Abstract

160 Neurons are known to die continuously during the whole life of a human or animals [1]. However, until advanced age or even death, this neuronal loss does not influence negatively the functioning of the brain, including its involvement in neural or neuroendocrine regulation of the most important body functions. Even an increase in the rate of demise of specific neurons induced by unknown reasons in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease (PD), and others, does not impair brain func� tions, such as cognitive functions in Alzheimer’s dis� ease or motor functions in PD, for several decades [1]. This may be explained by compensation of functional insufficiency caused by neuronal loss related to the mechanisms of brain plasticity. However, at a certain threshold level of neuronal degeneration, compensa� tory capabilities of the brain become insufficient or exhausted, which results in impairments of specific body functions [2]. From the viewpoint of basic neu� rophysiology, it is important to understand the tempo� ral and functional relationships between two linked processes, neurodegeneration and compensation of functions of dead neurons, which continuously occur in the brain. This basic knowledge is very important for medicine too, because it may allow us to understand the mechanisms of regulation of both processes and to cope with them using prospective drugs. The aim of the present study was to examine the development of the linked processes of degeneration

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