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Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases
Nixon RA, Rubinsztein DC.. Nature reviews. Molecular cell biology, 2024-08-06
Topic: Brain proteins, microglia and lab models
Autophagy is a lysosome-based degradative process used to recycle obsolete cellular constituents and eliminate damaged organelles and aggregate-prone proteins. Their postmitotic nature and extremely polarized morphologies make neurons particularly vulnerable to disruptions caused by autophagy-lysosomal defects, especially as the brain ages. Consequently, mutations in genes regulating autophagy and lysosomal functions cause a wide range of neurodegenerative diseases.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Nixon, R. A., & Rubinsztein, D. C. (2024). Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases. Nature reviews. Molecular cell biology. https://doi.org/10.1038/s41580-024-00757-5
Vancouver
Nixon RA, Rubinsztein DC. Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases. Nature reviews. Molecular cell biology. 2024. doi:10.1038/s41580-024-00757-5. PMID: 39107446.
BibTeX
@article{nixon2024-39107446,
author = {Nixon, R. A. and Rubinsztein, D. C.},
title = {{Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases}},
journal = {Nature reviews. Molecular cell biology},
year = {2024},
doi = {10.1038/s41580-024-00757-5},
pmid = {39107446},
url = {https://doi.org/10.1038/s41580-024-00757-5}
}
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Key findings
- Their postmitotic nature and extremely polarized morphologies make neurons particularly vulnerable to disruptions caused by autophagy-lysosomal defects, especially as the brain ages.
- Consequently, mutations in genes regulating autophagy and lysosomal functions cause a wide range of neurodegenerative diseases.
- Here, we review the role of autophagy and lysosomes in neurodegenerative diseases such as Alzheimer disease, Parkinson disease and frontotemporal dementia.
- We also consider the strong impact of cellular ageing on lysosomes and autophagy as a tipping point for the late-age emergence of related neurodegenerative disorders.
Why it matters
This review discusses how problems with autophagy and lysosome function contribute to neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. It is a review of mechanisms and does not report any treatment, cure, or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 60/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature reviews. Molecular cell biology) |
| Journal's citation record | 4 / 4 | Nature Reviews Molecular Cell Biology: journal h-index 622 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2024 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 396 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 99.0 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 6 / 6 | Cited 42.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 10 other studies in this library |
| Still being cited | 4 / 4 | Cited 395 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author David Chaim Rubinsztein: h-index 144 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Cambridge: institution h-index 1,973 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39107446) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 60 / 100 | — |
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