Dll4 signalling inhibits tumour growth by deregulating angiogenesis
Ridgway, J., Zhang, G., Wu, Y., Stawicki, S., Liang, W.-C., Chanthery, Y., Kowalski, J., Watts, R. J., Callahan, C., Kasman, I., et al. (2006) · Nature · doi:10.1038/nature05313 · Cited by 986
Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke
Sacco, R. L., Diener, H.-C., Yusuf, S., Cotton, D., Ôunpuu, S., Lawton, W. A., Palesch, Y., Martin, R. H., Albers, G. W., Bath, P., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0805002 · Cited by 961
Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke
Clarkson, A. N., Huang, B. S., MacIsaac, S. E., Mody, I., & Carmichael, S. T. (2010) · Nature · doi:10.1038/nature09511 · Cited by 869
Neuroplasticity in the context of motor rehabilitation after stroke
Dimyan, M. A., & Cohen, L. G. (2011) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.200 · Cited by 732
Research works printed but not linked: 1
- Cui, 2010, Niacin treatment of stroke increases synaptic plasticity and axon growth in rats, Stroke, 41, 2044, 10.1161/strokeaha.110.589333 · DOI · Paper page
Cited by
Sorted by citations
Doeppner, T. R., Herz, J., Görgens, A., Schlechter, J., Ludwig, A., Radtke, S., de Miroschedji, K., Horn, P. A., Giebel, B., & Hermann, D. M. (2015) · Stem Cells Translational Medicine · doi:10.5966/sctm.2015-0078 · Cited by 789
Self-citationSokoła-Wysoczańska, E., Wysoczański, T., Wagner, J., Czyż, K., Bodkowski, R., Lochyński, S., & Patkowska-Sokoła, B. (2018) · Nutrients · doi:10.3390/nu10101561 · Cited by 376
Exosomes/miRNAs as mediating cell-based therapy of stroke
Xin, H., Li, Y., & Chopp, M. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00377 · Cited by 307
Self-citationDávalos, A., Álvarez‐Sabín, J., Castillo, J., Díez‐Tejedor, E., Ferro, J. M., Martínez‐Vila, E., Serena, J. L., Segura, T., Cruz, V. T., Masjuán, J., et al. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60813-7 · Cited by 304
Human umbilical cord mesenchymal stem cells: an overview of their potential in cell-based therapy
Tan, L., Xia, M., Gao, Y., Chen, Y., & Xu, Y. (2015) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.2015.1051528 · Cited by 259
Metadata
- Authors
- Hermann, D. M., & Chopp, M.
- Affiliations
- Essen University Hospital (DE)
- Oakland University (US)
- Corresponding author
- Hermann, Dirk M
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 11
- Issue
- 4
- Pages
- 369-380
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC3964179
- OpenAlex
- W2112095855
- Cited by
- 333
- References
- 102
- Citations by year
- 2026: 15 · 2025: 10 · 2024: 15 · 2023: 14 · 2022: 15 · 2021: 21 · 2020: 35 · 2019: 28 · 2018: 24 · 2017: 25 · 2016: 35 · 2015: 33 · 2014: 20 · 2013: 36 · 2012: 7
- FWCI
- 3.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- German Research Foundation ((HE3173/2-1 and HE3173/3-1))
- National Institutes of Health ((AG037506))
- Topics
- Health Sciences › Medicine › Rehabilitation › Stroke Rehabilitation and Recovery
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- stroke recovery, neuroplasticity, neurorestoration, cell therapy, pharmacotherapy, cerebral microvasculature, glial cells, neural progenitor cells, perilesional tissue, ischemic stroke, alteplase thrombolysis, adverse effects, clinical translation, time window for treatment
- MeSH terms
- Animals, Neuronal Plasticity, Neovascularization, Physiologic, Stroke, Rats, Neurogenesis, Translational Research, Biomedical
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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