Evidence map›Paper›PMID 37227619›Full record

ReviewCellular and molecular neurobiology2023

Roles of ApoE4 on the Pathogenesis in Alzheimer's Disease and the Potential Therapeutic Approaches.

Yu-Ying Sun, Zhun Wang, Han-Chang Huang

Open access · bronzeAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
13.8field-weighted citation impact, top 1% of its field
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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Brain, behavior, & immunity - health · 2026
    Article
  4. Article
  5. Review
  6. Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026
    Review
  7. Alcohol use andAlzheimer's & dementia. Behavior & socioeconomics of aging · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Yu-Ying SunBeijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-5524-9810
Zhun WangBeijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-1153-6148
Han-Chang HuangBeijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China. hanchang@buu.edu.cn.ORCID https://orcid.org/0000-0002-3574-5286
Beijing Union University · CN

Funding

Academic Research Projects of Beijing Union University JZ10202001Academic Research Projects of Beijing Union University XP202008Academic Research Projects of Beijing Union University ZK70202101
6 · The paper itself

Abstract

The Apolipoprotein E ε4 (ApoE ε4) allele, encoding ApoE4, is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). Emerging epidemiological evidence indicated that ApoE4 contributes to AD through influencing β-amyloid (Aβ) deposition and clearance. However, the molecular mechanisms of ApoE4 involved in AD pathogenesis remains unclear. Here, we introduced the structure and functions of ApoE isoforms, and then we reviewed the potential mechanisms of ApoE4 in the AD pathogenesis, including the effect of ApoE4 on Aβ pathology, and tau phosphorylation, oxidative stress; synaptic function, cholesterol transport, and mitochondrial dysfunction; sleep disturbances and cerebrovascular integrity in the AD brains. Furthermore, we discussed the available strategies for AD treatments that target to ApoE4. In general, this review overviews the potential roles of ApoE4 in the AD development and suggests some therapeutic approaches for AD. ApoE4 is genetic risk of AD. ApoE4 is involved in the AD pathogenesis. Aβ deposition, NFT, oxidative stress, abnormal cholesterol, mitochondrial dysfunction and neuroinflammation could be observed in the brains with ApoE4. Targeting the interaction of ApoE4 with the AD pathology is available strategy for AD treatments.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4Apolipoproteins EBrainHumansAmyloid beta-PeptidesApolipoprotein E4Apolipoproteins EAlzheimer’s disease (AD)Apolipoprotein E4 (ApoE4)Therapyβ-Amyloid (Aβ)

Identifiers

PMID37227619
PMCPMC10211310
OpenAlexW4378172805

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.