IntroductionAlzheimer’s disease (AD) accounts for almost 70% of dementia cases, and its pathophysiology is characterized by an accumulation of small peptides, amyloid-β (Aβ), in fibrils and plaques, followed by hyperphosphorylation, misfolding, and aggregation into neurofibrillary tangles of another protein, tau. Both aggregates are associated with strong inflammatory responses, synaptic dysfunction, and neuronal injury, causing considerable brain damage and impairing cognitive processes.1,2 In ...