Evidence map›Paper›PMID 23328732›Full record

ReviewFree radical biology & medicine2013

Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.

Laurie H Sanders, J Timothy Greenamyre

Abstract readReview
In one paragraph

Review 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 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
18.8field-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

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 341 citations in OpenAlex.

  1. A systematic review of molecular approaches that link mitochondrial dysfunction and neuroinflammation in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  2. Gender-specific gene profiling inIBRO neuroscience reports · 2026
    Article
  3. Article
  4. Environmental science. Processes & impacts · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Rescue of a Rotenone Model of Parkinson's Disease inInternational journal of molecular sciences · 2025
    Article
  19. Monoamine Oxidase Inhibitors in Toxic Models of Parkinsonism.International journal of molecular sciences · 2025
    Review
  20. Review

82 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

2 authors at 1 institution in 1 country.

Laurie H SandersPittsburgh Institute for Neurodegenerative Diseases, Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15260, USA.
J Timothy GreenamyrePittsburgh Institute for Neurodegenerative Diseases, Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15260, USA. Electronic address: jgreena@pitt.edu.
Institute for Neurodegenerative Disorders · US

Funding

VARIABILITY, STABILITY & SMOOTHNESS OF WALKINGP30AG024827 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JENNIFER S BRACH · 2004 to 2026
$28.6M
Stress Proteins and Neuroprotection Against Parkinsonian Cell DeathP01NS059806 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2009 to 2013
$6.3M
MtDNA damage as a biomarker for environmental mitochondrial toxicityR01ES020718 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENAMYRE, J TIMOTHY · 2011 to 2015
$2.6M
NIA NIH HHS P30 AG024827NIEHS NIH HHS R01 ES020718NINDS NIH HHS P01 NS059806
6 · The paper itself

Abstract

Parkinson disease (PD), the most common neurodegenerative movement disorder, is associated with selective degeneration of nigrostriatal dopamine neurons. Although the underlying mechanisms contributing to neurodegeneration in PD seem to be multifactorial, mitochondrial impairment and oxidative stress are widely considered to be central to many forms of the disease. Whether oxidative stress is a cause or a consequence of dopaminergic death, there is substantial evidence for oxidative stress both in human PD patients and in animal models of PD, especially using rotenone, a complex I inhibitor. There are many indices of oxidative stress, but this review covers the recent evidence for oxidative damage to nucleic acids, lipids, and proteins in both the brain and the peripheral tissues in human PD and in the rotenone model. Limitations of the existing literature and future perspectives are discussed. Understanding how each particular macromolecule is damaged by oxidative stress and the interplay of secondary damage to other biomolecules may help us design better targets for the treatment of PD.

Indexed as

Oxidative StressAnimalsDisease Models, AnimalDNA DamageDopaminergic NeuronsHumansLipid MetabolismParkinson DiseaseParkinson Disease, SecondaryProteinsRotenoneProteinsRotenone4-hydroxy-2-nonenaladenosine-5′-triphosphateATPcerebrospinal fluidCSFDAdopamineelectron transport chainETCFree radicalsHNEhydroxyl radicalLBL-DOPAlevodopa, l-3,4-dihydroxyphenylalanineLewy bodyMacromoleculesmalondialdehydeMDAmitochondrial DNAmtDNAO(2)(−)OH(•)Oxidative damageParkinson diseasePDpolyunsaturated fatty acidPUFAreactive oxygen speciesROSRotenoneSNsubstantia nigra pars compactasuperoxideventral tegmental areaVTA

Identifiers

PMID23328732
PMCPMC3677955
OpenAlexW2070066327

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.