Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

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 40 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer disease (AD) is the most common form of dementia with hallmarks of β-amyloid deposits, neurofilament tangles, synaptic loss and neuronal death in the patient's brain. AD is a heavy burden in an ageing society as there are no effective therapies in treating the causes or slowing down its progression. Autophagy is a conserved process through formation of double membrane structure, namely autophagosome which is delivered to lysosome to digest cellular disposals. Autophagy maintains homoeostasis in the brain and is generally considered to protect brain functions against ageing. The first evidence of autophagy involvement in AD is that there is decreased expression of autophagy essential genes in post-mortem AD brains. Autophagy is also believed to be protective in neurodegeneration. However, the molecular and cellular mechanisms for dysfunction of autophagy in AD are not fully understood. Recent studies of autophagy regulation in AD cover the findings not only in neurons, but also from fast growing evidence for their importance in glia and brain vascular system. Thus, this review composes pertinent information regarding the involvement of autophagy in neurons, glias (including microglia, astrocyte, and oligodendrocyte), and brain vascular cells in AD, and their unique cellular mechanisms of this connection in AD pathology. We will provide effectual insights both in investigating autophagy in AD pathological mechanisms and in establishing a strategic approach for developing autophagy-based AD therapies.

Key findings

Why it matters

This review describes autophagy as a protective process in the brain and notes that autophagy-related genes are decreased in post-mortem Alzheimer's brains, with roles in neurons, glia, and blood vessels. It provides insights for future research but does not report an effective treatment.

Study details

How this study scored 40/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 0 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 3 of 7; Citations per year 2 of 5; Impact for its field and year 4 of 6; Cited by studies here 0 of 6; Still being cited 2 of 4; Senior author's track record 1 of 4; Institution's track record 1 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 40 of 100.40 of 100 points earned60 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 (Autophagy Reports)
Journal's citation record 0 / 4 Autophagy Reports: journal h-index 14 (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 3 / 7 Cited 16 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 5.3 citations a year over 3 year(s) since 2025
Impact for its field and year 4 / 6 Cited 10.0× 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 2 / 4 Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author Chenran Wang: h-index 9 (OpenAlex, whole career)
Institution's track record 1 / 3 Rutgers, The State University of New Jersey: institution h-index 1,147 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 40395993)
Free to read 2 / 2 Free to read
Total 40 / 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).

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

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.

APA 7th

Angst, G., Jia, N., Esqueda, L. T., Fan, Y., Cai, Q., & Wang, C. (2025). Autophagy in alzheimer disease pathogenesis and its therapeutic values. Autophagy Reports. https://doi.org/10.1080/27694127.2025.2471677

Vancouver

Angst G, Jia N, Esqueda LT, Fan Y, Cai Q, Wang C. Autophagy in alzheimer disease pathogenesis and its therapeutic values. Autophagy Reports. 2025. doi:10.1080/27694127.2025.2471677. PMID: 40395993.

BibTeX

@article{angst2025-40395993,
  author  = {Angst, Gabrielle and Jia, Nuo and Esqueda, Luis Tron and Fan, Yanbo and Cai, Qian and Wang, Chenran},
  title   = {{Autophagy in alzheimer disease pathogenesis and its therapeutic values}},
  journal = {Autophagy Reports},
  year    = {2025},
  doi     = {10.1080/27694127.2025.2471677},
  pmid    = {40395993},
  url     = {https://doi.org/10.1080/27694127.2025.2471677}
}

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here. Showing 12 of 26.

Related studies in Inflammation and the immune system

Also in Inflammation and the immune system

138 studies in the library are filed under Inflammation and the immune system with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Inflammation and the immune system hub.

Similar studies

More on Inflammation and the immune system

See all studies in Inflammation and the immune system →