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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.
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...
8 sty 2024 · Neuronal APOE4 removal protects against tau-mediated gliosis, neurodegeneration and myelin deficits. Article Open access 20 February 2023. APOE4 impairs the microglial response in Alzheimer’s...
2 dni temu · The team created a new research model for studying Alzheimer's that involved transplanting human neurons producing the APOE4 protein into the brains of mice. When they removed microglia from the ...
2 dni temu · Huang and colleagues examine the effects of APOE4 and microglial depletion on Alzheimer’s disease (AD) pathogenesis in a chimeric mouse model with transplanted human induced pluripotent stem cell-derived neurons. They demonstrate the importance of neuronal APOE and the role of both APOE4 and microglia in promoting AD pathologies.
The ɛ4 allele of the apolipoprotein E gene (APOE) is the strongest genetic risk factor for late-onset Alzheimer disease (AD). Within the CNS, APOE is produced by a variety of cell types under different conditions, posing a challenge for studying its roles in AD pathogenesis.
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.
