Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease.
Sodium dependent D-aspartate and Ca2+/Cl-independent L-glutamate binding assays were used to assess the integrity of glutamate uptake sites and postsynaptic NMDA receptor levels in control and Alzheimer's disease temporal cortex. The number of glutamate uptake sites was significantly and substantially reduced in accordance with previous findings. However, NMDA receptor levels were unchanged. This finding suggests that glutamatergic presynaptic elements are severely reduced in Alzheimer's disease, whilst postsynaptic elements remain intact.
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism*; D001224:Aspartic Acid / Q000378:metabolism; D005260:Female; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D006801:Humans; D008297:Male; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D013702:Temporal Lobe / Q000378:metabolism*
D005971:Glutamates; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D018698:Glutamic Acid