Summary
Emerging evidence demonstrates that thrombin exerts physiological and pathological
functions in the central nervous system. Both prothrombin and its active form thrombin
have been detected locally in the brain. The cellular functions of thrombin are mainly
regulated by G protein-coupled protease-activated receptors (PARs). Thrombin can signal
via PAR-1, PAR-3 and PAR-4. Some neurological diseases (e.g. Alzheimer’s disease or
Parkinson’s disease) are characterized by increased levels of both active thrombin
and PAR-1. This indicates that thrombin and its receptor may be closely involved in
the development of neurodegenerative processes. The role of thrombin in brain injury
can be either protective or deleterious, depending on the concentration of thrombin.
Thrombin at high concentrations exacerbates brain damage. In contrast, low concentrations
of thrombin rescue neural cells from death after brain insults. Also thrombin preconditioning
has neuroprotective effects. Therefore, thrombin and thrombin receptors represent
novel therapeutic targets for treating neurodegenerative diseases.
Keywords
Thrombin - PAR - central nervous system - neurodegeneration - neuroprotection