The role of astrocytes in parkinson's disease
2014 Springer International Publishing Switzerland. All rights reserved. Unlike other disorders, astrocytes in regions undergoing neurodegeneration in patients with Parkinson's disease do not become reactive. Instead gray matter protoplasmic astrocytes accumulate α-synuclein, withdraw their processes from damaged neurons, and show altered expression of constituent proteins, including PINK-1, parkin, and DJ-1 (gene products associated with recessive Parkinson's disease). These and other gene products are normally up-regulated in astrocytes by disease states. Combined, these data suggest that protoplasmic astrocytes lose their protective function in patients with Parkinson's disease, leaving neurons vulnerable to perturbations and insults they would normally be protected from. Recent work also shows that astrocytes are able to take up and metabolize L-DOPA, the drug of choice for standard therapy for Parkinson's disease. It is therefore possible that ongoing astrocytic dysfunction may compromise the efficacy of L-DOPA therapy. These unique astrocytic responses to the disease process and current main therapy support the concept that astrocytes play a critical, under-recognized role in the initiation, progression, and treatment response of patients with Parkinson's disease.