Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disease histologically characterized by the presence of extraneuronal plaques, mainly formed by the 42-aminoacid isoform of amyloid-β (Aβ1–42), and by intraneuronal neurofibrillary tangles, mainly formed by the tau protein and its hyperphosphorylated isoforms (p-tau). AD is the most common cause of dementia, with an estimated lifetime risk of about 1 in 10 for men and 1 in 5 for women. As of 2020, there were approximately 50 million people living with dementia worldwide, a number set to increase to 152 million by 2050 (Scheltens et al., 2021). Two forms of AD exist. The most common form is late-onset AD with onset at ≥ 65 years which in most cases is a sporadic disorder with a number of genetic risk factors (e.g., APOE, CLU, CR1, TREM2, and PICALM). Early-onset AD occurs at ≤ 65 years and accounts for 5% to 6% of total cases of which about 10% have an autosomal-dominant form associated with point mutations of genes codifying for amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2), which are involved in Aβ production. Clinical features of sporadic and autosomal-dominant AD are similar, with early and prominent episodic memory loss (Scheltens et al., 2021). The Aβ cascade hypothesis of AD postulates that the accumulation of Aβ in the brain is the initial causative event of the disease process, starting 15–20 years before the onset of clinical symptoms. The accumulation of Aβ in the brain would trigger the aggregation of tau protein in neurofibrillary tangles. These effects are interconnected with microglial activation and astrocyte reactivity leading to neuritic dystrophy and disease progression. Over the past 30 years, this hypothesis has inspired intense research efforts to develop and test compounds that counteract the accumulation of Aβ in the brain (Karran et al., 2022).