Disorders of energy metabolism play a significant role in the development of Alzheimer’s disease (BA), an atrophic brain disease that occurs at a later age and leads to total dementia. The disease is characterized by a gradual little noticeable onset at the age of 40-90, but more often after 65 years, a relatively slow, but steadily progressive course with a gradual decrease in memory, the disintegration of higher mental (cognitive) functions and mental activity in general (G. McKhann et al., 1984; SI Gavrilova et al., 1992). Pathologically, BA is characterized by atrophy and abnormally high density of senile plaques and neurofibrillary tangles (ZS Khatchaturian, 1985).
BA is a heterogeneous disease, various forms of which differ in their clinical picture, genetics and pathogenesis. BA is distinguished from early (aged up to 65 years) and late onset (aged 65 and older), which according to the previously existing national classification corresponded to Alzheimer’s disease and senile dementia of Alzheimer’s type (SDAT) (S.I. Gavrilova et al., 1992 ). Early-onset BAs are also referred to as BA of the presenile type.
The etiopathogenesis of AD is complex and not fully elucidated, but there is no doubt that genetic and age factors are leading in the development of the disease. Their influence on the pathogenesis of BA is largely mediated by changes in cerebral energy metabolism.