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8 sty 2024 · APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints. Article 25 September 2023. Introduction. Alzheimer disease (AD) is a neurodegenerative disorder...
18 wrz 2024 · We report that in ApoE4 mice perivascular macrophages are the sole source and effectors of the ApoE4 mediating the neurovascular dysfunction, enhanced white matter damage and cognitive...
2 lis 2020 · APOE4 is a strong genetic risk factor for late-onset Alzheimer’s disease. Here, the authors show that APOE4 is associated with AD features in hiPSCs-derived cerebral organoids.
16 paź 2023 · Here, the authors developed fully automated chemiluminescence enzyme-immunoassay kit for ApoE4 and Pan-ApoE, and evaluated their diagnostic concordance with the APOE genotyping.
Here, we review these scientific advances and propose a cell type-specific APOE4 cascade model of AD. In this model, neuronal APOE4 emerges as a crucial pathological initiator and driver of AD pathogenesis, instigating glial responses and, ultimately, neurodegeneration.
2 cze 2023 · This review focuses on the pathophysiology of neuronal ApoE4 and explains how neuronal ApoE4 mediates Aβ deposition, pathological mechanisms of tau protein hyperphosphorylation, and potential...
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 inuencing β-amyloid (Aβ) deposition and clearance.