Evidence map›Paper›PMID 36278358›Full record

ReviewJournal of Parkinson's disease2022

Unraveling Parkinson's Disease Neurodegeneration: Does Aging Hold the Clues?

Colin Coleman, Ian Martin

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.0field-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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  13. Article
  14. Article
  15. The centenarian blueprint: lessons in defying Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  16. Review
  17. Noninvasive Therapies: A Forthcoming Approach to Parkinson's Treatment.CNS & neurological disorders drug targets · 2025
    Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Colin ColemanDepartment of Neurology, Jungers Center for Neurosciences, Oregon Health and Science University, Portland, OR, USA.
Ian MartinDepartment of Neurology, Jungers Center for Neurosciences, Oregon Health and Science University, Portland, OR, USA.
Oregon Health & Science University · US

Funding

Neuroscience of Aging, Neurodegeneration and Alzheimer’s DiseaseT32AG055378 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI JACOB RABER, HENRYK F URBANSKI · 2018 to 2026
$4.3M
LRRK2 in Parkinson's Disease NeurodegenerationR01NS119226 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI Ian Martin · 2022 to 2026
$1.4M
Conserved Aging Mechanisms Impacting Dopamine Neuron SurvivalR21AG075320 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI MARTIN, IAN · 2022 to 2023
$424k
NIA NIH HHS R21 AG075320NIA NIH HHS T32 AG055378NINDS NIH HHS R01 NS119226
6 · The paper itself

Abstract

Aging is the greatest risk factor for Parkinson's disease (PD), suggesting that mechanisms driving the aging process promote PD neurodegeneration. Several lines of evidence support a role for aging in PD. First, hallmarks of brain aging such as mitochondrial dysfunction and oxidative stress, loss of protein homeostasis, and neuroinflammation are centrally implicated in PD development. Second, mutations that cause monogenic PD are present from conception, yet typically only cause disease following a period of aging. Third, lifespan-extending genetic, dietary, or pharmacological interventions frequently attenuate PD-related neurodegeneration. These observations support a central role for aging in disease development and suggest that new discoveries in the biology of aging could be leveraged to elucidate novel mechanisms of PD pathophysiology. A recent rapid growth in our understanding of conserved molecular pathways that govern model organism lifespan and healthspan has highlighted a key role for metabolism and nutrient sensing pathways. Uncovering how metabolic pathways involving NAD+ consumption, insulin, and mTOR signaling link to the development of PD is underway and implicates metabolism in disease etiology. Here, we assess areas of convergence between nervous system aging and PD, evaluate the link between metabolism, aging, and PD and address the potential of metabolic interventions to slow or halt the onset of PD-related neurodegeneration drawing on evidence from cellular and animal models.

Indexed as

Parkinson DiseaseAgingAnimalsMitochondriaOxidative StressSignal TransductionAgingmetabolismmitochondriaParkinson’s disease

Identifiers

PMID36278358
PMCPMC9837701
OpenAlexW4307166650

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.