Evidence map›Paper›PMID 42712882›Full record

ArticleMedComm2026

Multi-Omics Analysis Reveals That Aβ42- Me3 Co-Aggregation Induces Mitophagy Blockade in Early Stages of Alzheimer's Disease.

Wenjie Zhu, Yuanyuan Zhang, Pengjie Li, Yingying Zhong, Yawei Lin, Xin Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Wenjie ZhuThe Key Laboratory for Biomedical Photonics of MOE At Wuhan National Laboratory for Optoelectronics-Hubei Bioinformatics and Molecular Imaging Key Laboratory Systems Biology Theme Department of Biomedical Engineering College of Life Science and Technology Huazhong University of Science and Technology Wuhan China.
Yuanyuan ZhangThe Key Laboratory for Biomedical Photonics of MOE At Wuhan National Laboratory for Optoelectronics-Hubei Bioinformatics and Molecular Imaging Key Laboratory Systems Biology Theme Department of Biomedical Engineering College of Life Science and Technology Huazhong University of Science and Technology Wuhan China.
Pengjie LiThe Key Laboratory for Biomedical Photonics of MOE At Wuhan National Laboratory for Optoelectronics-Hubei Bioinformatics and Molecular Imaging Key Laboratory Systems Biology Theme Department of Biomedical Engineering College of Life Science and Technology Huazhong University of Science and Technology Wuhan China.
Yingying ZhongThe Key Laboratory for Biomedical Photonics of MOE At Wuhan National Laboratory for Optoelectronics-Hubei Bioinformatics and Molecular Imaging Key Laboratory Systems Biology Theme Department of Biomedical Engineering College of Life Science and Technology Huazhong University of Science and Technology Wuhan China.
Yawei LinSchool of Chemistry Chemical Engineering and Life Sciences Wuhan University of Technology Wuhan China.
Xin LiuThe Key Laboratory for Biomedical Photonics of MOE At Wuhan National Laboratory for Optoelectronics-Hubei Bioinformatics and Molecular Imaging Key Laboratory Systems Biology Theme Department of Biomedical Engineering College of Life Science and Technology Huazhong University of Science and Technology Wuhan China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is one of the earliest pathological features of Alzheimer's disease (AD), preceding overt neurodegeneration and cognitive decline. Amyloid-β (Aβ) accumulation has long been considered a central pathogenic event in AD, yet how Aβ toxicity is mechanistically linked to mitochondrial impairment during early disease stages remains incompletely understood. To address this, we combined multi-omics with in vivo and in vitro genetic interventions. Here, we show that malic enzyme 3 (Me3) links Aβ aggregation to mitochondrial dysfunction in APP/PS1 mice and neuronal cells. At ultra-early and early AD stages (3 and 6 months), Me3 was upregulated and accumulated within mitochondria, where it colocalized with Aβ42 and physically interacted with it, an association linked to oxidative stress and impaired mitophagy. Knockdown of Me3 reduced mitochondrial reactive oxygen species, improved mitochondrial morphology, and alleviated mitophagy defects in both cellular and mouse models, with statistical significance across these functional measurements (

Indexed as

Alzheimer's diseasemalic enzyme 3mitophagyproteomicsβ‐amyloid

Identifiers

PMID42712882
PMCPMC13551346

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.