Mechanisms of cognitive aging: norm and pathology

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Abstract

Cognitive aging is a multifactorial process that manifests itself in the deterioration of attention, memory, learning ability, decreased speed of information processing and decision-making, language capabilities, and impairment of executive functions. The mechanisms underlying these processes are not fully understood. The literature contains data on age-related changes in the structure, metabolism and activity of the brain, the occurrence of inflammatory processes and oxidative stress, as well as the influence of genetic and environmental factors. Although considerable evidence has been found of natural changes in the aging brain, they are not clearly integrated. At the same time, understanding the mechanisms of these processes will allow developing strategies for the prevention and treatment of cognitive impairment in old age to achieve a full quality of life at any stage. In neurophysiology, a distinction is made between “healthy aging” with minor changes in the cognitive function, and “pathological aging”, aggravated by the development of neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), characterized by a sharp decline in mental abilities, up to dementia. Changes in the brain of patients with AD and PD differ from those observed during normal aging. However, the mechanisms by which aging increases the risk of developing AD and PD remain unclear. To slow down/prevent the processes of cognitive decline, it is important to understand what compensatory mechanisms of the brain (cognitive reserve) exist that increase resistance to cognitive aging. This review briefly describes the main neural and network changes observed in healthy older people and leading to certain difficulties in memorization, problem solving and decision making. The main focus is on the consideration of the putative causes of cognitive aging. Part of the review concerns the contribution of aging mechanisms to the development of neurodegenerative diseases such as AD and PD. Data on the existing cognitive reserve and ways to maintain it are also provided.

About the authors

V. F. Kitchigina

Institute of Theoretical and Experimental Biophysics RAS

Author for correspondence.
Email: vkitchigina@gmail.com
Pushchino, Moscow Region, Russia

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