Abstract
Alzheimer's disease (AD) is the most common cause of dementia and contributes significantly to overall morbidity and mortality in the population. Despite the global and social importance of AD and dementia, despite extensive research, the etiopathogenetic mechanisms associated with AD have not yet been fully elucidated.
The disease can be divided into early onset or familial AD and sporadic or late onset AD, which differ in etiopathogenesis, prevalence, course, and genetic predisposition. The sporadic form of AD represents 99% of cases of the disease.
Its etiology is complex and largely unclear; it probably results from an interplay of many endogenous and exogenous factors. The present article provides a basic overview of hypotheses explaining the origin and progress of AD with emphasis on the most common amyloid hypothesis regarding excessive synthesis or insufficient clearance of toxic forms of amyloid peptides as the key factor of AD pathophysiology.
Other theories tend to explain AD development by the primary impact of other factors, such as tau protein, the inappropriate effects of some neurotransmitters, metabolic, neurovascular, inflammatory, infectious, and other factors. The article also summarizes some controversial conclusions on the pathophysiology of the disease, which probably stem from the general application of knowledge gained in the research on different forms of the disease and direct translation of research results on experimental models of AD to human disease.
Despite enormous advances in AD research, causal treatment of this devastating disease has not yet been found.