Evidence map›Paper›PMID 35655270›Full record

ReviewTranslational neurodegeneration2022

Defective mitophagy and the etiopathogenesis of Alzheimer's disease.

Kuan Zeng, Xuan Yu, Yacoubou Abdoul Razak Mahaman, Jian-Zhi Wang, Rong Liu, Yi Li, Xiaochuan Wang

Abstract readReview
In one paragraph

Review in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. International journal of molecular sciences · 2026
    Review
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  8. Programmed cell death: a promising management for Alzheimer's disease.Apoptosis : an international journal on programmed cell death · 2026
    Review
  9. 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

7 authors.

Kuan Zeng *Department of Psychiatry, Wuhan Mental Health Center, Wuhan, 430012, China.
Xuan Yu *Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yacoubou Abdoul Razak MahamanDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jian-Zhi WangCo-Innovation Center of Neurodegeneration, Nantong University, Nantong, 226001, China.
Rong LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yi LiDepartment of Psychiatry, Wuhan Mental Health Center, Wuhan, 430012, China. psylee@163.com.
Xiaochuan WangCo-Innovation Center of Neurodegeneration, Nantong University, Nantong, 226001, China. wxch@mails.tjmu.edu.cn.ORCID 0000-0001-8207-0042

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of impaired mitochondria and energy metabolism disorders are non-negligible features of both aging and age-related neurodegeneration, including Alzheimer's disease (AD). A growing number of studies suggest that mitophagy disorders play an important role in AD occurrence and development. The interaction between mitophagy deficits and Aβ or Tau pathology may form a vicious cycle and cause neuronal damage and death. Elucidating the molecular mechanism of mitophagy and its role in AD may provide insights into the etiology and mechanisms of AD. Defective mitophagy is a potential target for AD prevention and treatment.

Indexed as

Alzheimer DiseaseMitophagyHumansMitochondriaNeuronsAlzheimer’s diseaseAβMitophagyPINK1Tau

Identifiers

PMID35655270
PMCPMC9164340

What OpenQuestion holds

Textmetadata
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.