Evidence map›Paper›PMID 39367555›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2025

Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?

Zoë P Van Acker, Thomas Leroy, Wim Annaert

Abstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Neurodegenerative Diseases in Children: A Comprehensive Review.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    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

3 authors.

Zoë P Van AckerLaboratory for Membrane Trafficking, VIB Center for Brain & Disease Research, Leuven, Belgium.
Thomas LeroyLaboratory for Membrane Trafficking, VIB Center for Brain & Disease Research, Leuven, Belgium.
Wim AnnaertLaboratory for Membrane Trafficking, VIB Center for Brain & Disease Research, Leuven, Belgium.ORCID https://orcid.org/0000-0003-0150-9661

Funding

Alzheimer's Association AARF-20-677499Fonds Wetenschappelijk Onderzoek 11K1122NFonds Wetenschappelijk Onderzoek 1250425NFonds Wetenschappelijk Onderzoek G0C3620NFonds Wetenschappelijk Onderzoek G0C4220NFonds Wetenschappelijk Onderzoek I001322NKU Leuven C14/21/095KU Leuven SMINF KA/20/085Stichting Alzheimer Onderzoek #2020/030Stichting Alzheimer Onderzoek 2022/022Stichting Alzheimer Onderzoek 2023/034Vlaams Instituut voor Biotechnologie
6 · The paper itself

Abstract

Neurodegenerative diseases encompass a spectrum of conditions characterized by the gradual deterioration of neurons in the central and peripheral nervous system. While their origins are multifaceted, emerging data underscore the pivotal role of impaired mitochondrial functions and endolysosomal homeostasis to the onset and progression of pathology. This article explores whether mitochondrial dysfunctions act as causal factors or are intricately linked to the decline in endolysosomal function. As research delves deeper into the genetics of neurodegenerative diseases, an increasing number of risk loci and genes associated with the regulation of endolysosomal and autophagy functions are being identified, arguing for a downstream impact on mitochondrial health. Our hypothesis centers on the notion that disturbances in endolysosomal processes may propagate to other organelles, including mitochondria, through disrupted inter-organellar communication. We discuss these views in the context of major neurodegenerative diseases including Alzheimer's and Parkinson's diseases, and their relevance to potential therapeutic avenues.

Indexed as

LysosomesMitochondriaNeurodegenerative DiseasesAlzheimer DiseaseAnimalsAutophagyHumansNeuronsParkinson Diseaselysosomal homeostasismitochondrial homeostasisneurodegenerative diseases

Identifiers

PMID39367555
PMCPMC11662158

What Socratic 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 Socratic graph.