Evidence map›Paper›PMID 40558538›Full record

ReviewCells2025

Autophagy and Alzheimer's Disease: Mechanisms and Impact Beyond the Brain.

Zaw Myo Hein, Thirupathirao Vishnumukkala, Barani Karikalan, Aisyah Alkatiri, Farida Hussan, Saravanan Jagadeesan, Mohd Amir Kamaruzzaman, Muhammad Danial Che Ramli, Che Mohd Nasril Che Mohd Nassir, Prarthana Kalerammana Gopalakrishna

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

10 authors.

Zaw Myo HeinDepartment of Basic Medical Sciences, College of Medicine, Ajman University, Ajman P.O. Box 346, United Arab Emirates.ORCID 0000-0001-7621-7132
Thirupathirao VishnumukkalaAnatomy Discipline, Human Biology Department, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Barani KarikalanDepartment of Pathology, Faculty of Medicine, MAHSA University, Bandar Saujana Putra, Petaling Jaya 42610, Selangor, Malaysia.
Aisyah AlkatiriAnatomy Discipline, Human Biology Department, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Farida HussanAnatomy Discipline, Human Biology Department, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0002-0197-4646
Saravanan JagadeesanDepartment of Anatomy, School of Medicine, Lakeside Campus, Taylor's University, Subang Jaya 47500, Selangor, Malaysia.
Mohd Amir KamaruzzamanDepartment of Anatomy, Faculty of Medicine, University Kebangsaan Malaysia, Jalan Yaacob Latif, Bandar Tun Razak, Cheras, Kuala Lumpur 56000, Malaysia.ORCID 0000-0003-4163-2234
Muhammad Danial Che RamliFaculty of Health and Life Sciences, Management and Science University, Seksyen 13, Shah Alam 40100, Selangor, Malaysia.ORCID 0000-0002-5261-0391
Che Mohd Nasril Che Mohd NassirDepartment of Anatomy and Physiology, Faculty of Medicine, University Sultan Zainal Abidin, Kuala Terengganu 20400, Terengganu, Malaysia.ORCID 0000-0002-2019-4565
Prarthana Kalerammana GopalakrishnaPhysiology Discipline, Human Biology Department, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0002-1428-5305

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles. Recent evidence highlights autophagy as a pivotal mechanism in cellular homeostasis, mediating the clearance of misfolded proteins and damaged organelles. However, impaired autophagy contributes significantly to AD pathogenesis by disrupting proteostasis, exacerbating neuroinflammation, and promoting synaptic dysfunction. This review aims to scrutinize the intricate relationship between autophagy dysfunction and AD progression, explaining key pathways including macroautophagy, chaperone-mediated autophagy (CMA), and selective autophagy processes such as mitophagy and aggrephagy. This further extends the discussion beyond the central nervous system, evaluating the role of hepatic autophagy in Aβ clearance and systemic metabolic regulation. An understanding of autophagy's involvement in AD pathology via various mechanisms could give rise to a novel therapeutic strategy targeting autophagic modulation to mitigate disease progression in the future.

Indexed as

Alzheimer DiseaseAutophagyBrainAmyloid beta-PeptidesAnimalsHumansMitophagyAmyloid beta-PeptidesAlzheimer’s diseaseamyloid-beta clearanceautophagyneurodegenerationtau pathology

Identifiers

PMID40558538
PMCPMC12191281

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.