Apolipoprotein E (APOE) is a protein that plays an important role in lipid metabolism (including cholesterols), and has been implicated in synaptogenesis, repair of injured nerve tissue and the modulation of beta-amyloid plaques and neurofibrillary tangles that characterise Alzheimer’s Disease (AD) (for review, see Rocchi, Pellegrini, Siciliano, & Murri, 2003; Belloy, Napolioni, & Greicius, 2019). The gene coding for APOE is located on chromosome 19 and is polymorphic in the general population. The three most common alleles are ε2, ε3, and ε4, with approximate allele frequencies of 6%, 78% and 15% in healthy Caucasian Europeans (Eisenberg et al., 2010). Possession of the ε4 allele has been associated with poorer cognitive abilities and more rapid longitudinal decline in healthy older people, particularly in episodic memory (e.g., Schiepers et al., 2012; Jack et al., 2015; Jochemsen, Muller, van der Graaf, & Geerlings, 2012; Jorm et al., 2007; Marioni et al., 2016; Mondadori et al., 2007; Schultz et al., 2008; Shin et al., 2014; Lyall et al., 2019; see Wisdom, Callahan & Hawkins, 2011, for a meta-analysis). It has also been associated with a three-to-fourfold increase in the risk of late onset AD in a gene dose-dependent manner (Farrer et al., 1997) and with an earlier age at onset by nearly 6 years on average for ε4 carriers (Blacker et al., 1997). Indeed, some have argued that APOE has no influence on cognition in mid- or late-life beyond increasing risk for AD, such that effects found on cognition reflect the decades of a pre-symptomatic period of AD pathology (e.g., Vemuri et al., 2010; see also O’Donoghue, Murphy, Zamboni, Nobre, & Mackay, 2018).