Evidence map›Paper›PMID 40659647›Full record

Reviewnpj aging2025

The Rab3 family proteins in age-related neurodegeneration: unraveling molecular pathways and potential therapeutic targets.

Haijun He, Ruixue Ai, Evandro Fei Fang, Konstantinos Palikaras

Abstract readReview
In one paragraph

Review in npj aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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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.

Haijun HeDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 157 27, Athens, Greece.
Ruixue AiDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1474, Lørenskog, Norway.
Evandro Fei FangDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1474, Lørenskog, Norway.
Konstantinos PalikarasDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 157 27, Athens, Greece. palikarask@med.uoa.gr.

Funding

Akershus University Hospital (#269901, #261973, #262960European Commission GA101077374-SynaptoMitophagyFondation Santé 19656Greece 2.0, National Recovery and Resilience Plan Flagship program TAEDR-0535850the National Natural Science Foundation of China 81971327the Rosa sløyfe/Norwegian Cancer Society & Norwegian Breast Cancer Society 207819Wellcome Trust
6 · The paper itself

Abstract

The Rab3 protein family is composed of a series of small GTP-binding proteins, including Rab3a, Rab3b, Rab3c, and Rab3d, termed Rab3s. They play crucial roles in health, including in brain function, such as through the regulation of synaptic transmission and neuronal activities. In the high-energy-demanding and high-traffic neurons, the Rab3s regulate essential cellular processes, including trafficking of synaptic vesicles and lysosomal positioning, which are pivotal for the maintenance of synaptic integrity and neuronal physiology. Emerging findings suggest that alterations in Rab3s expression are associated with age-related neurodegenerative pathologies, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, among others. Here, we provide an overview of how Rab3s dysregulation disrupts neuronal homeostasis, contributing to impaired autophagy, synaptic dysfunction, and eventually leading to neuronal death. We highlight emerging questions on how Rab3s safeguards the brain and how their dysfunction contributes to the different neurodegenerative diseases. We propose fine-tuning the Rab3s signaling directly or indirectly, such as via targeting their upstream protein AMPK, holding therapeutic potential.

Identifiers

PMID40659647
PMCPMC12260062

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Registered trials

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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.