PLATELETS AS PERIPHERAL MODEL OF GLUTAMATE-RELATED EXCITOTOXICITY IN PARKINSON'S DISEASE

Over-stimulation of glutamate receptors and oxidative stress are two possible mechanisms that cooperate to selective degeneration of dopaminergic cells in Parkinson’s Disease (PD)1,2,3. Defects in mitochondrial enzymes, which make dopaminergic cells more susceptible to oxidative stress, have been found not only in substantia nigra of PD patients4, but also in their peripheral tissues5and blood platelets6,7,8,9. Recent studies also indicated that impaired mitochondrial function in platelets of PD patients is a characteristic of the disease and is not a consequence of pharmacological treatment10.