Zhurnal Vysshei Nervnoi Deyatelnosti Imeni I.P. Pavlova

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.

This study aimed to investigate resting-state network functional connectivity in patients with temporal lobe epilepsy (TLE) with and without comorbid depression. Using resting-state functional magnetic resonance imaging (rs-fMRI) and the XCP-D software package, we assessed functional connectivity between nodes of major resting-state neural networks: the default mode network (DMN), salience network (SN), dorsal attention network (DAN), somatomotor network (SMN), and frontoparietal control network (FPCN). The study included 77 patients with TLE (36 with depression, 41 without) and 48 healthy controls. Compared with both TLE without depression and healthy controls, patients with TLE and depression demonstrated decreased functional connectivity between key nodes of the SN, DAN, and DMN. In contrast, TLE without depression was characterized by increased connectivity between nodes of the DMN, FPCN, and SMN. A common feature for both TLE groups was increased connectivity between prefrontal nodes of the DMN and FPCN. These findings suggest distinct mechanisms of network reorganization in TLE depending on the presence of comorbid depression and highlight the importance of an integrative neuroimaging approach to epilepsy research.

In the study behavioral and neurophysiological indices of processing emotional facial expressions of anger, fear, joy, surprise, disgust and sadness in girls with single panic attacks (PA) and girls without panic attacks (norm), all the students of the medical university, were compared. In the PA group, facial expressions of anger and fear were recognized with an increased reaction time compared to joyful ones; in the norm group, differences associated with the type of expression were absent. Compared with the norm, in PA, a clear increase in the amplitude of the occipital components P100 and P200 to emotional faces was recorded, indicating increased exogenous attention to the facial emotions, with a more pronounced response to anger compared to other emotional expressions. An increase in the amplitudes of the P100 and P200 components in the ERP of the temporal regions in PA indicates increased activity of the limbic formations, which also leads to increased ascending attention to facial expression. In the frontal cortex, in PA the amplitude of the ERP components is increased, that is combined with signs of insensitivity of the early negativity of N90 to the type of emotional expressions. The results indicate an altered state of the attention network and limbic-prefrontal complex in a nonclinical group of girls with isolated panic attacks.

To clarify the informative value of EEG markers in the study of neural network organization of human brain, a quantitative assessment and analysis of the spatial organization of coherence (CohEEG), as well as a number of local and global graph analysis (GA) metrics based on this characteristic, were performed in 20 healthy subjects at resting state. The topograms of CohEEG and local GA metrics were compared with cortical projections of the four most significant neural networks: default mode network, sensorimotor network, executive function network, and frontoparietal network. For frequency bands theta2 (5.9–7.4 Hz), alpha1 (7.8–9 Hz), and, especially, alpha2 (9.4–10.2 Hz), a neural network non-specificity of the topography of a number of characteristics was revealed, i.e., the spatial coincidence of maximum values with cortical projections of several neural networks. It was suggested that there are two neural network hubs: sensorimotor hub and frontal hub, which are active even in resting state. The preliminary data obtained clarify the understanding of neural network EEG markers, the cerebral organization of resting state in norm, and can serve as a reference for similar comparative studies in brain pathology.

The effects of the transglutaminase inhibitor monodansylcadaverine on context memory maintenance and reconsolidation practically are not investigated. This work was devoted to the analysis of the role of transglutaminase (TG) in the formation, maintenance, and reconsolidation of long-term context memory in the terrestrial snail Helix lucorum. We used the transglutaminase inhibitor monodansylcadaverine and demonstrated an irreversible loss of memory if the inhibitor was injected 24 hrs after training. In conditions of memory reactivation effects of TG inhibitor were absent or diminished suggesting a role of TG in memory maintenance. Obtained results can be explained by participation of TG in epigenetic regulation. Exact mechanisms should be investigated in future.