Because of its incidence and devastating consequences, Alzheimer’s disease (AD) has attracted much research attention in the last decades. Intensive work led to the identification of a number of cellular and molecular pathophysiologic mechanisms including Tau alterations, β-amyloid deposition, lipid homeostasis dysregulation, excitotoxicity, neuroinflammation or autophagy defects (Di Paolo and Kim, 2011; Ittner and Gotz, 2011; Heppner et al., 2015; Menzies et al., 2015; Wang and Mandelkow, 2015). Despite of the efforts, how these different pathways interact and contribute to disease pathogenesis remains poorly understood. Nonetheless, the presence of Aβ plaques, formed by the sequential cleavage of the amyloid precursor protein (APP), is a prominent neuropathologic feature of the disease and is still thought to be central to AD development (Nhan et al., 2015).