Abstract: Amyloid-β (Aβ) and tau, the two hallmark proteins associated with Alzheimer’s disease (AD), exhibit distinct toxic effects but also interact synergistically within the disease pathology. The prevailing theory in AD pathology—the amyloid cascade hypothesis—highlights the pivotal role of increased processing of the amyloid precursor protein (APP). Initially cleaved by the major β-secretase (β-amyloid cleaving enzyme-1, BACE1) in the brain, then undergoes further cleavage by the γ-secretase complex, resulting in the production of Aβ40–42 and a set of intracellular C-terminal peptides known as Aβ and APP intracellular domain (β-AICDs) and soluble amyloid precursor protein β (sAPPβ) (Orobets and Karamyshev, 2023).