Evidence map›Paper›PMID 31432604›Full record

ReviewAging cell2019

Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease.

Benjamin G Trist, Dominic J Hare, Kay L Double

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 411 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
411citing papers in PubMed, 6 pooled it
43.2field-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

411 citing papers in PubMed, 6 syntheses or guidelines pooled it, 717 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Are high copper levels related to Alzheimer's and Parkinson's diseases? A systematic review and meta-analysis of articles published between 2011 and 2022.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Pooled it
  6. Pooled it
  7. Taurochenodeoxycholic acid alleviates MPPIBRO neuroscience reports · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

351 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.

Benjamin G TristBrain and Mind Centre and Discipline of Pharmacology, Faculty of Medical and Health, The University of Sydney, Sydney, NSW, Australia.
Dominic J HareThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Vic., Australia.
Kay L DoubleBrain and Mind Centre and Discipline of Pharmacology, Faculty of Medical and Health, The University of Sydney, Sydney, NSW, Australia.ORCID 0000-0001-8712-7781
The University of Sydney · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease prevalence is rapidly increasing in an aging global population. With this increase comes exponentially rising social and economic costs, emphasizing the immediate need for effective disease-modifying treatments. Motor dysfunction results from the loss of dopaminergic neurons in the substantia nigra pars compacta and depletion of dopamine in the nigrostriatal pathway. While a specific biochemical mechanism remains elusive, oxidative stress plays an undeniable role in a complex and progressive neurodegenerative cascade. This review will explore the molecular factors that contribute to the high steady-state of oxidative stress in the healthy substantia nigra during aging, and how this chemical environment renders neurons susceptible to oxidative damage in Parkinson's disease. Contributing factors to oxidative stress during aging and as a pathogenic mechanism for Parkinson's disease will be discussed within the context of how and why therapeutic approaches targeting cellular redox activity in this disorder have, to date, yielded little therapeutic benefit. We present a contemporary perspective on the central biochemical contribution of redox imbalance to Parkinson's disease etiology and argue that improving our ability to accurately measure oxidative stress, dopaminergic neurotransmission and cell death pathways in vivo is crucial for both the development of new therapies and the identification of novel disease biomarkers.

Indexed as

AgingCellular SenescenceOxidative StressAnimalsCalciumHumansMitochondriaParkinson DiseaseSubstantia NigraCalciumantioxidantoxidative stressParkinson's diseasereactive oxygen species

Identifiers

PMID31432604
PMCPMC6826160
OpenAlexW2969573657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.