ReviewMolecular neurobiology2025
Apolipoprotein E in Alzheimer's Disease: Focus on Synaptic Function and Therapeutic Strategy.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- ZuoGui Pill Ameliorates Alzheimer's Disease-Like Pathology in 3xTg-AD Mice by Targeting Aβ Production, Tau Phosphorylation, Synaptic Loss, and Neuroinflammation.Molecular neurobiology · 2025Article
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Advances of therapeutic strategies for Alzheimer's disease.Journal of neurology · 2025Review
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
- Integrating genetic and immune profiles for personalized immunotherapy in Alzheimer's disease.Frontiers in medicine · 2025Review
- On the Therapeutic Use of Monoclonal Antibodies Against Amyloid Plaques in Older Adults with Down Syndrome: A Narrative Review and Perspective.Brain sciences · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Synaptic dysfunction is a critical pathological feature in the early phase of Alzheimer's disease (AD) that precedes typical hallmarks of AD, including beta-amyloid (Aβ) plaques and neurofibrillary tangles. However, the underlying mechanism of synaptic dysfunction remains incompletely defined. Apolipoprotein E (APOE) has been shown to play a key role in the pathogenesis of AD, and the ε4 allele of APOE remains the strongest genetic risk factor for sporadic AD. It is widely recognized that APOE4 accelerates the development of Aβ and tau pathology in AD. Recent studies have indicated that APOE affects synaptic function through a variety of pathways. Here, we summarize the mechanism of modulating synapses by various APOE isoforms and demonstrate the therapeutic potential by targeting APOE4 for AD treatment.
Indexed as
Identifiers
39214953What 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.