The strong prevalence of annexin A6 over A1 and A2 in neurons, along with the observation that A6 localizes to sites of injury in neurons [29] and is the key factor for initiation of membrane repair in myofibers [30, 31], led us to focus on annexin A6 expression as a potential approach for reducing Aβ-associated membrane damage, DN formation, and pathologic tau generation in AD. Here, TWF1 is linked to Alzheimer disease.