Evidence map›Paper›PMID 40071644›Full record

ArticleAdvanced biology2025

The Aging Substantia Nigra is Characterized by ROS Accumulation Potentially Resulting in Increased Neuroinflammation and Cytoskeletal Remodeling.

Britta Eggers, Simone Steinbach, Isabel Gil Aldea, Sharon Keers, Mariana Molina, Lea T Grinberg, Helmut Heinsen, Renata E Paraizo Leite, Johannes Attems, Caroline May and 1 more

Abstract read
In one paragraph

Article in Advanced biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
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  3. Review
  4. Article
  5. Article
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

11 authors.

Britta EggersMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801, Bochum, Germany.ORCID https://orcid.org/0000-0002-6553-4631
Simone SteinbachMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801, Bochum, Germany.
Isabel Gil AldeaNavarrabiomed Biobank, Hospital Universitario de Navarra, Pamplona, Navarra, 31008, Spain.
Sharon KeersInstitute of Neuroscience and Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, NE1 7RU, UK.
Mariana MolinaPhysiopathology in Aging Lab/Brazilian Aging Brain Study Group-LIM22, University of São Paulo Medical School, São Paulo, CEP 01246 903, Brazil.
Lea T GrinbergPhysiopathology in Aging Lab/Brazilian Aging Brain Study Group-LIM22, University of São Paulo Medical School, São Paulo, CEP 01246 903, Brazil.
Helmut HeinsenInstitute of Forensic Medicine, University of Wuerzburg, Versbacher Str. 3, 97078, Wuerzburg, Germany.
Renata E Paraizo LeitePhysiopathology in Aging Lab/Brazilian Aging Brain Study Group-LIM22, University of São Paulo Medical School, São Paulo, CEP 01246 903, Brazil.
Johannes AttemsTranslational and Clinical Research Institute, Newcastle University, Edwardson building, Campus for Ageing and Vitality, Newcastle-upon-Tyne, NE4 5PL, UK.
Caroline MayMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801, Bochum, Germany.
Katrin MarcusMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801, Bochum, Germany.

Funding

Investigating regional and cellular vulnerabilities to tau pathology in young-onset Alzheimer's diseaseR01AG075802 · NIA · MAYO CLINIC JACKSONVILLE · PI BERNARDINO Francesco GHETTI, Lea Tenenholz Grinberg · 2022 to 2026
$15.5M
Alzheimer's Society and Alzheimer's Research UKBundesministerium für Bildung und Forschung FZ 01GS08143Bundesministerium für Bildung und Forschung NGFNplusConselho Nacional de Desenvolvimento Científico e Tecnológico CNPQ 466763/2014-0Deutsche Forschungsgemeinschaft MA 325/5-1Germany and FoRUM F781-13HUPO Brain Proteome ProjectMinisterium für Innovation, Wissenschaft und Forschung des Landes Nordrhein-Westfalen 233-1.08.03.03-031‑68079Ministerium für Kultur und Wissenschaft des Landes Nordrhein-Westfalen 111.08.03.05-133974National Science Foundation K24053435National Science Foundation R01AG075802NIA NIH HHS R01 AG075802NIHR Newcastle Biomedical Research CentreUK Medical Research Council G0400074Verein zur Durchführung Neurowissenschaftlicher Tagungen e.V, Berlin
6 · The paper itself

Abstract

Aging is a progressive and irreversible process, serving as the primary risk factor for neurodegenerative disorders. This study aims to identify the molecular mechanisms underlying physiological aging within the substantia nigra, which is primarily affected by Parkinson's disease, and to draw potential conclusions on the earliest events leading to neurodegeneration in this specific brain region. The characterization of essential stages in aging progress can enhance knowledge of the mechanisms that promote the development of Parkinson's disease. To gain a comprehensive overview three study groups are utilized: young individuals (mean age: 28.7 years), middle-aged (mean age: 62.3 years), and elderly individuals (mean age: 83.9 years). Using the proteomic approach, crucial features of physiological aging are able to be identified. These include heightened oxidative stress, enhanced lysosomal degradation, autophagy, remodeling of the cytoskeleton, changes in the structure of the mitochondria, alterations in vesicle transportation, and synaptic plasticity.

Indexed as

AgingCytoskeletonNeuroinflammatory DiseasesReactive Oxygen SpeciesSubstantia NigraAdultAgedAged, 80 and overAutophagyFemaleHumansMaleMiddle AgedOxidative StressParkinson DiseaseReactive Oxygen Speciesagingdata independent acquisitiondopaminergic neuronslaser microdissectionproteomicssubstantia nigra

Identifiers

PMID40071644
PMCPMC12001008

What OpenQuestion holds

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LicenceCC BY
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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.