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Autor:
Sang-Bae Han, Dae Yeun Hwang, Hwan-Soo Yoo, Mi Hee Park, Jin Tae Hong, Jin-Yi Han, Hae Won Jin, Dong Young Choi, Ki-Wan Oh
Publikováno v:
Journal of neuropathology and experimental neurology. 71(2)
Senile plaques composed of β-amyloid (Aβ) are a pathological hallmark of Alzheimer disease. Presenilin 2 (PS2) mutations increase Aβ generation in the brains of Alzheimer disease patients, but the underlying mechanism of Aβ generation by PS2 muta