Alzheimer’s disease (AD) is characterized by a progressive cognitive decline linked to both the extracellular deposition of aggregated amyloid-β (Aβ) peptides into plaques and the intraneuronal aggregation of hyperphosphorylated tau (p-tau) proteins.1 AD risk depends on various genetic and environmental factors.2,3 Among protective factors, several epidemiological studies have reported an inverse relationship between caffeine intake and both age-related cognitive impairments and the risk of developing AD later in life (for reviews, see Flaten et al.,4 Cunha5 and Yelanchezian et al. 6). This evidence concerns the gene MAPT and Alzheimer disease.