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Mitochondrial Approaches for Neuroprotection
Open accessAbstract
A large body of evidence from postmortem brain tissue and genetic analysis in humans and biochemical and pathological studies in animal models (transgenic and toxin) of neurodegeneration suggest that mitochondrial dysfunction is a common pathological mechanism. Mitochondrial dysfunction from oxidative stress, mitochondrial DNA deletions, pathological mutations, altered mitochondrial morphology, and interaction of pathogenic proteins with mitochondria leads to neuronal demise. Therefore, therapeutic approaches targeting mitochondrial dysfunction and oxidative damage hold great promise in neurodegenerative diseases. This review discusses the potential therapeutic efficacy of creatine, coenzyme Q10, idebenone, synthetic triterpenoids, and mitochondrial targeted antioxidants (MitoQ) and peptides (SS‐31) in in vitro studies and in animal models of Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. We have also reviewed the current status of clinical trials of creatine, coenzyme Q10, idebenone, and MitoQ in neurodegenerative disorders. Further, we discuss newly identified therapeutic targets, including peroxisome proliferator‐activated receptor‐γ‐coactivator and sirtuins, which provide promise for future therapeutic developments in neurodegenerative disorders.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that mitochondrial dysfunction and oxidative damage are common pathological mechanisms in Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. It evaluates mitochondria-targeted neuroprotective agents—including creatine, coenzyme Q10, idebenone, MitoQ, SS-31, and synthetic triterpenoids—and highlights PGC-1α and sirtuins as emerging therapeutic targets.
Key findings
- Mitochondrial dysfunction is implicated across neurodegenerative diseases: complex-I inhibition by MPTP/rotenone in PD models; reduced complexes II–III and aconitase in HD; impaired TCA enzymes and respiratory complexes I, III, and IV in AD; and mutant SOD1-associated mitochondrial defects in ALS.
- Creatine showed neuroprotection in multiple models, including MPTP-treated mice, G93A ALS mice, and R6/2 and N-171-82Q HD mice. In early PD, a phase II trial of creatine 10 g/day plus minocycline reported tolerability of 91% for creatine versus 77% for minocycline, and UPDRS progression slowed by almost 50% at 1 year compared with DATATOP controls; an NIH phase III trial planned to randomize 1720 participants to 10 g creatine or placebo. In HD, creatine 8 g/day for 16 weeks in 64 subjects was safe, bioavailable to brain, and decreased serum 8-hydroxy-2-deoxyguanosine.
- CoQ10 at 360 mg/day reduced occipital cortex lactate concentrations by 37% in 18 HD patients. In the CARE-HD trial of 340 patients, CoQ10 600 mg/day produced a 14% decrease in disease progression over 30 months, while remacemide showed no efficacy. A phase II early-PD trial using 300, 600, or 1,200 mg/day for 16 months found a statistically significant dose-dependent reduction in UPDRS score; high doses up to 3,600 mg/day were safe, though plasma CoQ10 plateaued at 2,400 mg/day.
- Mitochondrial-targeted agents showed preclinical promise: MitoQ entered a phase II PD trial; SS-31 at 5 mg/kg daily intraperitoneally from 30 days of age improved survival and motor performance in G93A ALS mice; CDDO-MA reduced MPTP and 3-NP toxicity; and PGC-1α and sirtuin/resveratrol pathways were protective in models of neurodegeneration.
Methods
- Design: narrative review; no systematic review, meta-analysis, or formal search methodology is stated.
- Data/sample: evidence from post-mortem human tissue, genetic analyses, in vitro cell models, transgenic and toxin animal models, and clinical trials in PD, HD, AD, and ALS.
- Analysis: qualitative synthesis of preclinical and clinical findings for mitochondrial-targeted neuroprotective agents and emerging targets including PGC-1α and sirtuins.
Limitations
- The paper states no explicit limitations.
- Evident from the text: as a narrative review, it lacks systematic search criteria, inclusion/exclusion criteria, and quantitative synthesis.
- Evident from the text: several cited findings are unpublished (e.g., Chaturvedi et al., Kipiani et al., Yang et al., Kiaei et al.), and clinical results for idebenone are described as controversial, with one large trial showing no benefit.
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Claims the paper makes
93 Not checked yet · 24 Own interpretation · 2 Own result
In the paper
“We observed G11778A mtDNA point mutation in a subunit of mitochondrial complex-I in a family with parkinsonism and multisystem degeneration19.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial dysfunction in Parkinson's disease (PD)
What the sources say
- Not checked yetcites [19] Simon DK 1999 Familial multisystem degeneration with parkinsonism associated with the 11778 mitochondrial DNA mutation Neurology 53 1787 93 10563629 source
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“We also identified high levels of somatic mtDNA point mutations in elderly PD patients20.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial dysfunction in Parkinson's disease (PD)
What the sources say
- Not checked yetcites [20] Simon DK 2004 Somatic mitochondrial DNA mutations in cortex and substantia nigra in aging and Parkinson's disease Neurobiol Aging 25 71 81 14675733 source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“We found neuroprotective effects against DA depletion, loss of TH-IR neurons in the SN and the development of α–synuclein aggregates.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [147] Cleren C 2007 Therapeutic effects of coenzyme Q(10) (Q(10)) and reduced CoQ(10) in the MPTP model of Parkinsonism J Neurochem 17973981
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Recently, we found that a combination of creatine and CoQ10 exerts synergistic neuroprotective effects in the MPTP model of PD (Yang et al., unpublished findings).”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites Yang et al., unpublished findings
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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In the paper
“We demonstrated CoQ10 provided significant protection against MPTP induced dopamine depletion and loss of TH-IR neurons in aged mice146.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [146] Beal MF 1998 Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3,tetrahydropyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice Brain Res 783 109 14 9479058 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“We found neuroprotective effects against DA depletion, loss of TH-IR neurons in the SN and the development of α–synuclein aggregates.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [147] Cleren C 2007 Therapeutic effects of coenzyme Q(10) (Q(10)) and reduced CoQ(10) in the MPTP model of Parkinsonism J Neurochem 17973981
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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In the paper
“We found neuroprotective effects against DA depletion, loss of TH-IR neurons in the SN and the development of α–synuclein aggregates.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [147] Cleren C 2007 Therapeutic effects of coenzyme Q(10) (Q(10)) and reduced CoQ(10) in the MPTP model of Parkinsonism J Neurochem 17973981
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“We observed that CoQ10 treatment produced a 37% reduction in occipital cortex lactate concentrations, which was reversed following withdrawal of therapy39.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [39] Koroshetz WJ 1997 Energy metabolism defects in Huntington's disease and effects of coenzyme Q10 Ann Neurol 41 160 5 9029064 source
plaindirectn = 18- Asserted: passes — The authors put it forward as true.
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In the paper
“More recently, we found that dietary administration of either of two formulations of CoQ10 resulted in significant protection in a chronic MPTP model induced by the administration of MPTP by Alzet pump for 1 month147.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [147] Cleren C 2007 Therapeutic effects of coenzyme Q(10) (Q(10)) and reduced CoQ(10) in the MPTP model of Parkinsonism J Neurochem 17973981
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“We found SS-31 mediated significant neuroprotection against cell death induced by hydrogen peroxide in SOD1 neuronal cells.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [180] Petri S 2006 Cell-permeable peptide antioxidants as a novel therapeutic approach in a mouse model of amyotrophic lateral sclerosis J Neurochem 98 1141 8 16895581 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 41
- Probably not a substantial claim. 4
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
“We observed significantly reduced cellular respiration and COX activity in myoblasts from HD patients, and these defects were exacerbated in chronic energy deprivation conditions (Chaturvedi et. al., unpublished findings).”
§ Mitochondrial approaches for neuroprotection > Mitochondrial dysfunction in Huntington's disease (HD)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“We found that oral administration of creatine at a dose of 8 g/day for 16 weeks is well tolerated, safe and bioavailable to the brain, and it decreased serum 8-hydroxy-2-deoxyguanosine levels, a marker for oxidative stress.”
§ Mitochondrial approaches for neuroprotection > Creatine
What the sources say
- Not checked yetcites [134] Hersch SM 2006 Creatine in Huntington disease is safe, tolerable, bioavailable in brain and reduces serum 8OH2'dG Neurology 66 250 2 16434666 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Recently, we found that CoQ10 treatment decreases brain oxidative stress, Aβ42 levels, β-amyloid plaque area and number, and improves cognitive performance in Tg19959 mice, a transgenic mouse model of AD (Kipiani et al., unpublished findings).”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites Kipiani et al., unpublished findings
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
“We found that creatine significantly improves survival, improves motor performance, slows the development of brain atrophy, increases brain ATP levels, delays atrophy of striatal neurons and the formation of Htt-positive aggregates in the R6/2 and N-171-82Q transgenic mouse models of HD118-120.”
§ Mitochondrial approaches for neuroprotection > Creatine
What the sources say
- Not checked yetcites [118] Andreassen OA 2001 Creatine increase survival and delays motor symptoms in a transgenic animal model of Huntington's disease Neurobiol Dis 8 479 91 11447996 source
- Not checked yetcites [119] Dedeoglu A 2003 Creatine therapy provides neuroprotection after onset of clinical symptoms in Huntington's disease transgenic mice J Neurochem 85 1359 67 12787055 PMC2866522 source
- Not checked yetcites [120] Ferrante RJ 2000 Neuroprotective effects of creatine in a transgenic mouse model of Huntington's disease J Neurosci 20 4389 97 10844007 PMC6772461 source
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“We found that creatine produced protection against dopamine loss, as well as an attenuation of neuron loss in the SN of mice treated with MPTP.”
§ Mitochondrial approaches for neuroprotection > Creatine
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 this study, oral administration of CoQ10 in PD patients was well tolerated and resulted in significant, dose-dependent increases in plasma CoQ10 levels.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [159] Shults CW 1997 Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects Ann Neurol 42 261 4 9266740 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Both SS-31 and SS-20 also produce complete protection against MPTP neurotoxicity (Yang et al., unpublished findings).”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites Yang et al., unpublished findings
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
“We found a significant reduction in CoQ10 levels in mitochondria isolated from platelets of PD patients, that directly correlated with a decrease in complex-I activity159.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [159] Shults CW 1997 Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects Ann Neurol 42 261 4 9266740 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“It reduces t-butylhydroperoxide induced ROS generation, attenuates MPTP-induced nigrostriatal dopaminergic neurodegeneration and reduces 3-NP induced striatal lesions.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites Yang et al., unpublished findings
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
“Mitochondrial dysfunction due to oxidative stress, mitochondrial DNA deletions, pathological mutations, altered mitochondrial morphology and interaction of pathogenic proteins with mitochondria leads to neuronal demise.”
§ Mitochondrial approaches for neuroprotection > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Creatine was shown to reduce the UPDRS scores, and could not be rejected as futile based on the 30% DATATOP futility threshold.”
§ Mitochondrial approaches for neuroprotection > Creatine
What the sources say
- Not checked yetcites [130] 2006 A randomized, double-blind, futility clinical trial of creatine and minocycline in early Parkinson disease Neurology 66 664 71 16481597 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Oral administration of creatine produces a dose-dependent improvement in motor performance and extends survival in G93A transgenic ALS mice, where it protects against loss of both motor neurons and SN neurons114.”
§ Mitochondrial approaches for neuroprotection > Creatine
What the sources say
- Not checked yetcites [114] Klivenyi P 1999 Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis Nat Med 5 347 50 10086395 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
“There is ample evidence showing involvement of mitochondrial dysfunction in the pathogenesis of neurodegenerative disorders, therefore, one would predict that agents that alleviate mitochondrial dysfunction could be beneficial and exert neuroprotective effects.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Mitochondrial dysfunction is a valid therapeutic target for neurodegenerative diseases.
None of the sources cited for this claim have been checked yet.
In the paper
“Similarly, we and others, by using CoQ10 and remacemide (NMDA antagonist) combination therapy observed significantly improved motor performance and increased survival in the R6/2 and the N-171-82Q transgenic mouse models of HD151, 154.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [151] Ferrante RJ 2002 Therapeutic effects of coenzyme Q10 and remacemide in transgenic mouse models of Huntington's disease J Neurosci 22 1592 9 11880489 PMC6758854 source
- Not checked yetcites [154] Schilling G 2001 Coenzyme Q10 and remacemide hydrochloride ameliorate motor deficits in a Huntington's disease transgenic mouse model Neurosci Lett 315 149 53 11716985 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The combination therapy of CoQ10 and minocycline in R6/2 transgenic mouse model of HD resulted in a significantly increased amelioration of behavioral and neuropathological deficits, extended survival, improved rotarod performance and attenuated striatal neuron atrophy, as compared to either minocycline or CoQ10 alone153.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [153] Stack EC 2006 Combination therapy using minocycline and coenzyme Q10 in R6/2 transgenic Huntington's disease mice Biochim Biophys Acta 1762 373 80 16364609 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A dose ranging and efficacy study of highdose coenzyme Q10 formulations in the R6/2 HD transgenic mice demonstrated that high-dose CoQ10 significantly extends survival, improves motor performance, grip strength and reduces brain atrophy in R6/2 HD mice, in a dose-dependent manner152.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [152] Smith KM 2006 Dose ranging and efficacy study of high-dose coenzyme Q10 formulations in Huntington's disease mice Biochim Biophys Acta 1762 616 26 16647250 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Subsequently, in two other clinical trials, idebenone was safe and tolerable up to 360 mg/day and slowed progression of cognitive deficits in patients with AD168, 169.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [168] Gutzmann H Hadler D 1998 Sustained efficacy and safety of idebenone in the treatment of Alzheimer's disease: update on a 2-year double-blind multicentre study J Neural Transm Suppl 54 301 10 9850939 source
- Not checked yetcites [169] Gutzmann H 2002 Safety and efficacy of idebenone versus tacrine in patients with Alzheimer's disease: results of a randomized, double-blind, parallel-group multicenter study Pharmacopsychiatry 35 12 8 11819153 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Mitochondrial-targeted antioxidants including mitochondrial CoQ10 (MitoQ) and Szeto-Schiller peptide (SS-31) play an important role in modulating ROS induced mitochondrial permeability transition and cell death, and were found to be protective in several in vitro and in vivo models of ischemia, reperfusion injury and neurodegeneration173.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [173] Armstrong JS 2007 Mitochondria-Directed Therapeutics. Antioxid Redox Signal 18092938
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
“These findings strongly support the notion that creatine, CoQ10 and idebenone are promising neuroprotective agents in debilitating neurodegenerative disorders.”
§ Mitochondrial approaches for neuroprotection > CoQ10
boostedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Similarly, a novel peptide antioxidant (SS-31) targeted to the inner mitochondrial membrane prevents apoptosis, necrosis, oxidative stress and inhibition of the mitochondrial electron transport chain176.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [176] Szeto HH 2007 Mitochondria-Targeted Cytoprotective Peptides for Ischemia-Reperfusion Injury Antioxid Redox Signal 17999629
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“SS-31 protects neuronal cells against tert-butyl-hydroperoxide (tBHP) induced mitochondrial depolarization and apoptotic cell death by reducing intracellular ROS, decreasing markers of apoptotic cell death and caspase activity177.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [177] Zhao K 2005 Mitochondria-targeted peptide prevents mitochondrial depolarization and apoptosis induced by tert-butyl hydroperoxide in neuronal cell lines Biochem Pharmacol 70 1796 806 16216225 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This trial was powered to be able to determine a 40% attenuation of total functional capacity decline with 80% power.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [155] 2001 A randomized, placebo-controlled trial of coenzyme Q10 and remacemide in Huntington's disease Neurology 57 397 404 11502903 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“MitoQ reduces ROS formation and preserves mitochondrial function after glutathione depletion, even in the cells lacking mitochondrial DNA175.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [175] Lu C 2007 Is Antioxidant Potential of the Mitochondrial Targeted Ubiquinone Derivative MitoQ Conserved in Cells Lacking mtDNA? Antioxid Redox Signal 17999633
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
“MitoQ is a derivative of CoQ10 conjugated to triphenylalkylphosphonium ions, which promotes uptake into mitochondria, where it can combat ROS originating in mitochondria174.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [174] Tauskela JS 2007 MitoQ--a mitochondria-targeted antioxidant IDrugs 10 399 412 17642004
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
“The ratio of reduced to oxidized CoQ10 is significantly reduced in the platelets and cerebrospinal fluid (CSF) of PD patients156, 157 and in plasma of ALS patients158.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [156] Gotz ME 2000 Altered redox state of platelet coenzyme Q10 in Parkinson's disease J Neural Transm 107 41 8 10809402 source
- Not checked yetcites [157] Isobe C 2007 Increase of oxidized/total coenzyme Q-10 ratio in cerebrospinal fluid in patients with Parkinson's disease J Clin Neurosci 14 340 3 16647853 source
- Not checked yetcites [158] Sohmiya M 2005 An increase of oxidized coenzyme Q-10 occurs in the plasma of sporadic ALS patients J Neurol Sci 228 49 53 15607210 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“CoQ10 was safe and well tolerated at dosages of up to 1200 mg/day and a statistically significant dose-dependent reduction in UPDRS score was evident in subjects assigned to CoQ10 compared to those assigned to placebo.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
- Not checked yetcites [160] Shults CW 2002 Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline Arch Neurol 59 1541 50 12374491 source
plain- 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
“However, plasma CoQ10 levels reached a plateau at the 2400 mg/day dosage and did not increase further at the 3000 mg/day dosage in PD, HD or ALS patients161, 162.”
§ Mitochondrial approaches for neuroprotection > CoQ10
What the sources say
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.
In the paper
“SS-31 also prevents Ca2+ induced cytochrome c release and inhibits 3-NP-induced activation of the MPT pore and mitochondrial depolarization in isolated mitochondria178.”
§ Mitochondrial approaches for neuroprotection > Mitochondrial targeted antioxidants/peptides
What the sources say
- Not checked yetcites [178] Zhao K 2004 Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury J Biol Chem 279 34682 90 15178689 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
“Following activation by TP, Nrf2 dissociates from Keap1, translocates to the nucleus, and binds to the ARE promoter sequences, leading to coordinated induction of a battery of cytoprotective genes including antioxidant and anti-inflammatory genes182.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [182] Lee JM 2005 Nrf2, a multi-organ protector? Faseb J 19 1061 6 15985529 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 studies suggest a potential neuroprotective effect of triterpenoids in cell and animal models of neurodegenerative disorders, and these compounds hold great promise as therapeutic agents for these disorders.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
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.
In the paper
“In the Nrf2 knockout (Nrf2−/−) mice, injection of the mitochondrial complex-II inhibitor 3-NP causes increased motor deficits and striatal lesions as compared to the Nrf2+/+ mice, and these toxic effects of 3-NP were protected by adenoviral mediated over expression of Nrf2185.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [185] Shih AY 2005 Induction of the Nrf2-driven antioxidant response confers neuroprotection during mitochondrial stress in vivo J Biol Chem 280 22925 36 15840590 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
“Sirtuin activation improves mitochondrial function, extends lifespan, and promotes longevity in various species including yeast193.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
What the sources say
- Not checked yetcites [193] Dali-Youcef N 2007 Sirtuins: the ‘magnificent seven’, function, metabolism and longevity Ann Med 39 335 45 17701476 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
“Synthetic TP compounds are potent inducers of the antioxidant response element (ARE)–Nrf2–Keap1 signaling pathway and are useful in a variety of the cancers including leukemia, multiple myeloma, osteosarcoma, breast and lung cancer181.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [181] Liby KT Yore MM Sporn MB 2007 Triterpenoids and rexinoids as multifunctional agents for the prevention and treatment of cancer Nat Rev Cancer 7 357 69 17446857 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
“Synthetic triterpenoids (TP), analogues of oleanolic acid, are powerful inhibitors of oxidative stress and cellular inflammatory processes, and thus may be neuroprotective in neurodegeneration.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [181] Liby KT Yore MM Sporn MB 2007 Triterpenoids and rexinoids as multifunctional agents for the prevention and treatment of cancer Nat Rev Cancer 7 357 69 17446857 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.
In the paper
“Additionally, the Nrf2 activator tertbutylhydroquinone, has attenuated 3-NP toxicity in Nrf2+/+ mice, but not in Nrf2−/− mice185.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [185] Shih AY 2005 Induction of the Nrf2-driven antioxidant response confers neuroprotection during mitochondrial stress in vivo J Biol Chem 280 22925 36 15840590 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
“Neuronal cultures derived from the Nrf2 knockout mice show increased susceptibility to oxidative stress, as well as damage produced by mitochondrial electron transport chain complex inhibitors such as MPP+ and rotenone184.”
§ Mitochondrial approaches for neuroprotection > Triterpenoids
What the sources say
- Not checked yetcites [184] Lee JM 2003 NF-E2-related factor-2 mediates neuroprotection against mitochondrial complex I inhibitors and increased concentrations of intracellular calcium in primary cortical neurons J Biol Chem 278 37948 56 12842875 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
“These studies provide compelling evidence for a role of PGC-1α in the pathogenesis of neurodegenerative diseases, and thus it is a promising therapeutic target for neurodegenerative disorders2, 72.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
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.
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
“Several agents, including creatine, CoQ10, MitoQ and idebenone are presently in clinical trials and show promising neuroprotective effects in these disorders.”
§ Mitochondrial approaches for neuroprotection > Conclusion and future perspective
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.
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
“Identification of new therapeutic targets including PGC-1α and Sirtuins may provide new avenues for therapy of neurodegenerative diseases.”
§ Mitochondrial approaches for neuroprotection > Conclusion and future perspective
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.
In the paper
“SIRT-1 activation by resveratrol increases survival of motor neurons from transgenic ALS mice and reduces learning impairment and neurodegeneration in AD mouse models by decreasing the acetylation of SIRT1 substrates PGC-1α and p53194.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
What the sources say
- Not checked yetcites [194] Kim D 2007 SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis Embo J 26 3169 79 17581637 PMC1914106 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
“Altogether, theses studies provide strong evidence for involvement of Sirtuins in neuroprotection and targeting of Sirtuins could be an attractive therapeutic approach in neurodegenerative disorders.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
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.
In the paper
“Increased intracellular NAD+ concentration activates SIRT1 in brain following caloric restriction and this results in a reduction in amyloid pathology in a mouse model of Alzheimer disease197.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
What the sources say
- Not checked yetcites [197] Qin W 2006 Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction J Biol Chem 281 21745 54 16751189 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
“Similarly, resveratrol in another study improved motor function in mice which was accompanied by a decrease in PGC1α acetylation leading to increased activity and mitochondrial biogenesis196.”
§ Mitochondrial approaches for neuroprotection > PGC-1α and Sirtuins (Sir2)
What the sources say
- Not checked yetcites [196] Lagouge M 2006 Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha Cell 127 1109 22 17112576 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.
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, therapeutic agents having the ability to target mitochondria and reduce mitochondrial dysfunction hold great promise for therapeutic interventions.”
§ Mitochondrial approaches for neuroprotection > Conclusion and future perspective
plaindirect- 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.
The paper relies on this without support.
Animal model results for neuroprotective agents predict clinical efficacy in human neurodegenerative diseases.
“The success of creatine in experimental studies led to clinical trials in neurodegenerative diseases including PD, HD and ALS.”
The paper relies on this without support.
Mitochondrial dysfunction is a valid therapeutic target for neurodegenerative diseases.
“There is ample evidence showing involvement of mitochondrial dysfunction in the pathogenesis of neurodegenerative disorders, therefore, one would predict that agents that alleviate mitochondrial dysfunction could be beneficial and exert neuroprotective effects.”
The paper relies on this without support.
Neuroprotective effects observed in animal models of neurodegenerative diseases predict neuroprotective efficacy in human patients.
“On the basis of results from animal studies, we and others initiated several clinical trials of CoQ10 in neurodegenerative disorders.”
The paper relies on this without support.
Plasma CoQ10 levels are a valid basis for selecting the dose for phase III clinical trials in HD.
“This dose was chosen based on the studies of plasma CoQ10 concentrations discussed above.”
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
“Furthermore, CoQ10 offers neuroprotection in animal models of neurodegenerative diseases (e.g. Parkinson’s) [179, 180].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [179]
Citations
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Metadata
- Authors
- Chaturvedi, R. K., & Beal, M. F.
- Affiliations
- Cornell University (US)
- Corresponding author
- Chaturvedi, Rajnish K.
- Beal, M. Flint
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2008-12
- Volume
- 1147
- Issue
- 1
- Pages
- 395-412
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC2605644
- OpenAlex
- W2157205154
- Cited by
- 294
- References
- 314
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 13 · 2023: 17 · 2022: 14 · 2021: 10 · 2020: 12 · 2019: 9 · 2018: 13 · 2017: 9 · 2016: 11 · 2015: 15 · 2014: 21 · 2013: 15 · 2012: 27
- FWCI
- 2.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS039258)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- mitochondrial dysfunction, neuroprotection, neurodegenerative diseases, oxidative stress, mitochondrial DNA deletions, creatine, coenzyme Q10, idebenone, synthetic triterpenoids, MitoQ, SS-31, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Alzheimer's disease, PPARγ coactivator, sirtuins, mitochondria-targeted antioxidants
- MeSH terms
- Animals, Humans, Mitochondria, Neuroprotective Agents, Neurodegenerative Diseases
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