FAIM and Alzheimer disease: Thus, diminished FAIM expression in AD patients, combined with our previous report of increased protein aggregation in several organs after oxidative stress is delivered to FAIM-deficient mice (Kaku and Rothstein, 2020), and our current finding that FAIM prevents and disrupts Aβ oligomers and fibrils, demonstrates that FAIM is pathophysiologically relevant to current paradigms for the origin and/or progression of neurodegenerative diseases that involve disruption of proteostasis.