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Vitamin metabolic disorders can cause diverse dysfunctions of both the peripheral and central nervous systems. There is conclusive evidence that cyanocobalamin (vitamin B12) and folic acid deficiencies may lead to diminished cognitive functions even to the extent of developing dementia. Cognitive impairments may be accompanied by involvement of other regions of the central nervous system, the corticospinal tract in particular, less frequently by brainstem and cerebellar disorders. Changes in nervous system functions in the presence of cyanocobalamin deficiency may predominate in the clinical picture, ahead of the occurrence of hematological changes. The paper considers the possible mechanisms for involvement of brain neurons in deficiency of cyanocobalamin and in that of folic acid in particular in patients with hyperhomocysteinemia. The low serum concentration of folic acid or cyanocobalamin in the elderly raises the risk of developing Alzheimer’s disease in future (by almost twice) and vascular dementia. The authors give the results of randomized clinical trials evaluating the efficacy of the vitamins used in patients with cognitive impairments. Thus, there are data that the use of cyanocobalamin in patients with lacunar infarcts and moderate cognitive impairments may give rise to their complete recovery and reduce the risk of depressive disorders. Intramuscular cyanocobalamin used in a daily dose of 1000 μg for 5 days, then 1000 μg once monthly is demonstrated to be efficacious. This therapy may be effective in patients with different types of dementia and cognitive diminution, primarily in those with these conditions and its serum concentration of less 150 pmol/l. Among the side effects while taking folic acid, there may be higher incidence rates of convulsive attacks. A number of trials have shown the efficacy of cyanocobalamin, pyridoxine, and folic acid in preventing acute cerebral ischemic episodes; however, not all the investigations could confirm this relationship. This may be related to patients’ age, therapy duration, blood inflammatory marker concentrations, and other factors.

Cognitive impairment (CI) develops not only in structural damage to the central nervous system, but also in encephalopathies of dysmetabolic and deficiency etiology. Recently, special attention is focused on the appearance of CI due to the deficiency of cobalamin (vitamin B 12 ) and folic acid (FA), the change in the level of homocysteine (HC). To detect vitamin B 1 2 deficiency is possible by examining key biomarkers in serum based on a decrease in the levels of vitamin B 1 2 and holotranscobalamin, and levels of methylmalonic acid (MMA) and HC. The article presents an analysis of studies conducted in Norway, Korea, India, and other countries to assess the risks of CI in the presence of reduced levels of vitamin B 1 2 in the elderly, which demonstrated a decrease in brain volume in the elderly (according to MRI data) in combination with altered test parameters that assess cognitive functions. In many studies, female patients with reduced levels of vitamin B 1 2 predominated among the studied patients. Also, some studies have demonstrated the effectiveness of complex CI therapy with the inclusion of vitamin B 1 2 (both for oral and intravenous administration). Oral vitamin B 1 2 therapy at a dose of 1000 μg has been shown to be adequate for the treatment of vitamin B 1 2 deficiency. Also, the administration of vitamin B 1 2 for prophylactic purposes is recommended for patients with subnormal or borderline concentrations of vitamin B 1 2 in the blood serum.