Defective autophagy and Alzheimer’s disease: is calcium the key?

作     者：Riccardo Filadi Paola Pizzo 

作者机构：Department of Biomedical Sciences University of Padua and Neuroscience Institute-Italian National Research Council (CNR) 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2019年第14卷第12期

页      面：2081-2082页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100203[医学-老年医学] 10[医学] 

基　　金：supported by Italian Ministry of University and Scientific Research,the University of Padua(to PP) the EU Joint Programme-Neurodegenerative Disease Research(CeBioND)(to PP) UNIPD Funds for Research Equipment-2015 

主　　题：Alzheimer is cell tens has PS1 PS2 

摘      要：Presenilins and autophagy: Presenilin 1 (PS1) and presenilin 2 (PS2) are homologous, multi-pass transmembrane proteins endowed with pleiotropic functions, ranging from the regulation of membrane trafficking to cell differentiation. Their catalytic activity within the γ-secretase complex, an aspartyl-protease responsible for the intramembrane cleavage of several different type I transmembrane proteins, has been intensively studied in the context of Alzheimer’s disease (AD). Indeed, tens of autosomal dominant mutations in the PSEN1 and PSEN2 genes (encoding PS1 and PS2, respectively) have been associated with the rare familial forms of AD (FAD).