Evidence map›Paper›PMID 23200807›Full record

ArticleFree radical biology & medicine2013

Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease.

Michael H Yan, Xinglong Wang, Xiongwei Zhu

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 338 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
338citing papers in PubMed, 3 pooled it
17.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

338 citing papers in PubMed, 3 syntheses or guidelines pooled it, 719 citations in OpenAlex.

  1. Are high copper levels related to Alzheimer's and Parkinson's diseases? A systematic review and meta-analysis of articles published between 2011 and 2022.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
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  11. Au-PtNPs@MnACS omega · 2026
    Article
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  19. Synergistic Effects of Anthocyanin-EnrichedFoods (Basel, Switzerland) · 2025
    Article
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278 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Michael H YanDepartment of Pathology.
Xinglong WangDepartment of Pathology; Department of Neurology, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: Xinglong.wang@case.edu.
Xiongwei ZhuDepartment of Pathology; Department of Neurology, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: xiongwei.zhu@case.edu.
Case Western Reserve University · US

Funding

Mitochondrial Fission and Fusion in Alzheimer DiseaseR01AG031852 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI ZHU, XIONGWEI · 2008 to 2012
$1.6M
LRRK2 and mitochondrial dysfunctionR21NS071184 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI ZHU, XIONGWEI · 2010 to 2011
$427k
Role of PS1 in Mitochondria Dynamics and Mitochondria FunctionR03AG044680 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI WANG, XINGLONG · 2013 to 2014
$158k
NIA NIH HHS AG031852NIA NIH HHS R01 AG031852NIA NIH HHS R03 AG044680NINDS NIH HHS NS071184NINDS NIH HHS R21 NS071184
6 · The paper itself

Abstract

Alzheimer disease (AD) and Parkinson disease (PD) are the two most common age-related neurodegenerative diseases characterized by prominent neurodegeneration in selective neural systems. Although a small fraction of AD and PD cases exhibit evidence of heritability, among which many genes have been identified, the majority are sporadic without known causes. Molecular mechanisms underlying neurodegeneration and pathogenesis of these diseases remain elusive. Convincing evidence demonstrates oxidative stress as a prominent feature in AD and PD and links oxidative stress to the development of neuronal death and neural dysfunction, which suggests a key pathogenic role for oxidative stress in both AD and PD. Notably, mitochondrial dysfunction is also a prominent feature in these diseases, which is likely to be of critical importance in the genesis and amplification of reactive oxygen species and the pathophysiology of these diseases. In this review, we focus on changes in mitochondrial DNA and mitochondrial dynamics, two aspects critical to the maintenance of mitochondrial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCell DeathHumansMitochondriaNerve DegenerationNeuronsOxidative StressParkinson DiseaseReactive Oxygen SpeciesAmyloid beta-PeptidesReactive Oxygen Species1-methyl-4-phenyl-1,2,3,6-tetrahydropyradineADADDLAlzheimer diseaseamyloid-βamyloid-β protein precursorApoE4apolipoprotein EAPPAβAβ-derived diffusible ligandCOXcytochrome c oxidaseDLP1, aka Drp1dynamin-like protein 1electron transport chainETCFree radicalsLeber's hereditary optic neuropathyleucine-rich repeat kinase 2LHONLRRK2 or PARK8MERRFMfnmitochondrial DNAMitochondrial DNAMitochondrial dynamicsMitochondrial dysfunctionmitochondrial membrane potentialmitofusinMMPMPTPmtDNAmyoclonic epilepsy with red ragged fibers syndromeOMMOPA-1optic atrophy protein 1outer mitochondrial membraneoxidative phosphorylationOxidative stressOXPHOSParkinson diseasePDPINK1 or PARK6presenilinPSPTEN-induced putative kinasereactive oxygen speciesROSsingle-nucleotide polymorphismSNPSODsuperoxide dismutase

Identifiers

PMID23200807
PMCPMC3744189
OpenAlexW2027783468

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.