The neuropathological hallmarks of AD – amyloid β-protein (Aβ) plaques and neurofibrillary tangles (NFTs) comprised of hyperphosphorylated pTau protein – are well established and characterized in the brains of AD patients (Goedert et al., 1989; Hardy and Selkoe, 2002; Selkoe, 2004, 2008; Perrin et al., 2009; Goedert, 2015; Avila et al., 2016). These hallmark pathologies are hypothesized to induce and amplify inflammation and vascular abnormalities, drive synaptic and neuronal loss, and eventually lead to clinical AD-dementia (Choi et al., 2014; Ontiveros-Torres et al., 2016). The preclinical phase of AD-related pathological buildup is an insidious process which can take up to 20 years (Perrin et al., 2009; Bateman et al., 2012; Dubois et al., 2015; Bilgel et al., 2016; De Strooper and Karran, 2016; Dubois, 2018; Douglas and Scharre, 2019). Intervention during this preclinical stage, before definitive clinical symptoms appear and when synaptic and neuronal damage is still limited, should hold promise for increased therapeutic efficacy.