ReviewMolecular neurobiology2025
The Synergistic Role of ApoE4 and GSK3β in Alzheimer's Disease: Pathological Mechanisms and Therapeutic Implications.
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 4 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
4 citing papers in PubMed.
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- Article
- The APOE4-estrogen-microglia axis in perimenopausal cognitive changes: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Association between apolipoprotein E gene polymorphisms and the effects of high-intensity interval training on body composition in university students.Frontiers in nutrition · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by significant cognitive decline. Glycogen synthase kinase-3β (GSK3β), a key regulator in the pathological process of AD, exacerbates neuronal damage by phosphorylating tau proteins and promoting Aβ production. The activity of GSK3β is modulated by multiple signaling cascades, including the PI3K/AKT and Wnt/β-catenin transduction pathways. Furthermore, Apolipoprotein E ε4 (ApoE4) has been identified as a major genetic risk factor for increased susceptibility to AD. ApoE4 aggravates lipid metabolism disorders by interfering with LRP1 receptor function, inhibiting insulin signaling, and promoting the release of inflammatory factors (IL-6, TNF-α) and GSK3β. Specifically, ApoE4 may intensify the pathological process of AD by interacting with GSK3β, altering the balance of lipid metabolism in the body, regulating GSK3β activity, and modulating neuroinflammatory responses. This article systematically reviews the synergistic mechanisms of ApoE4 and GSK3β in AD and provides a new theoretical basis and potential intervention strategies for early diagnosis and targeted therapy of AD.
Indexed as
Identifiers
41222729What OpenQuestion 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 OpenQuestion graph.