Abstract
Alzheimer's disease (AD) is among the main causes of cognitive impairment, memory loss, and dementia, particularly in old adults. It has been listed as one of the most expensive, lethal, and burdening diseases of the 21st century and develops with the process of aging worldwide (Scheltens et al., 2021). Currently, it is widely acknowledged that the typical pathogenesis of AD involves the deposition of amyloid-β (Aβ) and Tau proteins in the cerebral parenchyma and vasculature, intraneuronal neurofibrillary tangles, and the gradual degeneration of synapses (Scheltens et al., 2016; Rostagno, 2022). According to several hypotheses, abnormalities and dysfunctions in vascular structure, mitochondrial metabolism, oxidative stress, glucose utilization, and neuroinflammation are considered fundamental for AD pathology (Scheltens et al., 2016).