AB is a progressive neurodegenerative disease and the most common type of dementia. It accounts for at least two-thirds of all dementia cases in people aged 65 and older. It was named after the famous doctor Alois Alzheimer, who described the first case of the disease. The etiology of AD has not yet been fully known. There are numerous acquired, environmental and genetic risk factors. The disease occurs as a result of the accumulation of amyloid that forms plaques and tau-protein that forms neurofibrillary tangles in the brain. The amyloid hypothesis remains the dominant hypothesis in the pathogenesis of AD. Tau protein, mitochondrial dysfunction, glucose metabolism disorder, inflammation, dysfunction of the autophagy-lysosomal pathway, etc., play an important role in the pathogenesis of the disease. The onset of the disease is insidious and can only be dated imprecisely. We distinguish the preclinical stadium; MCI due to ADi; mild, moderate and severe dementia due to AD. The preclinical stage implies the existence of pathological changes in the brain, but without clinical manifestations of AD and this term is used only in research. For the diagnosis of AD, a detailed anamnesis, heteroanamnesis, physical examination with mental status examination, laboratory testing, neuroimaging and sometimes genetic testing is essential. The initial and most common symptom is episodic short-term memory loss. Impairment of short-term memory is accompanied by disruption of other cognitive domains. As the disease progresses, neuropsychiatric symptoms are common. The first forms of pharmacological treatment included the use of cholinesterase inhibitors and memantine, and neuropsychiatric symptoms were treated with antidepressants, antipsychotics and antiepileptics. The new approved drugs are aducanumab and lekanemab. The development of new methods for AD treatment are ongoing.