The DOI matches its Crossref record; 136 of the 136 references it cites were found in a registry or an index; 50 of the 166 sources its claims cite were checked for support.
The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease
Open accessAbstract
Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer's disease (AD). We examined the ability of the novel mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienl-yl) decyl triphenylphosphonium methanesulfonate]) to prevent AD-like pathology in mouse cortical neurons in cell culture and in a triple transgenic mouse model of AD (3xTg-AD). MitoQ attenuated β-amyloid (Aβ)-induced neurotoxicity in cortical neurons and also prevented increased production of reactive species and loss of mitochondrial membrane potential (Δψ(m)) in them. To determine whether the mitochondrial protection conferred by MitoQ was sufficient to prevent the emergence of AD-like neuropathology in vivo, we treated young female 3xTg-AD mice with MitoQ for 5 months and analyzed the effect on the progression of AD-like pathologies. Our results show that MitoQ prevented cognitive decline in these mice as well as oxidative stress, Aβ accumulation, astrogliosis, synaptic loss, and caspase activation in their brains. The work presented herein suggests a central role for mitochondria in neurodegeneration and provides evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative stress and metabolic failure, namely AD.
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Written from the paper’s full text.
TL;DR
MitoQ, a mitochondria-targeted antioxidant, prevented Aβ-induced oxidative stress and mitochondrial depolarization in cultured cortical neurons and blocked early cognitive decline and neuropathology in young female 3xTg-AD mice. The authors conclude that mitochondria-derived reactive species contribute centrally to early AD-like progression and that mitochondria-targeted therapy warrants further testing.
Key findings
- In cortical neuron cultures, Aβ(22–35) reduced survival to ~35% of untreated controls by 48 h; low nanomolar MitoQ (1–100 nM) greatly inhibited this toxicity, and 1 nM MitoQ also prevented death induced by full-length Aβ(1–40).
- Aβ(22–35) for 24 h increased CM-H2DCFDA intensity 3.4 ± 0.2-fold and depolarized Δψm; MitoQ (1 and 5 nM) prevented the reactive-species increase and maintained Δψm at control levels. In 3xTg-AD cortical cultures, 25 μM Aβ(22–35) increased CM-H2DCFDA 3.4 ± 0.2-fold (n = 34), and 10 nM MitoQ prevented this (0.3 ± 0.19-fold, n = 49).
- In female 3xTg-AD mice treated with 100 μM MitoQ in drinking water from 2–7 months of age, MitoQ prevented the long-term spatial memory retention deficit in the Morris water maze; acquisition performance was significantly improved versus untreated 3xTg-AD (p < 0.01), while the control compound dTPP had no effect (p > 0.05).
- MitoQ prevented brain oxidative stress markers (GSH/GSSG decrease, MDA increase, 3-nitrotyrosine increase), synaptic loss (synaptophysin), astrogliosis (GFAP), soluble and intraneuronal Aβ(1–42) accumulation, and caspase 3/7 activation; untreated 7-month 3xTg-AD mice showed a 3.0 ± 0.6-fold increase in cerebral caspase 3/7 activity versus nonTg, which MitoQ completely blocked.
Methods
- In vitro: primary mouse cortical neurons treated with Aβ(22–35) or Aβ(1–40), with or without MitoQ or dTPP; survival counted by phase-bright morphology, reactive species measured with CM-H2DCFDA, and mitochondrial membrane potential measured with TMRM+ confocal microscopy.
- In vivo: female 3xTg-AD and nonTg mice received 100 μM MitoQ or 100 μM dTPP continuously in drinking water from 2 to 7 months of age (5 months); a total of 117 mice were used. Spatial learning and memory retention were assessed by Morris water maze after 4.5 months of treatment.
- Postmortem analyses at 7 months included immunohistochemistry for Aβ(1–42), immunoblotting for Δtau, 3-nitrotyrosine, synaptophysin, and GFAP, ELISA for soluble Aβ(1–42), TBARS for lipid peroxidation, GSH/GSSG assay, and caspase 3/7 activity assay; statistics used Kruskal–Wallis one-way ANOVA on ranks with post hoc pairwise comparisons.
Limitations
- The paper states that only female mice were studied to minimize sex-related variability and reduce animal numbers, so findings may not generalize to male 3xTg-AD mice.
- The study assessed only early AD-like pathologies; the authors note that testing effects on neurofibrillary tangle formation would require treatment for up to 18 months, and Δtau was below detectable levels in 7-month-old untreated 3xTg-AD mice.
- The caspase assay does not distinguish between caspase 3 and caspase 7 activities. Evident from the text: in vivo MitoQ was adsorbed to cyclodextrin in a 1:2 complex, whereas the dTPP control was not cyclodextrin-complexed, so a cyclodextrin/vehicle effect was not fully controlled.
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Claims the paper makes
47 Own result · 29 Own interpretation · 26 Partly supported · 21 Not checked yet · 17 No full text of the sources · 11 Sources not found · 7 Supported · 4 Supported so far · 3 Own method · 2 No basis given · 1 Mixed support · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“To date, none of the tested compounds have proven effective (Sano et al., 1997; Petersen et al., 2005; Pham and Plakogiannis, 2005; DeKosky et al., 2008).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
What the sources say
- Disputedcites Sano et al., 1997 sourceExperimental — accuracy not yet measured
The Discussion reports that selegiline and alpha-tocopherol were beneficial in delaying the primary outcome of disease progression in patients with Alzheimer's disease. The paper does not report improved cognition, and the unadjusted analysis found no significant difference, but its adjusted analysis found significant delays. Its conclusion therefore runs contrary to the claim that none of the tested compounds had proven effective. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Partly supportedcites Petersen et al., 2005 sourceExperimental — accuracy not yet measured
The primary outcome measures report that vitamin E did not significantly reduce progression from mild cognitive impairment to Alzheimer’s disease. That supports a narrower claim about one antioxidant in a prevention trial, not a claim about all tested antioxidants treating Alzheimer’s disease. The paper’s introductory passage also reports evidence that vitamin E could delay important milestones in patients with moderately severe Alzheimer’s disease. (LLM, conf=0.86)
- Not matchedcites DeKosky et al., 2008
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Disputed
Every source the paper cites for this claim was checked and supports it.
In the paper
“Consistent with the findings of others (Saraiva et al., 2010), brief incubation with FCCP caused the loss of most CM-H2DCFDA fluorescence in Aβ(22–35)-treated cortical neurons (Fig. 2 B), suggesting that the RS detected by this dye was primarily of mitochondrial origin (Duchen, 1999).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Supportedcites Saraiva et al., 2010 source
The Results section ('Hexokinase activity blocks Aβ-induced generation of reactive oxygen species') reports that FCCP lowered ROS in Aβ-treated neurons below control levels and interprets this as evidence of a mitochondrial origin. The Methods section says ROS was measured in cortical neurons using CM-H2DCFDA. The Aβ(22–35) and Fig. 2B observations are the citing authors’ own experiment; Saraiva et al. provide the consistent finding attributed to them. (LLM, conf=0.90)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Extensive evidence indicates that alterations in glucose metabolism and mitochondrial energetics occur along with the accumulation of oxidative damage before the cardinal signs of AD pathogenesis in the brains of transgenic animal models and patients (Hoyer, 1996; Hirai et al., 2001; Rinaldi et al., 2003; Butterfield et al., 2006; Lin and Beal, 2006; Sultana et al., 2006a,b; Mosconi et al., 2008a;”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
What the sources say
- Not checked — no full text of the sourcecites Hoyer, 1996 source
- Not checked — no full text of the sourcecites Hirai et al., 2001 source
- Partly supportedcites Yao et al., 2009 sourceExperimental — accuracy not yet measured
The Results and Discussion report early mitochondrial dysfunction, altered glycolysis, and oxidative stress in female 3xTg-AD mice; the Discussion says mitochondrial dysfunction precedes plaque formation. It also describes reduced glucose use as an early finding in people at risk of AD, but does not establish that oxidative damage precedes the cardinal signs of AD in patients. (LLM, conf=0.86)
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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Aβ induces production of O2·- nitric oxide (NO·), and multiple RS downstream of these radicals in many cells, including cortical neurons (Keller et al., 1998; Longo et al., 2000; Keil et al., 2004; Malinski, 2007; Stepanichev et al., 2008; Díaz et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Partly supportedcites Keller et al., 1998 sourceExperimental — accuracy not yet measured
The Discussion links Aβ-induced apoptosis to superoxide and resulting peroxynitrite formation, and the results report increased peroxynitrite-related signals after Aβ exposure in PC6 cells (page unavailable in our copy). The paper does not show that Aβ induces nitric oxide production; it treats an NO-generating compound as a separate insult. The cited Aβ experiments also do not establish the claim specifically in cortical neurons or across many cell types. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites Longo et al., 2000 source
- Partly supportedcites Keil et al., 2004 sourceExperimental — accuracy not yet measured
The Discussion reports that increased Aβ levels led to increased nitric oxide production in APP-transfected PC12 and HEK cells, and discusses reactive nitrogen species and possible peroxynitrite-mediated damage. The passages do not establish Aβ-induced superoxide production or production of multiple downstream reactive species in cortical neurons; the neuronal-culture passage concerns mitochondrial activity, not those species. Page numbers are unavailable in our copy. (LLM, conf=0.87)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Furthermore, mitochondrial function and oxidative stress have been fully characterized only in female 3xTg-AD mice (Yao et al., 2009).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Mice
What the sources say
- Partly supportedcites Yao et al., 2009 sourceExperimental — accuracy not yet measured
The Results and Discussion (page not provided) characterize mitochondrial function and oxidative stress in female 3xTg-AD mice. The paper does not establish the broader claim that these measures had been fully characterized only in females. (LLM, conf=0.86)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Given the sensitivity of CM-H2DCFDA to oxidation by ONOO−, in combination with the propensity of ONOO− formation attributable to Aβ-induced stress, we reasoned that the primary RS detected in our paradigm was ONOO− (Setsukinai et al., 2003; Malinski, 2007).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Partly supportedcites Setsukinai et al., 2003 sourceExperimental — accuracy not yet measured
Table I reports a strong fluorescence increase when DCFH was exposed to ONOO−, supporting the peroxynitrite-sensitivity premise. The paper tested DCFH prepared from DCFH-DA, not CM-H2DCFDA, so it does not directly establish that probe’s sensitivity. The identification of ONOO− as the primary species in the citing authors’ paradigm is their own inference, not a finding attributed to this source. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites Malinski, 2007 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“There is a transient sex divergence in 3xTg-AD pathology, such that young- to middle-aged (6–12 month) female 3xTg-AD mice exhibit enhanced cognitive deficits compared with age-matched male 3xTg-AD (Clinton et al., 2007).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Mice
What the sources say
- Partly supportedcites Clinton et al., 2007 sourceExperimental — accuracy not yet measured
The Results report greater cognitive deficits in female 3xTg-AD mice at 6 months, still evident at 9 months, but not from 12 months onward. The Discussion also reports no significant sex differences in AD-related pathology at any age, so the citing sentence's references to a 6–12-month cognitive disparity and a divergence in pathology are not supported. (LLM, conf=0.88)
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.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer’s disease (AD).”
- Also stated in: § Introduction · hedged
“Extensive evidence indicates that alterations in glucose metabolism and mitochondrial energetics occur along with the accumulation of oxidative damage before the cardinal signs of AD pathogenesis in the brains of transgenic animal models and patients (Hoyer, 1996; Hirai et al., 2001; Rinaldi et al., 2003; Butterfield et al., 2006; Lin and Beal, 2006; Sultana et al., 2006a,b; Mosconi et al., 2008a;”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Abstract
What the sources say
- Not checked — no full text of the sourcecites Hoyer, 1996 source
- Not checked — no full text of the sourcecites Hirai et al., 2001 source
- Supportedcites Yao et al., 2009 source
The paper’s introduction describes mitochondrial dysfunction as a plausible contributor to AD pathogenesis and links oxidative stress to cognitive decline. The Discussion says elevated oxidative stress plays an important role in AD pathogenesis, supporting the citing sentence’s qualified claim. (LLM, conf=0.91)
hedgeddirect- 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.
- Also stated in: § Introduction · hedged
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Consistent with the findings of others (Saraiva et al., 2010), brief incubation with FCCP caused the loss of most CM-H2DCFDA fluorescence in Aβ(22–35)-treated cortical neurons (Fig. 2 B), suggesting that the RS detected by this dye was primarily of mitochondrial origin (Duchen, 1999).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Partly supportedcites Duchen, 1999 sourceExperimental — accuracy not yet measured
The paper’s discussion of FCCP (indexed as Abstract; page unavailable) supports the mechanistic premise that FCCP disrupts mitochondrial membrane potential. It does not report CM-H2DCFDA fluorescence or establish that the reactive species detected in Aβ(22–35)-treated cortical neurons were primarily mitochondrial. (LLM, conf=0.82)
hedgeddirect- 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: By decreasing the proton gradient across the inner mitochondrial membrane, FCCP increases the rate of electron transport through the respiratory chain, thereby inhibiting electron leakage and consequently mitochondrial O2·- production.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“mitochondrial dysfunction and oxidative stress may encourage the development of amyloid plaques and NFTs”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Could not verifycites Hardy, 2006 sourceExperimental — accuracy not yet measured
The passages on amyloid deposition and neurofibrillary tangles (labeled Abstract; no page supplied) discuss APP, presenilin, and MAPT mutations, but do not link mitochondrial dysfunction or oxidative stress to the development of either lesion. Searches for “mitochondrial,” “oxidative stress,” and “reactive oxygen species” found no passage addressing that proposed link. (LLM, conf=0.74)
- Supportedcites Gibson and Shi, 2010 source
Section 5.2 reports that impaired mitochondrial function and oxidative stress promote plaque formation, including increased plaque burden in mouse models. It also links impaired oxidation to tangle formation; Sections 5.1 and 5.2 describe oxidative stress and disturbed metabolism promoting tau changes associated with neurofibrillary tangles. No page numbers are supplied in our copy. (LLM, conf=0.91)
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.
- Could not verify
- Probably not a substantial claim. 30
- It may state two separate claims as one. 25
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It has the experimental advantage for in vitro studies of rapidly aggregating in aqueous solutions (Pike et al., 1993).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Partly supportedcites Pike et al., 1993 sourceExperimental — accuracy not yet measured
The PAP aggregation section and Table 1 (p. 1687) show that freshly prepared Aβ(25–35) forms visible aggregates in aqueous stock solution. The cited paper reports this for Aβ(25–35), not the claimed Aβ(22–35), so it does not establish that the specified fragment rapidly aggregates. (LLM, conf=0.84)
plain- 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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They also demonstrated that MitoQ enhances neurite outgrowth in cultured hippocampal neurons from AβPP-expressing mice but did not present direct evidence of a protective effect of MitoQ on the mitochondria in these cells.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Supportedcites Manczak et al., 2010 source
The Conclusions report significantly increased neurite outgrowth in primary neurons from AβPP transgenic mice treated with MitoQ. The Materials and Methods identify the cultured neurons as hippocampal neurons. (LLM, conf=0.93)
boosteddirect- 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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The recently developed, mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienlyl) decyl triphenylphosphonium methanesulfonate]) possesses these qualities (James et al., 2005, 2007; Murphy and Smith, 2007).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
What the sources say
- Partly supportedcites James et al., 2005 sourceExperimental — accuracy not yet measured
The passage labeled Abstract states that MitoQ10 selectively accumulates within mitochondria in isolated preparations, cells, and in vivo. It does not establish that MitoQ crosses the blood-brain barrier; a search for blood-brain barrier and brain penetration found no supporting passage in our copy. (LLM, conf=0.86)
- Partly supportedcites James et al., 2007 sourceExperimental — accuracy not yet measured
The Abstract states that MitoQ10 accumulates within mitochondria, driven by its triphenylphosphonium cation. The supplied passages and a search of our copy for blood–brain barrier and brain penetration do not establish that MitoQ crosses the blood–brain barrier. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Murphy and Smith, 2007 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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Manczak et al. (2010) recently demonstrated that MitoQ protects mitochondria from Aβ-induced toxicity in N2a cells.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Supportedcites Manczak et al., 2010 source
The Results (Mitochondrial dysfunction) report that MitoQ-treated N2a cells incubated with Aβ had significantly higher mitochondrial membrane potential and cytochrome oxidase activity than cells incubated with Aβ alone. The Discussion (Mitochondrial function) concludes that MitoQ protects N2a cells from Aβ toxicity. (LLM, conf=0.94)
boosteddirect- 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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This characterization shows that CM-H2DCFDA is trapped in neurons, is insensitive to pH changes within the physiological range, and is not photo-oxidized by the laser power and exposure time used in these experiments.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Microscopy
What the sources say
- Partly supportedcites Kirkland and Franklin, 2001 sourceExperimental — accuracy not yet measured
The ROS measurement section (page unavailable) says CM-H2DCFDA is trapped inside cells and reports no significant leakage from neurons. The mitochondrial ROS section finds that the acidification tested did not quench the dye, but does not establish insensitivity across the physiological pH range. The ROS measurement section calls the dye relatively insensitive to photo-oxidation at low laser intensity; it does not say photo-oxidation was absent at the laser power and exposure time claimed. (LLM, conf=0.86)
- Partly supportedcites Kirkland et al., 2002 sourceExperimental — accuracy not yet measured
The ROS measurement section (page not specified) says CM-H2DCFDA is trapped in cells and reports little dye leakage from neurons. It does not establish that the dye is insensitive to physiological pH changes or that the laser power and exposure time used prevent photo-oxidation; searches for those properties found only the microscopy settings. (LLM, conf=0.86)
boosted- 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.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Therefore, it cannot substitute for endogenous ubiquinone in the electron transport chain but primarily acts as an antioxidant capable of continuous regeneration by complex II (James et al., 2005, 2007; Rodriguez-Cuenca et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
What the sources say
- Supportedcites James et al., 2005 source
The Discussion states that MitoQ10 could not restore respiration in mitochondria lacking CoQ because MitoQ analogs are not oxidized by complex III. The Results report that complex II rapidly reduces MitoQ10 while complex III oxidizes it negligibly, keeping it in the antioxidant-active reduced form under most conditions. Page numbers are not provided in our copy. (LLM, conf=0.94)
- Supportedcites James et al., 2007 source
The Discussion states that MitoQ10 cannot be oxidized by complex III and therefore does not function as an electron carrier in mitochondrial respiration. It also says MitoQ10 acts as a chain-breaking antioxidant and is recycled to its active ubiquinol form by complex II. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Rodriguez-Cuenca et al., 2010 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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Aβ is reported to increase RS in neurons via multiple mechanisms, including direct Aβ-induced RS production, elevated NADPH oxidase activity, interaction with mitochondria-associated Aβ alcohol dehydrogenase, inhibition of cytochrome oxidase (respiratory complex IV), and by causing leakage of electrons from the mitochondrial electron transport chain (Hensley et al., 1994; Canevari et al., 1999; L”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Partly supportedcites Hensley et al., 1994 sourceExperimental — accuracy not yet measured
The Results and Discussion report that Aβ peptides generate free radicals and that the Aβ(25–35) fragment produces reactive oxygen species in cell-free experiments. They do not establish increased reactive species in neurons or address the listed NADPH oxidase, Aβ alcohol dehydrogenase, cytochrome oxidase, and mitochondrial electron-leakage mechanisms. No page numbers are available in our copy. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Canevari et al., 1999 source
- Not checked — no full text of the sourcecites Lustbader et al., 2004 source
hedgeddirect- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Notably, the earliest pathological changes in 3xTg-AD mice involve mitochondrial impairment and increased oxidative stress (Resende et al., 2008; Yao et al., 2009).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
What the sources say
- Partly supportedcites Resende et al., 2008 sourceExperimental — accuracy not yet measured
The Results and Discussion report increased oxidative stress in 3–5-month-old 3×Tg-AD mice before plaques and tangles appear. They do not establish mitochondrial impairment as an early change in these mice; the Discussion’s mention of mitochondrial vulnerability concerns a different tau-transgenic model. (LLM, conf=0.88)
- Partly supportedcites Yao et al., 2009 sourceExperimental — accuracy not yet measured
The Discussion identifies elevated oxidative stress as among the earliest indicators of dysfunction and says mitochondrial dysfunction preceded plaque formation. The study examined female 3xTg-AD mice, so it does not establish the same sequence for 3xTg-AD mice generally. (LLM, conf=0.84)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recent evidence suggests that executioner caspases 3 and 7 may contribute to tau, the protein responsible for forming NFTs, pathology by cleaving tau after Asp421 to yield a cytotoxic Δtau fragment (Rissman et al., 2004; Rohn et al., 2008; de Calignon et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased caspase activation in the cortex of 3xTg-AD mice
What the sources say
- Not checked yetcites Rissman et al., 2004 source
Checked before — its earlier verdict is held back until a new check runs.
- Partly supportedcites Rohn et al., 2008 sourceExperimental — accuracy not yet measured
The Results section (page unavailable) reports caspase-cleaved tau at Asp421 in the mouse model, and the Discussion links caspase cleavage of tau to NFT pathology. The paper identifies caspase-3 as an executioner caspase, but the passages do not identify caspase-7 as a tau-cleaving enzyme or describe the resulting fragment as cytotoxic Δtau. (LLM, conf=0.86)
- Partly supportedcites de Calignon et al., 2010 sourceExperimental — accuracy not yet measured
The supplied Abstract passage says caspases cleave tau at Asp421, producing truncated tau associated with tangles, and reports that a caspase-3/7 probe colocalized with tangles. It implicates caspase 3 and caspase 6 in cleavage, however; it does not establish that caspase 7 cleaves tau or that the resulting fragment is cytotoxic. The paper instead suggests that soluble tau species may be the critical toxic form. (LLM, conf=0.86)
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.
Probably not a substantial claim.
- Not checked yet
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“This hypothesis is supported by the early Aβ accumulation in the rare, autosomal dominant forms of AD, by transgenic mice harboring these human mutations (Hardy and Selkoe, 2002), and by recent studies suggesting that mitochondrial Aβ may be responsible for synaptic degeneration and the onset of cognitive impairment in AD models of Aβ enrichment (Zhao et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased Aβ accumulation in the brains of 3xTg-AD mice
What the sources say
- Not checked — no full text of the sourcecites Hardy and Selkoe, 2002 source
- Supportedcites Zhao et al., 2010 source
The Discussion reports that Aβ accumulates in mitochondria and that blocking its interactions with mitochondrial proteins prevents or reduces cognitive deficits in AD mice. It also reports that Aβ-expressing flies lose presynaptic mitochondria before other synaptic changes, supporting the cited sentence’s hedged link between mitochondrial Aβ and synaptic dysfunction. (LLM, conf=0.86)
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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Among these markers were decreased levels of GSH, increased levels of GSSG, and increased levels of malondialdehyde (MDA), a marker for lipid peroxidation.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased oxidative stress, synaptic loss, and astrogliosis in the cortex of 3xTg-AD mice
What the sources say
- Supportedcites Resende et al. (2008) source
The Results section reports significantly decreased GSH and increased GSSG in 3×Tg-AD mice, as well as increased brain MDA. It also identifies MDA as a product of lipid peroxidation. These findings concern the mouse model studied, not Alzheimer disease patients. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Lipid-derived radicals may contribute to nitration of proteins associated with biological membranes (Bartesaghi et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased oxidative stress, synaptic loss, and astrogliosis in the cortex of 3xTg-AD mice
What the sources say
- Supportedcites Bartesaghi et al., 2010 source
The Discussion states that lipid peroxyl radicals participate in tyrosine oxidation in hydrophobic compartments and that this provides a mechanism for protein nitration in lipoproteins and biomembranes. The claim’s cautious wording matches that conclusion; the study used a membrane model rather than directly measuring nitration of membrane-associated proteins. (LLM, conf=0.93)
hedgedconditional- 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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Because the intrinsic apoptotic pathway may involve mitochondrial RS generation (Kirkland et al., 2001), we hypothesized that the decrease in oxidative stress caused by MitoQ treatment may prevent aberrant caspase activity in the 3xTg-AD model (Rohn et al., 2008).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased caspase activation in the cortex of 3xTg-AD mice
What the sources say
- Supportedcites Kirkland et al., 2001 source
The Discussion reports ROS bursts during apoptotic death of NGF-deprived sympathetic neurons and says that blocking mitochondrial oxidative phosphorylation blocked those bursts, suggesting the ROS came from the mitochondrial electron transport chain. This supports the hedged claim that the intrinsic apoptotic pathway may involve mitochondrial reactive-species generation. (LLM, conf=0.92)
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.
Probably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The amyloid hypothesis states that Aβ peptides lie upstream of all the pathological events occurring in AD, including NFT formation, synaptic dysfunction, and neuronal death (Oddo et al., 2003b; Hardy, 2006).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased Aβ accumulation in the brains of 3xTg-AD mice
What the sources say
- Not matchedcites Oddo et al., 2003b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Hardy, 2006 sourceExperimental — accuracy not yet measured
The passage labeled Abstract (page unavailable) describes amyloid deposition as central to the amyloid hypothesis and discusses Aβ toxicity and electrophysiological effects. It does not state that Aβ lies upstream of all AD pathology, specifically NFT formation, synaptic dysfunction, and neuronal death. (LLM, conf=0.82)
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.
Probably not a substantial claim.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Modification of mitochondrial enzymes and components of the respiratory chain by RS may contribute to impaired glucose metabolism found in preclinical AD subjects”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Sultana and Butterfield, 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Yao et al., 2009 sourceExperimental — accuracy not yet measured
The Discussion reports that oxidative damage to mitochondrial proteins impairs oxidative phosphorylation, and links reduced PDH and COX activity to altered glucose metabolism in AD-model mice. It also cites decreased glucose uptake in people at increased risk of AD. It does not establish that reactive-species modification of respiratory-chain components causes the impaired glucose metabolism observed in preclinical human subjects. (LLM, conf=0.84)
hedgedconditional- 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.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Several antioxidants are reported to lessen pathologies found in transgenic mouse models of AD”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Partly supportedcites Lim et al., 2001 sourceExperimental — accuracy not yet measured
The Discussion and the section on plaque burden report that curcumin, an antioxidant, reduced oxidative damage and amyloid pathology in APPSw transgenic mice. The paper establishes this result for curcumin, not for several antioxidants, so the claim’s plural generalization is not supported by this source. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Stackman et al., 2003 source
- Supportedcites Nicolakakis et al., 2008 source
The section on normalization of cerebrovascular reactivity reports that the antioxidants NAC and tempol reversed impaired vascular responses in aged transgenic APP mice. The Conclusions also report reduced abnormal SOD2 immunoreactivity after antioxidant treatment. These findings support the broad claim that antioxidants lessen pathologies in a transgenic mouse model of AD; the paper does not claim they reduced amyloid plaques. (LLM, conf=0.90)
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.
Probably not a substantial claim.
- Partly supported
A result the paper reports from its own data — 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 concentrations also blocked an Aβ-induced increase in NO·-associated RS and Aβ-induced depolarization of Δψm.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rather, MitoQ enhanced learning and spatial memory retention.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
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
“Aβ(22–35) forms amyloid fibrils in vitro resembling those of the β-amyloid protein in senile plaques and exhibits a toxicity profile that parallels that of full-length Aβ(1–40) and Aβ(1–42) in hippocampal and cortical neurons in cell culture (Pike et al., 1995; Casley et al., 2002b).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Not checked — no full text of the sourcecites Pike et al., 1995 source
- Not matchedcites Casley et al., 2002b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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
“A similar amyloid fragment has been reported to impair mitochondrial function in isolated brain mitochondria (Canevari et al., 1999).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Not checked — no full text of the sourcecites Canevari et al., 1999 source
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.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“There is extensive in vitro evidence that the concentrations of MitoQ used here have no impact on mitochondrial functions, such as ATP production, membrane potential, or ROS production in cells or mitochondria, but do prevent mitochondrial oxidative damage under conditions that lead to oxidative stress (Kelso et al., 2001; Jauslin et al., 2003; Saretzki et al., 2003; Asin-Cayuelaa et al., 2004).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
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.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Aβ, and its precursor APP, localize, in part, to mitochondria in which they can cause mitochondrial dysfunction as evidenced by increased production of RS, enzyme inhibition, loss of cytochrome c, and depolarization of Δψm (Casley et al., 2002a; Kim et al., 2002; Anandatheerthavarada et al., 2003; Jang and Surh, 2003; Lustbader et al., 2004; Liang et al., 2009; Takuma et al., 2009).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
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
“MitoQ rapidly crosses the blood– brain barrier and neuronal membranes and concentrates several hundred-fold in mitochondria driven by the high membrane potential across the inner mitochondrial membrane (IMM; Murphy and Smith, 2007).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
What the sources say
- Not checked — no full text of the sourcecites Murphy and Smith, 2007 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 other studies, the EC50 for MitoQ in cultured cells was <0.5 nM, and the protective effect then plateaued over several logs of concentration (Jauslin et al., 2003).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Not checked — no full text of the sourcecites Jauslin et al., 2003 source
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. It may state two separate claims as one.
In the paper
“Δψm not only influences RS generation but other critical mitochondrial functions, such as nicotinamide adenine dinucleotide reduction, ATP synthesis, and Ca+ sequestration, and is therefore considered the primary dictator of mitochondrial energetics as well as an indicator of the overall health of mitochondria in neurons (Nicholls and Ward, 2000).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ-induced RS and mitochondrial damage in cortical neurons in cell culture
What the sources say
- Not checked — no full text of the sourcecites Nicholls and Ward, 2000 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.
Probably not a substantial claim. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A number of studies show that, when MitoQ is administered to in vivo animal models of pathologies, it reduces both oxidative damage and the pathologies (Adlam et al., 2005; Lowes et al., 2008; Graham et al., 2009; Supinski et al., 2009; Chacko et al., 2010; Smith and Murphy 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
What the sources say
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.
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
“One possible explanation for these failures is that the compounds tested were not efficient at detoxifying relevant reactive species (RS), perhaps because they did not achieve sufficient concentrations at the site of most RS production, mitochondria.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Introduction
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.
Probably not a substantial claim.
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
“Therefore, our findings in neuronal cells are consistent with other studies.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
plain- 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Cortical neuron survival was determined by blinded counting of phase-bright/morphologically intact cells in 10 randomly selected fields of view per treatment and was normalized to the average percentage survival of nontreated, sibling cultures.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Cell culture
plain- 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.
In the paper
“Cued acquisition trials were conducted after the last probe trial to determine whether differences in learning and memory could be attributed to impaired eyesight, swimming ability, or motivation to escape (Morris, 1984).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Spatial learning and memory retention
What the sources say
- Not checked — no full text of the sourcecites Morris, 1984 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.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Confocal pinhole and gain were maintained at constant levels during each experiment.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Microscopy
plain- 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.
In the paper
“An even shorter peptide [Aβ(25–35)] causes memory impairment when injected into rat brains (Díaz et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ attenuated Aβ toxicity in cortical neurons in cell culture
What the sources say
- Not matchedcites Díaz et al., 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
In the paper
“When administered to wild-type mice for several months, MitoQ has no effect on the function of subsequently isolated mitochondria, on mtDNA, on nuclear or mitochondrial gene expression, on whole-body metabolism, on whole-body motor function, or on food and liquid consumption (Rodriguez-Cuenca et al., 2010).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Mice
What the sources say
- Not checked — no full text of the sourcecites Rodriguez-Cuenca et al., 2010 source
plain- 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. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All animal procedures were in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Materials and Methods > Mice
plain- 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.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“the rate of metabolic decline within the medial temporal lobe predicts the progression of cognitive deterioration from normal aging to AD”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Mosconi et al., 2008a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Mosconi et al., 2008b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- 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.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“Tyrosine nitration provides a footprint for free radical-mediated damage involving oxidation of NO· to ONOO− or products of its subsequent decomposition and the formation of a tyrosyl radical intermediate (Halliwell and Gutteridge, 2007; Malinski, 2007).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased oxidative stress, synaptic loss, and astrogliosis in the cortex of 3xTg-AD mice
What the sources say
- Not matchedcites Halliwell and Gutteridge, 2007
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Malinski, 2007 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.
Probably not a substantial claim.
- Not matched
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 effect of MitoQ on rate of learning in the 3xTg-AD mice could not be explained by a stimulatory effect of MitoQ or by an effect of MitoQ on vision.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
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.
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 average swim speed was ~ 21 cm/s for each group (p = 0.84), indicating that motor performance was the same for all and that the MitoQ did not have a stimulatory effect.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
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.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“overexpression of MnSOD decreases Aβ-processing”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
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.
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
“auxiliary approaches may be required for optimal therapeutic benefit and the effective prevention of AD.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
hedgedconditional- 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: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
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 data suggest that the death was associated with mitochondrial dysfunction and that it was caused by mitochondrial-derived RS.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
hedgeddirect- 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
“Aβ appears to enhance production of cellular RS, and these RS in turn may to contribute to Aβ toxicity.”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased Aβ accumulation in the brains of 3xTg-AD mice
What the sources say
hedgeddirect- 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
“Evidence also suggests that not only does Aβ increase cellular RS but that these RS may in turn increase production of Aβ in a destructive autocatalytic cycle (Misonou et al., 2000; Tamagno et al., 2002, 2005; Lin and Beal, 2006; Quiroz-Baez et al., 2009).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ decreased Aβ accumulation in the brains of 3xTg-AD mice
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.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Metabolic impairment induced by thiamine deficiency or respiratory chain inhibition augments β-secretase expression and activity”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Karuppagounder et al., 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Zhang et al., 2011
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
Probably not a substantial claim.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“preserves synaptic integrity”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
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.
In the paper
“This mouse strain develops cognitive dysfunction as well as both plaque and neurofibrillary tangle pathology in AD-relevant brain regions in an age-dependent manner, closely resembling AD progression in humans (Oddo et al., 2003b).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
What the sources say
- Not matchedcites Oddo et al., 2003b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Spatial retention deficits emerge in 3xTg-AD mice by 4–6 months of age and are reminiscent of spatial learning deficits in patients with mild cognitive impairment (MCI), a condition proposed to be prodromal for AD (Grundman et al., 2004; Mosconi et al., 2008a).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
What the sources say
- Not matchedcites Grundman et al., 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Mosconi et al., 2008a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“which may generate Aβ by directly cleaving APP (caspase 3)”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Newcombe et al., 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Chae et al., 2010 source
hedgedconditional- 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.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“may also be upregulated by RS”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Minopoli et al., 2007
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Guglielmotto et al., 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Oda et al., 2010 source
hedgedconditional- 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.
- Not matched
In the paper
“MitoQ has been though two phase II trials for other conditions”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Snow et al., 2010 source
plain- 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.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Intracellular Aβ may then enter the mitochondria in which it induces additional RS and magnifies the metabolic deficit”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
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.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“or via a process involving β-secretase (caspases 2 and 8”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Discussion
What the sources say
- Not matchedcites Newcombe et al., 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Chae et al., 2010 source
hedgedconditional- 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.
- Not matched
The paper relies on this without support.
Cognitive impairment in 3xTg-AD mice emerges as a long-term retention deficit at 4–6 months of age and further develops in an age-dependent manner.
“Cognitive impairment in 3xTg-AD mice emerges as a long-term retention deficit at 4–6 months of age and further develops in an age-dependent manner.”
The paper relies on this without support.
Cyclodextrin is widely used in drug delivery and is not thought to have any significant effects.
“Cyclodextrin is widely used in drug delivery and is not thought to have any significant effects.”
The paper relies on this without support.
By decreasing the proton gradient across the inner mitochondrial membrane, FCCP increases the rate of electron transport through the respiratory chain, thereby inhibiting electron leakage and consequently mitochondrial O2·- production.
“By decreasing the proton gradient across the IMM, FCCP increases rate of electron transport through the respiratory chain, thereby inhibiting electron leakage and consequently mitochondrial O2·- production.”
The paper relies on this without support.
Nitro-oxidative modification to proteins may dramatically alter their structure and biological activity and may play an important role in AD development.
“Nitro-oxidative modification to proteins may dramatically alter their structure and biological activity and may play an important role in AD development.”
The paper relies on this without support.
The brains of human AD patients exhibit extensive astrogliosis, a process indicative of neuronal damage.
“The brains of human AD patients exhibit extensive astrogliosis, a process indicative of neuronal damage.”
The paper relies on this without support.
The predominant pathway of Aβ production occurs by sequential cleavage of APP by β- and γ-secretases.
“The predominant pathway of Aβ production occurs by sequential cleavage of APP by β- and γ-secretases.”
The paper relies on this without support.
These antioxidants are nonspecific and should interact with ROS in all areas of the brain.
“However, these antioxidants are nonspecific and should interact with ROS in all areas of the brain.”
The paper relies on this without support.
MitoQ operates only within mitochondria.
“an antioxidant that only operates within mitochondria is protective”
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?
The cited source says what the claim attributes to it.
In the citing paper
“CoQ10 led to decreased Aβ pathology in aged transgenic mice with human AD presenilin-1 mutation, and in a different study, a quinone-containing derivative of CoQ10 (MitoQ) that targets mitochondria, improved memory, and neuropathology in a transgenic mouse model of AD [152,153].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [153]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
“After 4.5 months of treatment, the cognitive performance of these six groups was determined by performance in the MWM (Morris, 1984).”
§ The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease > Results > MitoQ improved cognitive performance in young 3xTg-AD mice
“Age-matched nonTg female mice either received no treatment or 100 μM MitoQ in their drinking water from 2–7 months of age.”
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Metadata
- Authors
- McManus, M. J., Murphy, M. P., & Franklin, J. L.
- Affiliations
- University of Georgia (US)
- MRC Mitochondrial Biology Unit (GB)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-11-02
- Volume
- 31
- Issue
- 44
- Pages
- 15703-15715
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3334845
- OpenAlex
- W1988664434
- Cited by
- 432
- References
- 135
- Citations by year
- 2026: 18 · 2025: 29 · 2024: 29 · 2023: 28 · 2022: 39 · 2021: 47 · 2020: 39 · 2019: 33 · 2018: 28 · 2017: 17 · 2016: 37 · 2015: 17 · 2014: 23 · 2013: 30 · 2012: 18
- FWCI
- 15.48
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R29NS037110, NS37110, R01NS037110)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- MitoQ, mitochondria-targeted antioxidants, Alzheimer's disease, 3xTg-AD mice, mitochondrial dysfunction, oxidative stress, amyloid-beta toxicity, mitochondrial membrane potential, cognitive decline, astrocyte activation, synaptic loss, caspase activation, neurodegeneration, mitochondrial protection
- MeSH terms
- Age Factors, Alzheimer Disease, Analysis of Variance, Animals, Animals, Newborn, Antioxidants, Cells, Cultured, Cerebral Cortex, Disease Models, Animal, Enzyme Inhibitors, Enzyme-Linked Immunosorbent Assay, Glial Fibrillary Acidic Protein, Gliosis, Glutathione, Humans, Memory Disorders, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Neurons, Organophosphorus Compounds, Peptide Fragments, Retention, Psychology, Rhodamines, Space Perception, Time Factors, Tyrosine, Ubiquinone, Lipid Peroxidation, Amyloid beta-Peptides, Cell Death, Oxidative Stress, Maze Learning, Caspases, Mice
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