APP and amyloidosis: Despite high Aβ levels, Aβ oligomers and amyloid pathology, the BRI2‐Aβ mice have intact cognitive performance, providing evidence that Aβ and amyloid pathology alone do not impair cognition and that other APP processing derivatives or APP overexpression or misexpression may play a major role in the APP TG models' cognitive decline (Kim et al, 2013).