Evidence map›Paper›PMID 33168089›Full record

ReviewActa neuropathologica communications2020

PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.

Peter M J Quinn, Paula I Moreira, António Francisco Ambrósio, C Henrique Alves

Open access · goldAbstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
285citing papers in PubMed, 3 pooled it
18.3field-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

285 citing papers in PubMed, 3 syntheses or guidelines pooled it, 429 citations in OpenAlex.

  1. Pooled it
  2. Rethinking 'rare'Journal of Parkinson's disease · 2025
    Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Cellular Mechanisms Enabling Mitochondria Transfer and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
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  20. Review

225 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

4 authors at 3 institutions in 2 countries.

Peter M J QuinnJonas Children's Vision Care, and Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative, Departments of Ophthalmology, Pathology and Cell Biology, Institute of Human Nutrition, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Paula I MoreiraCNC - Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
António Francisco AmbrósioCenter for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
C Henrique AlvesCenter for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal. chalves@fmed.uc.pt.ORCID 0000-0001-9776-5701
Association for Innovation and Biomedical Research on Light and Image · PTNewYork–Presbyterian Hospital · USUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson's disease (PD). PINK1, a protein kinase, and PARKIN, an E3 ubiquitin ligase, control the specific elimination of dysfunctional or superfluous mitochondria, thus fine-tuning mitochondrial network and preserving energy metabolism. PINK1 regulates PARKIN translocation in impaired mitochondria and drives their removal via selective autophagy, a process known as mitophagy. As knowledge obtained using different PINK1 and PARKIN transgenic animal models is being gathered, growing evidence supports the contribution of mitophagy impairment to several human pathologies, including PD and Alzheimer's diseases (AD). Therefore, therapeutic interventions aiming to modulate PINK1/PARKIN signalling might have the potential to treat these diseases. In this review, we will start by discussing how the interplay of PINK1 and PARKIN signalling helps mediate mitochondrial physiology. We will continue by debating the role of mitochondrial dysfunction in disorders such as amyotrophic lateral sclerosis, Alzheimer's, Huntington's and Parkinson's diseases, as well as eye diseases such as age-related macular degeneration and glaucoma, and the causative factors leading to PINK1/PARKIN-mediated neurodegeneration and neuroinflammation. Finally, we will discuss PINK1/PARKIN gene augmentation possibilities with a particular focus on AD, PD and glaucoma.

Indexed as

Alzheimer DiseaseAmyotrophic Lateral SclerosisAnimalsGene Knock-In TechniquesGlaucomaHumansHuntington DiseaseInflammationMacular DegenerationMiceMitochondriaMitophagyNeurodegenerative DiseasesParkinson DiseaseProtein KinasesPTEN-Induced Putative Kinaseparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesAlzheimer’s diseaseMitophagyNeurodegenerationPARKINParkinson’s diseasePINK1

Identifiers

PMID33168089
PMCPMC7654589
OpenAlexW3103775593

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.