Evidence map›Paper›PMID 23643800›Full record

ReviewProgress in neurobiology

Mitochondrial dysfunction and oxidative stress in Parkinson's disease.

Sudhakar Raja Subramaniam, Marie-Francoise Chesselet

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 457 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
457citing papers in PubMed, 5 pooled it
22.9field-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

457 citing papers in PubMed, 5 syntheses or guidelines pooled it, 856 citations in OpenAlex.

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  9. Phytochemical Profile and Bioactive Potential ofAntioxidants (Basel, Switzerland) · 2026
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397 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.

Sudhakar Raja SubramaniamDepartment of Neurology, David Geffen School of Medicine, UCLA, 710 Westwood Plaza, Los Angeles, CA 90095-1769, USA.
Marie-Francoise Chesselet
University of California, Los Angeles · US

Funding

UCLA CENTER FOR THE STUDY OF PARKINSON'S DISEASEP50NS038367 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHESSELET, MARIE-FRANCOISE S · 1999 to 2011
$15.3M
Project 4: Pesticides and Genes In PD: Studies In HumansP01ES016732 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHESSELET, MARIE-FRANCOISE S · 2008 to 2012
$6.7M
NIEHS NIH HHS P01 ES016732NIEHS NIH HHS P01ES016732NINDS NIH HHS P50 NS038367NINDS NIH HHS P50 NS38367
6 · The paper itself

Abstract

Parkinson's disease (PD) is a movement disorder that is characterized by the progressive degeneration of dopaminergic neurons in substantia nigra pars compacta resulting in dopamine deficiency in the striatum. Although majority of the PD cases are sporadic several genetic mutations have also been linked to the disease thus providing new opportunities to study the pathology of the illness. Studies in humans and various animal models of PD reveal that mitochondrial dysfunction might be a defect that occurs early in PD pathogenesis and appears to be a widespread feature in both sporadic and monogenic forms of PD. The general mitochondrial abnormalities linked with the disease include mitochondrial electron transport chain impairment, alterations in mitochondrial morphology and dynamics, mitochondrial DNA mutations and anomaly in calcium homeostasis. Mitochondria are vital organelles with multiple functions and their dysfunction can lead to a decline in energy production, generation of reactive oxygen species and induction of stress-induced apoptosis. In this review, we give an outline of mitochondrial functions that are affected in the pathogenesis of sporadic and familial PD, and hence provide insights that might be valuable for focused future research to exploit possible mitochondrial targets for neuroprotective interventions in PD.

Indexed as

AnimalsApoptosisDopaminergic NeuronsHumansMitochondriaMutationOxidative StressParkinson DiseaseMitochondrial dysfunctionParkinson's disease

Identifiers

PMID23643800
PMCPMC3742021
OpenAlexW2006696253

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.