Neuropharmacology

Biography

Biography: Ivanova E A

Abstract

Today neuroinflammation is considered a response of the CNS not only to acute brain damage, but also to neurodegeneration. While early inflammation as a reaction to damage is directed to the activation of neuroprotection, a transition to chronic neuroinflammation is harmful for the CNS. Nowadays attention is being increasingly focused on the role of protein-degrading enzymes in inflammation. The activity of prolylendopeptidase enzyme (PREP) is known to change in both inflammation and neurodegeneration. Dipeptidyl peptidase IV (adenosine deaminase (ADA) binding protein, DPP-4) and related peptidases hydrolyze cytokines, neuropeptides and immunopeptides. In our laboratory the activity of PREP, DPP-4 and ADA was measured in plasma and cerebrospinal fluid (CSF) of outbred rats with experimental Parkinson’s disease (PD). Enzyme activity assessment demonstrates that the activities of peptide (DPP-4, PREP) and purine metabolism (ADA) enzymes were altered in rats with PD induced by 6-hydroxydopamine (6-OHDA) injection in the left medial forebrain bundle and by intraperitoneal subchronical administration of rotenone. PREP activity increased in the plasma and DPP-4 activity increased in the CSF of rats with rotenone-induced PD. Rats with a more severe PD induced by 6-OHDA had increased activity of DPP-4 in plasma and decreased activity of DPP-4 and PREP in the CSF. Reduced ADA activity in plasma was demonstrated in both models of PD. In summary, the results demonstrate that the activity of peptide and purine metabolism enzymes is altered in both PD models and these changes can be considered a non-specific marker of neuroinflammation and a possible target of neuroprotective drugs.