Amyloid pores in mitochondrial membranes

作     者：Neville Vassallo Neville Vassallo

作者机构：Department of Physiology&BiochemistryFaculty of Medicine and SurgeryUniversity of MaltaMsida MSD 2080Malta 

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

年 卷 期：2021年第16卷第11期

页      面：2225-2226页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by grants from the Malta Council for Science and Technology(No.R&I-2012-066) Faculty of Medicine and Surgery of the University of Malta(Nos.MDSIN08-21 and MDSBM20-24)and the University of Malta(No.PHBR06) 

主　　题：Huntington membranes amyloid 

摘      要：Neurodegenerative diseases of the amyloid type include common conditions such as Alzheimer’s disease,Parkinson’s disease,Huntington’s disease and amyotrophic lateral *** the fact that the phenotypes of these neuropathic maladies differ widely,ranging from cognitive to motor and psychotic disturbances,they are all characterized by the pathological accumulation and deposition in the central nervous system of well-ordered protein aggregates known as amyloid *** evidence indicates that rather than the end-stage mature fibrils,however,it is the smaller,metastable intermediate forms(known as oligomers)of the aggregated protein and peptides which represent the most neurotoxic species(Chiti and Dobson,2017).One suggested mechanism for such toxicity appears to involve the ability of oligomers to interact with plasma membranes whilst inducing cell leakage(Surguchov et al.,2017).However,contemporary work increasingly points to mitochondria,and hence mitochondrial membranes,as preferential targets for the pathogenic action of oligomers in the neuronal cell(Ghio et al.,2016).