Alzheimer's disease: a tale of two diseases?
Eleonora Nardini1
Ryan Hogan2
Anthony Flamier1
Gilbert Bernier3
1.Whitehead Institute for Biomedical Research,Cambridge,MA,USA2.Stem Cell and Developmental Biology Laboratory,H?pital Maisonneuve-Rosemont,Montreal,QC,Canada3.Stem Cell and Developmental Biology Laboratory,H?pital Maisonneuve-Rosemont,Montreal,QC,Canada;Department of Neurosciences,University of Montreal,Montreal,QC,Canada
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 features. Hence, 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 trials. Unfortunately, such research has yielded little output in terms of therapeutics targeting the disease's development and progression. In 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.
机标关键词：
论文发表日期：2021-10-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：7( 1958-1964 )
英文信息