Alzheimer's disease: a tale of two diseases?

• Published in: Neural regeneration research Vol. 16; no. 10; pp. 1958 - 1964
• Main Authors: Nardini, Eleonora, Hogan, Ryan, Flamier, Anthony, Bernier, Gilbert
• Format: Journal Article
• Language: English
• Published: India Wolters Kluwer India Pvt. Ltd 01.10.2021; Medknow Publications and Media Pvt. Ltd; Medknow Publications & Media Pvt. Ltd; Whitehead Institute for Biomedical Research,Cambridge,MA,USA%Stem Cell and Developmental Biology Laboratory,H?pital Maisonneuve-Rosemont,Montreal,QC,Canada%Stem Cell and Developmental Biology Laboratory,H?pital Maisonneuve-Rosemont,Montreal,QC,Canada; Department of Neurosciences,University of Montreal,Montreal,QC,Canada; Wolters Kluwer - Medknow; Wolters Kluwer Medknow Publications
• Subjects: aging; alzheimer’s disease; bmi1; epigenetics; familial; late-onset; sporadic; Alzheimer's disease; Amyloid beta-protein; Care and treatment; Development and progression; Gene expression; Gene mutations; Genetic aspects; Health aspects; Presenilins; Review; Rodents; Canada; familial; sporadic; Alzheimer’s disease; aging; BMI1; late-onset; epigenetics; Alzheimer's disease
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.308070

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.