Cited by 35Stroke Rehabilitation and RecoveryNeurological Disorders and TreatmentsAcute Ischemic Stroke Management

Translating the frontiers of brain repair to treatments: Starting not to break the rules

Open access
Carmichael, S. Thomas·2010·Neurobiology of Disease

Abstract

The field of neural repair in stroke has identified cellular systems of reorganization and possible molecular mechanisms. Conceptual barriers now limit the generation of clinically useful agents. First, it is not clear what the causal mechanisms of neural repair are in stroke. Second, adequate delivery systems for neural repair drugs need to be determined for candidate molecules. Third, ad hoc applications of existing pharmacological agents that enhance attention, mood or arousal to stroke have failed. New approaches that specifically harness the molecular systems of learning and memory provide a new avenue for stroke repair drugs. Fourth, combinatorial treatments for neural repair need to be considered for clinical therapies. Finally, neural repair therapies have as a goal altering brain connections, cognitive maps and active neural networks. These actions may trigger a unique set of "neural repair side effects" that need to be considered in planning clinical trials.

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Crossref · 10.1016/j.nbd.2009.09.005

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  • Axonal sprouting after stroke shares similarities with the neuronal morphology changes in learning and memory paradigms, optic nerve and spinal cord regeneration and neurodevelopment.

    “Axonal sprouting after stroke shares similarities with the neuronal morphology changes in learning and memory paradigms, optic nerve and spinal cord regeneration and neurodevelopment36,37.”

    From GDF10 is a signal for axonal sprouting and functional recovery after stroke (2015) · cites this paper as [36]

    The “Learning and Memory, Peri-Infarct Cortex and Pharmacological Repair Therapies” section describes similar dendritic remodeling in stroke and learning-and-memory paradigms. “Combinatorial Treatments” discusses axonal growth in stroke, optic-nerve and spinal-cord injury models, and likens an induced growth state to an embryonic one. It does not establish the claimed similarity in neuronal morphology across all four settings; page numbers are unavailable in our copy. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

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Authors
Carmichael, S. T.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Carmichael, S. Thomas
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2010-02
Volume
37
Issue
2
Pages
237-242
ISSN
0969-9961 (ISSN-L)
OpenAlex
W2109474351
Cited by
35
References
88
Citations by year
2020: 2 · 2018: 2 · 2017: 5 · 2015: 2 · 2014: 2 · 2013: 7 · 2012: 2
FWCI
0.66
Type
journal article
Language
en
Open access
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (NS045729, NS053957)
  • Larry L. Hillblom Foundation
Topics
  • Health Sciences › Medicine › Rehabilitation › Stroke Rehabilitation and Recovery
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
Keywords
stroke, neural repair, neuroplasticity, drug delivery, combination therapy, neural network reorganization, cognitive maps, clinical translation
MeSH terms
Stroke Rehabilitation, Animals, Clinical Trials as Topic, Drug Evaluation, Preclinical, Humans, Nerve Regeneration, Neuronal Plasticity, Neuroprotective Agents, Nootropic Agents, Recovery of Function, Stroke, Physical Therapy Modalities, Translational Research, Biomedical

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