Although the mechanism underlying the onset and progression of AD is not fully clear, mutations of amyloid precursor protein that result in abnormal production of Aβ peptides (Ghiso et al., 2004), and the intracellular formation of neurofibrillary tangles (NFTs) in the brain (J. Z. Wang and Liu, 2008), have been suggested to play a dominant role in the pathogenesis of AD (Maldonado-Díaz et al., 2024). This evidence concerns the gene APP and Alzheimer disease.