Defects in mitochondrial enzymes have been found not only in substantia nig
ra, but also in platelets from Parkinson's Disease (PD) patients, suggestin
g a systemic impairment of energy metabolism. Since platelets present an en
ergy-dependent glutamate uptake similar to that described in central nervou
s system, glutamate uptake was determined in platelets from 34 PD patients
and 21 age-related normal controls, as Na+-dependent [H-3]glutamate influx;
glutamate level was also analyzed by reverse-phase HPLC. A 50% reduction o
f glutamate uptake (p < 0.001) was observed in idiopathic PD patients, resp
ect to controls and secondary parkinsonian syndromes. The decrease correlat
ed with the severity of PD, measured by the UPDRS (r = -0.54; P < 0.05). Gl
utamate level was increased in platelets of PD patients, but was not correl
ated to the uptake decrease. Both phoenomena may be explained by the modifi
cations of mitochondrial enzymes described in platelets, which could be use
d as a peripheral model of glutamatergic function in PD.