Platelet glutamate and aspartate uptake in Huntington's disease.
A possible involvement of amino acid uptake mechanisms in the etiology of the human neurodegenerative disease, Huntington's disease (HD), was investigated. Measurement of glutamate (Glu) and aspartate (Asp) uptake was performed in blood platelets, which have previously been shown to constitute a peripheral model system for central amino acid uptake processes. Analyses of Glu and Asp accumulation at 10(-7) M and kinetic examination of the high affinity site for Glu indicate no significant differences between control and HD platelets. A genetically determined defect in amino acid uptake therefore does not seem to underlie the nerve cell loss observed in HD patients.
D001224:Aspartic Acid / Q000097:blood*; D001692:Biological Transport; D001792:Blood Platelets / Q000378:metabolism*; D005971:Glutamates / Q000097:blood*; D018698:Glutamic Acid; D006801:Humans; D006816:Huntington Disease / Q000097:blood*; D007700:Kinetics; D012016:Reference Values
D005971:Glutamates; D001224:Aspartic Acid; D018698:Glutamic Acid