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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...
2 lis 2020 · APOE4 is the strongest genetic risk factor associated with late-onset Alzheimer’s disease (AD). To address the underlying mechanism, we develop cerebral organoid models using induced...
12 wrz 2024 · A variant called APOE4 is notorious for its link to Alzheimer’s. Can new insights into its function help stave off disease? 12 Sep 2024. 10:00 AM ET. By Jocelyn Kaiser. Ray Smith, 70 (left), and Carol Turner, 68 (right), with their mother Mattie Smith, 90, who has Alzheimer’s disease.
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.
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.
1 sie 2022 · Our current study shows that peripheral apoE4 is sufficient to impair brain functions and exacerbate amyloid pathogenesis.
19 gru 2023 · APOE4 +/+ restricts microglia in a non-responsive state (left part of the circle), resulting in exacerbated amyloid pathology (red) and dystrophic neurites (green). In contrast, deletion of APOE4 in microglia rescues these deficits (right part of the circle) Full size image.
