Evidence map›Paper›PMID 21039522›Full record

ArticleJournal of neurochemistry2010

Synergistic effects of environmental risk factors and gene mutations in Parkinson's disease accelerate age-related neurodegeneration.

Jun Peng, May Lin Oo, Julie K Andersen

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Positron Emission Tomography with [International journal of molecular sciences · 2024
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  15. Classic and new animal models of Parkinson's disease.Journal of biomedicine & biotechnology · 2012
    Review
  16. Article
  17. Parkinson's disease.Sub-cellular biochemistry · 2012
    Review
  18. Oxidative stress in genetic mouse models of Parkinson's disease.Oxidative medicine and cellular longevity · 2012
    Review
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.

Jun PengBuck Institute for Age Research, Novato, California 94945, USA.
May Lin Oo
Julie K Andersen
Buck Institute for Research on Aging · US

Funding

Toxicant-induced alpha-synuclein pathology in primatesU54ES012077 · NIEHS · PARKINSON'S INSTITUTE · PI LANGSTON, JAMES WILLIAM · 2002 to 2007
$7.4M
Subcellular localization of alpha-synuclein and its impact on neurodegenerationRL1NS062415 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI ANDERSEN, JULIE KAY · 2007 to 2011
$2.2M
NIEHS NIH HHS U54 ES012077NIEHS NIH HHS U54 ES12077NINDS NIH HHS RL1 NS062415
6 · The paper itself

Abstract

As Parkinson's disease appears to be a multifactoral disorder, the use of animal models to investigate combined effects of genetic and environmental risk factors are of great importance especially in the context of aging which is the single major risk factor for the disorder. Here, we assessed the combined effects of neonatal iron feeding and environmental paraquat exposure on age-related nigrostriatal degeneration in transgenic mice expressing the A53T familial mutant form of human α-synuclein within these neurons. We report here that A53T α-synuclein mice exhibit greater susceptibility to paraquat. Increased oral intake of iron in the neonatal period leads to a progressive age-related enhancement of dopaminergic neurodegeneration associated with paraquat neurotoxicity. Furthermore, neurodegeneration associated with these combined genetic and environmental risk factors could be attenuated by systemic treatment with the bioavailable antioxidant compound EUK-189. These data suggest that environmental factors previously identified as contributors to neurodegeneration associated with sporadic Parkinson's disease may also be candidates for observed variations in symptoms and disease progression in monogenic forms and that this may mechanistically involve increased levels of oxidatively-induced post-translational nitration of α-synuclein.

Indexed as

Agingalpha-SynucleinAnimalsCell LineCells, CulturedDisease ProgressionEnvironmental ExposureHumansIronMiceMice, TransgenicMutationNerve DegenerationParaquatParkinson DiseaseRatsalpha-SynucleinIronParaquat

Identifiers

PMID21039522
PMCPMC3595019
OpenAlexW1652666369

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.