Jiménez-Acosta Miguel A, Luckie-Duque Cristina A, Meraz-Ríos Marco A
Departamento de Biomedicina Molecular, CINVESTAV-IPN, Av. IPN 2508, San Pedro Zacatenco, 07360 Mexico City, Mexico.
J Leukoc Biol. 2025 Apr 23;117(4). doi: 10.1093/jleuko/qiaf007.
The seeded proliferation of harmful protein aggregates is fundamental to the pathophysiology of Alzheimer's disease (AD), although the initiation of this pathological cascade remains incompletely elucidated. Kaji et al. have developed a transgenic knockin mouse that expresses HaloTag-tagged APOE and discovered fibrillary aggregates of APOE in animals exhibiting amyloid-β (Aβ) amyloidosis. The APOE aggregates that tested positive for β-sheet-binding dyes induced Aβ amyloidosis in the endo-lysosomal system of microglia, a process modulated by microglial lipid metabolism and the JAK/STAT signaling pathway, indicating that the endocytic uptake and aggregation of APOE by microglia can initiate Aβ-plaque formation.
有害蛋白质聚集体的种子样增殖是阿尔茨海默病(AD)病理生理学的基础,尽管这一病理级联反应的起始机制仍未完全阐明。Kaji等人开发了一种表达HaloTag标记的载脂蛋白E(APOE)的转基因敲入小鼠,并在表现出淀粉样β蛋白(Aβ)淀粉样变性的动物中发现了APOE的纤维状聚集体。对β-折叠结合染料呈阳性反应的APOE聚集体在小胶质细胞的内溶酶体系统中诱导Aβ淀粉样变性,这一过程受小胶质细胞脂质代谢和JAK/STAT信号通路调节,表明小胶质细胞对APOE的内吞摄取和聚集可引发Aβ斑块形成。