| Summary: | This Thesis discusses the complex topic of the role of proteinase-activated receptors (PARs) in the physiology and pathophysiology of central nervous system diseases, and to some extent, the role of PARs in cancer pathobiology. Based on the results from this Thesis, we can conclude that PAR2 levels in the CSF do not track neuronal damage; therefore, PAR2 cannot be used as a marker of neuronal damage. Expression and activity of PAR2 in the brain appears to be mostly related to the activity of the disease process itself. To study the role of PAR2 in neurodegenerative diseases characterized by white matter and oligodendrocyte degeneration, a precise morphological descritption of individual diseases is essential. In the study aimed pathology of motor neuron disease we found reactive incre- ase in oligodendrocyte density in corticospinal tracts in reaction to white matter damage. In other study we confirmed the existence of a new variant of multiple system atrophy, atypical MSA (aMSA) charcterized by specific degenration of hippocampal neurons. Since the activity of kallikrein 6-PAR2 axis attenuates α-synuclein aggregation, its deficiency in hippocampus may be a prerequisite for its dominant degeneration leading to the develop- mant of α-synuclein neuronal inclusions and aMSA phenotype. Regarding the...
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