Evidence map›Paper›PMID 41703264›Full record

ReviewMolecular psychiatry2026

Protective mutations associated with APOE in Alzheimer's disease.

Yuejia Ma, Yanxi Li, Guangrun Wu, Lulu Liu, Mengjie Tian, Xinyu Han, Xinyi Chen, Xiuchen Xuan, Tianhu Zheng, Xu Gao and 3 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Yuejia Ma *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Yanxi Li *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Guangrun Wu *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Lulu LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Mengjie TianDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Xinyu HanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Xinyi ChenDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Xiuchen XuanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Tianhu ZhengDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Xu GaoDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Qing XiaDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China. j1995y@163.com.ORCID http://orcid.org/0000-0002-0506-9977
Fuyuan LiCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang, 150081, China. lifuyuan@hrbmu.edu.cn.ORCID http://orcid.org/0009-0001-2204-427X
Dayong WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, 150081, China. wangdayonghmu@126.com.ORCID http://orcid.org/0000-0002-9672-3347

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer' s disease (AD) is a progressive neurodegenerative disorder characterized by a spectrum of cognitive impairments, ranging from mild memory loss to severe cognitive decline and, ultimately, death. The global incidence of AD is projected to increase significantly, with late-onset AD being predominantly sporadic in nature. Over the past three decades, the Apolipoprotein E (APOE) gene has been recognized as the most important single genetic determinant of sporadic AD risk. The APOE4 allele is a major risk factor for AD and is known to exacerbate the pathological process for AD. Identifying protective variants that may reduce the risk or delay the onset of AD is of great significance for the development of effective treatments. This review comprehensively examines the protective effects of APOE and its related protective mutations. It also explores the impact of these unique protective variants at the cellular level during the pathological progression of AD. Furthermore, the review compiles new insights for AD treatment offered by these protective mutations, exploring the potential applications of APOE and its related protective variants in advanced therapeutic strategies, including gene editing, RNA editing, and stem cell therapy.

Indexed as

Alzheimer DiseaseApolipoproteins EAnimalsGenetic Predisposition to DiseaseHumansMutationApolipoproteins E

Identifiers

PMID41703264

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.