Evidence map›Paper›PMID 40719892›Full record

ReviewNeurochemical research2025

Mitochondrial Damage and Autophagy Dysregulation in Alzheimer's Disease: Mechanisms and Therapeutic Opportunities.

Qian Yu, Li Li, Shuyi Yu, Jialin Han, Qian Cheng, Zhikang Cui, Hang Chen, Ming Li, Zhiming Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

9 authors.

Qian YuDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Li LiDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Shuyi YuDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Jialin HanDepartment of Clinical Laboratory, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Qian ChengDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Zhikang CuiDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Hang ChenDepartment of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Ming Li *Department of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China. drmingli@yeah.net.
Zhiming Lu *Department of Clinical Laboratory Medicine, Shandong Provincial Hospital Afliated to Shandong First Medical University, Jinan, 250021, Shandong, China. luzhiming@sdu.edu.cn.

Funding

Key Technology Research and Development Program of Shandong Province 2022CXGC010507Taishan Scholars Program of Shandong Province tsqnz20240852
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that causes progressive neurodegeneration and a variety of cognitive deficits. Of note, mitochondrial malfunctions occur early in the disease's development. Mitophagy impairment leads to the build-up of damaged mitochondria inside the cells, causing malfunction and eventual death of the cells. This review summarizes the mechanisms linking mitochondrial damage and autophagy dysregulation to AD and highlights potential therapeutic opportunities. We summarize how mitochondrial dysfunction contributes to AD, including defects in mitochondrial biogenesis, impaired dynamics, the impact of AD-related protein aggregates on mitochondrial integrity, and defective axonal transport. We also explore the roles of mitophagy in AD, including its function in the removal of harmed proteins and organelles. Finally, we highlight the therapeutic strategies for the treatment of AD, targeting molecular components involved in mitochondrial damage and autophagy dysregulation in AD, i.e., antioxidants, mitochondrial modulators, and mitophagy enhancers.

Indexed as

Alzheimer DiseaseAutophagyMitochondriaAnimalsHumansMitophagyAlzheimer’s diseaseAβMitochondrial dysfunctionMitophagyp-tau

Identifiers

PMID40719892

What Socratic holds

Textmetadata
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 Socratic graph.