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In this model, neuronal APOE4 emerges as a crucial pathological initiator and driver of AD pathogenesis, instigating glial responses and, ultimately, neurodegeneration. In addition, we provide perspectives on future directions for APOE4 research and related therapeutic developments in the context of AD.
6 maj 2024 · New data confirm that APOE4 homozygosity is a major genetic cause of Alzheimer’s disease, warranting the development of specialized research strategies, treatment approaches and clinical trials.
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...
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...
1 cze 2023 · Recent studies have shown that neuronal ApoE4 may lead to greater neurotoxicity, which increases the risk of AD development. 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 therapeutic targets. 1.
APOE4 is the first identified genetic risk factor and remains as the strongest predictor for late-onset Alzheimer’s disease (AD). Studies of AD patients, AD patient-specific induced pluripotent stem cell-derived neurons and cerebral organoids, and ...
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 influencing β-amyloid (Aβ) deposition and clearance.
