Alzheimer’s disease:a tale of two diseases?

作     者：Eleonora Nardini Ryan Hogan Anthony Flamier Gilbert Bernier Eleonora Nardini;Ryan Hogan;Anthony Flamier;Gilbert Bernier

作者机构：Whitehead Institute for Biomedical ResearchCambridgeMAUSA Stem Cell and Developmental Biology LaboratoryHôpital Maisonneuve-RosemontMontrealQCCanada Department of NeurosciencesUniversity of MontrealMontrealQCCanada 

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10期

页      面：1958-1964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：This work was supported by grants from the National Science and Engineering Research Council of Canada(NSERC)(to GB) Canadian Institutes of Health Research(CIHR)(to GB) Maisonneuve-Rosemont Hospital Foundation and Fondation de la Famille Pierre Theroux(to GB).RH is supported by a fellowship from the Maisonneuve-Rosemont Hospital Foundation.AF is supported by post-doctoral fellowship from the Jane Coffin Childs Fund 

主　　题：aging Alzheimer’s disease BMI1 epigenetics familial late-onset sporadic 

摘      要：Sporadic late-onset Alzheimer’s disease(SLOAD)and familial early-onset Alzheimer’s disease(FEOAD)associated with dominant mutations in APP,PSEN1 and PSEN2,are thought to represent a spectrum of the same disorder based on near identical behavioral and histopathological ***,FEOAD transgenic mouse models have been used in past decades as a surrogate to study SLOAD pathogenic mechanisms and as the gold standard to validate drugs used in clinical ***,such research has yielded little output in terms of therapeutics targeting the disease’s development and *** this short review,we interrogate the widely accepted view of one,dimorphic disease through the prism of the Bmi1+/–mouse model and the distinct chromatin signatures observed between SLOAD and FEOAD brains.