In 1887, S.A. Belyakov, a physician of the Imperial Medical and Surgical Academy, first described amyloid deposits in the brain of patients with dementia. Later, in 1906, A. Alzheimer revealed amyloid plaques and tau tangles in a patient with clinical signs of dementia. Over the following 100 years, the development of the concept of the amyloid origin of Alzheimer's disease (AD) confirmed numerous relationships between the brain accumulation of APs and cognitive decline. And if at the beginning of the amyloid era many researchers considered that the disease was caused by amyloid beta (Aβ) protein overproduction, in recent years they have increasingly pointed to a defect in the mechanisms of Aβ clearance, especially after the discovery of the lymphatic system of the brain. The role of disturbed homeostasis of redox-active metals, primarily iron and copper, in the development of the disease is also considered.The amyloid hypothesis of AD has served as the basis for several areas in the design of drugs, such as secretase inhibitors, immunomodulatory drugs for active and passive immunization. However, only one drug (Akatinol memantine, an inhibitor of NMDA receptors and glutamatergic excitotoxicity) for the treatment of AD has been introduced into clinical practice over the past 20 years. Of interest are the data obtained in new studies of Akatinol memantine, which suggest that the latter is able to some extent affect the main pathophysiological processes underlying the development of cognitive impairment in Alzheimer-type pathology.
The idiopathic normal pressure hydrocephalus (Hakim – Adams syndrome) is characterized by the expansion of cerebrospinal cavities, which is clinically manifested by triad symptoms: cognitive impairment, impaired gait and urination. In this research the severity and modality of cognitive impairment, the pattern of gait changes and the levels of protein biomarkers of amyloidosis and neurodegeneration and neuroimaging changes was evaluated for idiopathic normal pressure hydrocephalus, Alzheimer's disease and their combination. It has been established that for patients with idiopathic normal pressure hydrocephalus the most characteristic is the dysregulatory type of disorders of higher brain functions, while for patients with a combination of Alzheimer's disease and idiopathic normal pressure hydrocephalus, mnemonic disorders are also detected. The specific changes of cerebrospinal fluid in patients with idiopathic normal pressure hydrocephalus are higher levels of amyloid beta, a decrease concentration of tau and phosphorylated tau-protein compared to patients with Alzheimer's disease. In the case of a combination of diseases (comorbidity), it was characterized by intermediate results by cerebrospinal fluid biomarkers. We also revealed patterns of transformation of moderate cognitive impairment into dementia (according to the ratio of tau/Aβ‑42 and ftau /Aβ‑42). The value of evaluating the results of magnetic resonance imaging using special techniques that evaluate both the expansion of the ventricular system and atrophy of the brain parenchyma. Comorbid patients are characterized by a combination of these processes based on the results of neuroimaging. That is why it is necessary to use complex visually analog neuroimaging scales for differential diagnosis and establishing diagnosis. Also, in the course of this work, an algorithm is proposed for mandatory clinical-neuropsychological and laboratory-instrumental examination of patients with cognitive impairment in idiopathic normal pressure hydrocephalus, Alzheimer's disease and their combination.
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