Apolipoprotein E4 Exacerbates Aβ Oligomer-Induced Synaptotoxicity through Promoting Autophagic Degradation of Glutathione Peroxidase 4
Extensive synaptic loss and progressive neurodegeneration are defining pathological hallmarks of Alzheimer's disease (AD), primarily driven by soluble A{beta} oligomers and neurofibrillary tangles. The apolipoprotein E4 (APOE4) isoform further aggravates these pathological cascades, yet the precise molecular mechanisms underlying AD pathogenesis remain poorly elucidated. Store-operated calcium…
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