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Age-related neurodegenerative diseases, including Parkinson's disease, are characterized by a number of pathomorphological signs, such as neuron loss in certain brain structures, gliosis, iron accumulation. However, the literature indicates that these signs can also be observed during normal (physiological) aging. The aim of our work was to evaluate qualitative and quantitative morphochemical changes in neurons and neuroglia, and also to localize iron (II) compounds in the human striatum during physiological aging. In the old age group, compared with the mature one, the size of the neuron bodies was significantly smaller, the neuronal distribution density did not differ, but the distribution density of both the overall glia and astrocytes was significantly higher. In the old age group, the accumulation of iron (II) compounds were seen along the walls of the vessels, as well as inside the cytoplasm of neurons and glial cells. We conclude that the results obtained may serve as a basis for the comparative study of the neurodegenerative process and for the earlier and more accurate diagnosis of neurodegenerative diseases associated with aging, including Parkinson's disease.

For investigation of pathogenetic patterns of Parkinson's disease, it is important to adequately assess the mechanisms of age-related involution and morphological changes that are formed in the brain during this process. Clinical symptoms, detected in Parkinson's disease (rigidity, hypokinesia, tremor), indicate the involvement in the pathological process of nigrostriate brain formations due to the death of dopamine neurons in the compact part of the substantia nigra. At the same time, the loss of these neurons, as well as the change in the number of neuroglia cells in the substantia nigra of the brain, are detected not only in Parkinson's disease, but also in physiological aging. This review presents and compares data on the morphological changes in the compact part of the substantia nigra of the human brain in physiological aging and Parkinson's disease.

Using surviving slices of guinea pig somatosensory cortex, it was shown that functionally different regulation of spontaneous firing activity in different neurons corresponded to irregular distribution of glial satellites. Maximal increase of spike activity induced by acetylcholine (up to 36 spikes per second) was detected in "silent" neurons which account for 37.2% of nerve cells in layer V. According to the morphometric analysis, the same relative number of neurons (38.6%) were surrounded with glial satellites. In spontaneously active neurons only a small elevation of firing activity (5-22 spikes per second) above the basal level was recorded. The results allow to suggest that M-cholinergic reaction, controlling the spontaneous activity level, requires the additional energy supply for its maximal expression in inactive neurons. This is achieved by contacts of neurons with the surrounding glial satellites.