Evidence map›Paper›PMID 41432841›Full record

ReviewMetabolic brain disease2025

Role of apolipoprotein E4 in alzheimer's disease pathogenesis and emerging therapeutic strategies.

Sribha Natarajan, Saraswathy Sundara Dhakshinamurthy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2025. 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

2 authors.

Sribha NatarajanDepartment of Biomedical Science, Bharathidasan University, Tiruchirappalli, India. sribha2001@gmail.com.ORCID 0009-0008-6420-7509
Saraswathy Sundara DhakshinamurthyDepartment of Biomedical Science, Bharathidasan University, Tiruchirappalli, India. sdswathy@bdu.ac.in.ORCID 0000-0002-7693-0322

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer’s disease, the leading cause of dementia worldwide, is profoundly influenced by the apolipoprotein E4 allele, the primary genetic risk factor for sporadic Alzheimer’s disease. This allele exacerbates amyloid-beta pathology, tau phosphorylation, mitochondrial dysfunction, neuroinflammation, synaptic impairment, vascular dysfunction, and gut-brain axis alterations, contributing to disease progression. Recent advances elucidate apolipoprotein E4’s molecular mechanisms, including its role in lipid metabolism and receptor interactions, which drive these pathological processes. This review synthesizes current understanding of apolipoprotein E4’s contributions to Alzheimer’s disease pathogenesis, evaluates emerging therapeutic strategies such as gene editing, immunotherapy, and non-pharmacological interventions, and addresses ethical considerations in gene therapy. By integrating insights from molecular biology, clinical research, and therapeutic development, the review highlights apolipoprotein E4’s potential as a therapeutic target. It emphasizes the importance of personalized medicine and combination therapies to mitigate disease progression and improve patient outcomes, while underscoring the need for ethical frameworks to guide novel interventions.

Indexed as

Alzheimer DiseaseApolipoprotein E4Amyloid beta-PeptidesAnimalsGenetic TherapyHumansAmyloid beta-PeptidesApolipoprotein E4Alzheimer’s diseaseAmyloid-betaAPOE GenotypingApolipoprotein E4DementiaMitochondrial dysfunctionNeurofibrillary tanglesNeuroinflammation

Identifiers

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.