Abstract: An update of the etiology of Alzheimer’s disease (AD): The current theory of the etiology of AD and the guidelines for most of the wide-ranging treatments activities are built around amyloid and tau protein as causative agents of the disease (Atlante et al., 2020). At present, based on a comprehensive evaluation of existing and contemporary studies, important questions arise regarding the causal role of amyloid and tau protein in the pathogenesis of AD (Morris et al., 2018). Analyzes of the available evidence does not allow obvious conclusion that amyloid, and especially tau protein, plays a key role in the etiology of AD (Morris et al., 2018). Evaluation of new data shows that accumulation of amyloid and altered tau protein is not the main cause of AD and more research is needed (Morris et al., 2018). As for the two substances planted to contribute to the development of AD, recent data indicate that the changes of amyloid and tau protein level and structure is triggered by some as yet unspecified factors, and then the triggered amyloid and tau protein interact with each other, exerting synergistic toxic effects on neurons and damaged neurons initiate the development of AD (Morris et al., 2018). It is certain that the pathology of amyloid and tau protein is currently ruled out as the sole cause of the development of dementia, as it cannot explain why about half of the world’s population have accumulation of different kinds of amyloid plaques and neurofibrillary tangles in the absence of dementia (Atlante et al., 2020). In these people, it was observed that the accumulation of neurofibrillary tangles increased exponentially with age (Atlante et al., 2020). In addition, it was noted that the appearance of hippocampus atrophy in elderly people with normal cognitive performance was not dependent on the presence of level and structure of amyloid (Atlante et al., 2020). Moreover, a multicenter study found that in patients diagnosed with AD, about one-third of the cases had no brain amyloid (Atlante et al., 2020).