While mechanisms underlying mitochondrial dysfunction in AD remain incompletely understood, recent studies from multiple groups demonstrated that abnormal mitochondrial dynamics and distribution are likely involved: overexpression of familial AD APP mutations or exposure to soluble Aβ oligomers induced profound mitochondrial fragmentation, ultrastructural damage, and reduced mitochondrial distribution in neuronal processes in neuronal culture (Du et al., 2010; Manczak et al., 2010; Wang et al., 2009; Wang, Su, Siedlak, et al., 2008). Here, APP is linked to Alzheimer disease.