Evidence map›Paper›PMID 33745923›Full record

ReviewBrain research2021

Is there a special relationship between complex I activity and nigral neuronal loss in Parkinson's disease? A critical reappraisal.

Nitya Subrahmanian, Matthew J LaVoie

Open access · hybridAbstract readReview
In one paragraph

Review in Brain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
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  5. Article
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  7. Review
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  9. Article
  10. Review
  11. Article
  12. Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024
    Article
  13. Article
  14. DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Review
  17. Article
  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.

Nitya SubrahmanianDepartment of Neurology, University of Florida, Gainesville, FL 32610, USA.
Matthew J LaVoieDepartment of Neurology, University of Florida, Gainesville, FL 32610, USA. Electronic address: mlavoie@ufl.edu.
University of Florida · US

Funding

Role of Parkin in Familial and Idiopathic Parkinson's DiseaseR01NS065013 · NINDS · UNIVERSITY OF FLORIDA · PI LAVOIE, MATTHEW J · 2010 to 2020
$3.8M
PATHOLOGIC LRRK2 SIGNALING IN FAMILIAL AND IDIOPATHIC PARKINSON'S DISEASER01NS110188 · NINDS · UNIVERSITY OF FLORIDA · PI LAVOIE, MATTHEW J · 2018 to 2022
$2.3M
NINDS NIH HHS R01 NS065013NINDS NIH HHS R01 NS110188
6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease manifesting both motor and non-motor symptoms. The motor features are generally ascribed to the selective loss of dopamine neurons within the substantia nigra pars compacta. While the precise etiology of PD remains elusive, multiple genetic and environmental elements have emerged as contributing factors. The discovery of MPTP-induced parkinsonism directed intense inquiry towards mitochondrial pathways, with a specific focus on mitochondrial complex I. Consisting of more than 40 subunits, complex I is the first enzyme of the electron transport chain that is required for mitochondrial ATP production. In this review, we present a critical analysis of studies assessing the prevalence and specificity of mitochondrial complex I deficiency in PD. In addition, we take the novel view of incorporating the features of genetically-defined bona fide complex I disorders and the prevalence of nigral involvement in such cases. Through this innovative bi-directional view, we consider both complex I changes in a disease of the substantia nigra and nigral changes in diseases of complex I. We assess the strength of association between nigral cell loss and complex I deficits, as well as the oft under-appreciated heterogeneity of complex I deficiency disorders and the variability of the PD data.

Indexed as

AnimalsCorpus StriatumDopamineDopaminergic NeuronsElectron Transport Complex IHumansMitochondriaMitochondrial DiseasesNeurodegenerative DiseasesParkinson DiseaseParkinsonian DisordersSubstantia NigraDopamineElectron Transport Complex IMitochondrial complex IMPTPNDUFAF2Parkinson’s diseasePINK1

Identifiers

PMID33745923
PMCPMC9520341
OpenAlexW3136710622

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.