Amyloid-β (Aβ) deposition is an ubiquitous finding in Alzheimer disease (AD), but the role of Aβ in the disease progression is subject to debate. Xie et al. found abnormalities in structure and function of mitochondria specifically in the vicinity of Aβ plaques in a mouse model of AD. The results provide evidence for involvement of Aβ neurotoxity in the pathological process that impairs mitochondrial function in AD.