Alzheimer’s disease is a neurodegenerative disease characterized by progressive neurocognitive dysfunction. Today, studying the pathogenesis of this disease remains an urgent problem. The review describes the pathogenetic basis of Alzheimer’s disease, including not only extracellular deposition of amyloid plaques and intracellular hyperphosphorylation of tau protein with subsequent formation of neurofibrillary tangles, but also mitochondrial dysfunction, impaired autophagy, neuroinflammation, etc. Data are presented on the effect of hyperphosphorylated tau protein on the breakdown and enhancement of β-amyloid peptide synthesis. Oligomerized tau protein causes proteasomal dysfunction and oxidative stress. Mitochondrial dysfunction is closely related to oxidative stress, which can be both a cause and a consequence. Autophagy, namely mitophagy, in turn, also plays an important role in the development of mitochondrial dysfunction. It can be argued that neuroinflammation is associated with all of the listed links in pathogenesis. This review also examines the influence of intestinal dysbiosis on the development of the disease. The complex mutual influence of pathogenetic mechanisms forms a multicomponent network of pathological processes. Understanding the Alzheimer’s disease pathogenesis is necessary in the search for methods for correcting impaired functioning mechanisms of the nervous system, which will help develop effective methods for treating this disease. In addition, to better understand the mechanisms of Alzheimer’s disease development, it is necessary to search for common pathogenetic factors with other neurodegenerative diseases.