ReviewCell death discovery2025
The multifaceted roles of apolipoprotein E4 in Alzheimer's disease pathology and potential therapeutic strategies.
Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed.
- Genetic Determinants of Tau-PET Imaging in Alzheimer's Disease: A Narrative Review of Genome-Wide and Candidate-Gene Studies.Journal of imaging · 2026Review
- ApoE4 as a Therapeutic Target in Epilepsy: From Pathogenic Mechanisms to Precision Medicine.CNS neuroscience & therapeutics · 2026Review
- Review
- Rodent Models of Alzheimer's Disease: Bridging the Translational Gap Through Systems-Level Integration.Biomedicines · 2026Review
- Article
- Exploring the associations between lifestyle and dietary patterns with preclinical alzheimer's disease: findings from La Rioja cohort study.European journal of nutrition · 2026Article
- Precision pathways: optimising amyloid PET for sustainable Alzheimer's disease care.Journal of neurology · 2026Review
- The iron-energy metabolism axis in Alzheimer's pathogenesis: from mechanisms to interventions.Cell death discovery · 2026Review
- Review
- Apolipoprotein E Deficiency Impairs Human Microglial Proliferation Accompanied by Elevated Cellular Oxidative Stress.Journal of cellular and molecular medicine · 2026Article
- A common 19 bp APOE enhancer deletion is protective against Alzheimer's disease in African Americans.Nature communications · 2026Article
- Artificial Intelligence for Natural Products Drug Discovery in Neurodegenerative Therapies: A Review.Biomolecules · 2026Review
- PathoAnalyzer-I: An Integrative Bioinformatics Platform for Chronic Disease Analysis.Bioinformatics and biology insights · 2026Article
- From plate to brain: role of mediators and moderators on the impact of diet on Alzheimer's disease.Frontiers in nutrition · 2026Review
- ApoE expression across the CNS: Who, What, Where, When, and How (much)?Molecular neurodegeneration advances · 2026Review
- The role of nutrition and multimodal lifestyle interventions in Alzheimer's prevention and management: a mini-review.Frontiers in nutrition · 2026Review
- Why 11β-HSD1 inhibitors show variable efficacy in Alzheimer's therapy: an APOE4-dependent HSD11B1 mechanism.Theranostics · 2026Article
- The Tetrapeptide HAEE Promotes Amyloid-Beta Clearance from the Brain.International journal of molecular sciences · 2025Article
- Low frequency BOLD oscillations,medRxiv : the preprint server for health sciences · 2025Article
- Orthobiologics and Peptide Therapy for Central Nervous System Repair in Neurodegenerative Conditions.Cells · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common dementia in the elderly, is marked by progressive cognitive decline and neurodegeneration. Core pathological hallmarks include amyloid-beta (Aβ) plaques, hyperphosphorylated tau aggregates, neuroinflammation, and metabolic dysfunction (e.g., impaired glucose utilization, mitochondrial deficits). Apolipoprotein E4 (ApoE4), the strongest genetic risk factor for AD, interacts with these processes, yet its precise pathogenic mechanisms remain unclear. This review examines ApoE4's multifaceted contributions to AD pathogenesis, focusing on its roles in Aβ accumulation, tau hyperphosphorylation, neuroinflammatory activation, and metabolic dysregulation. We further evaluate emerging therapeutic strategies targeting these pathways, including ApoE4 modulation, anti-amyloid/tau interventions, and metabolic rescue approaches. Elucidating the molecular interplay between ApoE4 and AD pathology is critical for developing targeted therapies to modify disease progression and mitigate cognitive decline in patients.
Identifiers
What Socratic holds
Registered trials
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.