According to current concepts, the excitatory amino acid glutamate is
involved in the pathogenesis of Parkinson's disease (PD). Overactivity
of glutamatergic projection neurons and beneficial effect of antiglut
amatergic substances in animal experiments suggest that excess supply
of glutamate might contribute to the pathophysiology of PD. Reduced ac
tivity of the glutamate metabolizing enzyme glutamine synthetase (GS)
leads to decreased uptake of glutamate and thus abundant glutamate. He
re we report that PD patients and age-matched controls are comparable
with respect to GS activity in peripheral blood mononuclear cells (PBM
C). These results imply no systemic dysregulation of the enzyme GS in
patients with PD.