Huntington's disease: N-methyl-D-aspartate receptor coagonist glycine is increased in platelets

Abstract

Experiments in vertebrates and striatal tissue cultures have provided evidence for a neuroexcitotoxic cause for the neurodegeneration in Huntington's disease (HD), via N-methyl-D-aspartate (NMDA) receptors. Glycine in vitro increases the response of NMDA receptors to its agonists via the NMDA receptor-associated glycine receptor, and the same effect has been observed in vivo. Significantly increased levels of glycine have previously been found in the cerebrospinal fluid of patients with HD. In this present study glycine was measured in platelets and plasma of patients with HD and in controls by high-pressure liquid chromatography. Mean glycine concentration was significantly increased (P < or = 0.01) in platelets in HD compared to controls, though plasma glycine was normal. A possible role for glycine in the pathogenesis of HD, based on the excitotoxicity hypothesis of HD, is discussed.