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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Risk genes beyond APOE

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease associated with accumulation of amyloid beta peptides and intracellular neurofibrillary tangles formed by hyperphosphorylated Tau. Autophagy, an evolutionarily conserved process of self-degradation and turnover of cellular constituents, is important for normal cell growth but may be defective in diseases. A growing body of data implies that autophagy strongly affects AD pathogenesis. Autophagy mediates degradation of damaged organelles and proteins as well as neurotoxic aggregates, by regulating their clearance. Thus, impaired autophagy may account for the accumulation of protein aggregates. Since AD is characterized by neuroinflammation, impaired mitochondrial and lysosomal functions, and the accumulation of protein aggregates, the roles of autophagy/mitophagy in Alzheimer's will be extensively evaluated. In the current review, we will discuss the connection between autophagy/mitophagy and Alzheimer's. It seems that Alzheimer-related proteins such as APOE4, TREM2, PSEN1/2, APP and Tau can regulate autophagy. In turn, depending on the cellular system and animal model, autophagy regulating proteins such as Atg7, BECN1, GSK3B, MAP1LC3B, SQSTM1, TFEB and VCP can affect AD progression as discussed. We will also describe the effect of sex and lifestyle impact on autophagy and AD. Finally, we will describe how the current knowledge may contribute to potential therapeutic strategies.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Nechushtai, L., Chen, D., Dan, F., & Pinkas‐Kramarski, R. (2025). The connection between autophagy and Alzheimer’s disease. Inflammation Research. https://doi.org/10.1007/s00011-025-02118-0

Vancouver

Nechushtai L, Chen D, Dan F, Pinkas‐Kramarski R. The connection between autophagy and Alzheimer’s disease. Inflammation Research. 2025. doi:10.1007/s00011-025-02118-0. PMID: 41123674.

BibTeX

@article{nechushtai2025-41123674,
  author  = {Nechushtai, Lior and Chen, D. and Dan, Frenkel and Pinkas‐Kramarski, Ronit},
  title   = {{The connection between autophagy and Alzheimer’s disease}},
  journal = {Inflammation Research},
  year    = {2025},
  doi     = {10.1007/s00011-025-02118-0},
  pmid    = {41123674},
  url     = {https://doi.org/10.1007/s00011-025-02118-0}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

Key findings

Why it matters

This review discusses how autophagy and mitophagy relate to Alzheimer's disease, noting that impaired autophagy may account for the accumulation of protein aggregates and that Alzheimer-related proteins such as APOE4, TREM2, PSEN1/2, APP and Tau can regulate autophagy. It is a review of existing evidence and does not report a new treatment, cure or prevention for patients.

Study details

How this study scored 38/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 4 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 2 of 7; Citations per year 2 of 5; Impact for its field and year 3 of 6; Cited by studies here 0 of 6; Still being cited 1 of 4; Senior author's track record 2 of 4; Institution's track record 1 of 3; Multi-centre collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 38 of 100.38 of 100 points earned62 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Inflammation Research)
Journal's citation record 1 / 4 Inflammation Research: journal h-index 138 (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 2025 — 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)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 2 / 7 Cited 14 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 4.7 citations a year over 3 year(s) since 2025
Impact for its field and year 3 / 6 Cited 7.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 1 / 4 Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 2 / 4 Last-listed author Ronit Pinkas‐Kramarski: h-index 47 (OpenAlex, whole career)
Institution's track record 1 / 3 Tel Aviv University: institution h-index 1,018 (OpenAlex)
Multi-centre collaboration 0 / 3 OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 41123674)
Free to read 2 / 2 Free to read
Total 38 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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