Evidence map›Paper›PMID 19526281›Full record

ArticleNeurotoxicity research2009

Mutant alpha-synuclein overexpression mediates early proinflammatory activity.

Xiaomin Su, Howard J Federoff, Kathleen A Maguire-Zeiss

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 152 citations in OpenAlex.

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  11. Role of cytokines and reactive oxygen species in brain aging.Mechanisms of ageing and development · 2023
    Review
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30 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 2 institutions in 1 country.

Xiaomin SuCenter for Aging and Developmental Biology, Aab Institute for Biomedical Research, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
Howard J Federoff
Kathleen A Maguire-Zeiss
University of Rochester · USGeorgetown University Medical Center · US

Funding

Toxicant, oxidative injury, dopamine & synuclein in PDR01ES014470 · NIEHS · UNIVERSITY OF ROCHESTER · PI MAGUIRE-ZEISS, KATHLEEN ANNE · 2007 to 2011
$1.7M
NIEHS NIH HHS R01 ES014470NIEHS NIH HHS R01ES014470
6 · The paper itself

Abstract

Microglia provide immune surveillance for the brain through both the removal of cellular debris and protection against infection by microorganisms and "foreign" molecules. Upon activation, microglia display an altered morphology and increased expression of proinflammatory molecules. Increased numbers of activated microglia have been identified in a number of neurodegenerative diseases including Parkinson's disease (PD). What remains to be determined is whether activated microglia result from ongoing cell death or are involved in disease initiation and progression. To address this question we utilized a transgenic mouse model that expresses a mutated form of a key protein involved in Parkinson's disease, alpha-synuclein. Herein, we report an increase in activated microglia and proinflammatory molecules in 1-month-old transgenic mice well before cell death occurs in this model. Frank microglial activation is resolved by 6 months of age while a subset of proinflammatory molecules remain elevated for 12 months. Both tyrosine hydroxylase mRNA expression and alpha-synuclein protein are decreased in the striatum of older animals evidence of dystrophic neuritic projections. To determine whether mutated alpha-synuclein could directly activate microglia primary microglia-enriched cell cultures were treated with exogenous mutated alpha-synuclein. The data reveal an increase in activated microglia and proinflammatory molecules due to direct interaction with mutated alpha-synuclein. Together, these data demonstrate that mutated alpha-synuclein mediates a proinflammatory response in microglia and this activity may participate in PD pathogenesis.

Indexed as

Age FactorsAnimalsAnimals, NewbornCalcium-Binding ProteinsCD36 AntigensCells, CulturedCerebral CortexCytokinesDisease Models, AnimalGene Expression RegulationHumansIntermediate Filament ProteinsMiceMice, Inbred C57BLMice, TransgenicMicrofilament ProteinsAif1 protein, mouseCalcium-Binding ProteinsCD36 AntigensCytokinesdesmuslinIntermediate Filament ProteinsMicrofilament ProteinsNitric Oxide Synthase Type IINos2 protein, mouseReactive Oxygen SpeciesRNA, MessengerTyrosine 3-Monooxygenase

Identifiers

PMID19526281
PMCPMC2877375
OpenAlexW2064978332

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.