Glutamatergic neurotransmission in Alzheimer's disease.

The studies described here provide convincing evidence of glutamatergic deafferentation in Alzheimer's disease. This deafferentation is presumed to represent the biochemical correlate of pyramidal neuron dysfunction in the disorder. In addition, there is a growing consensus of opinion that there is no widespread depletion of glutamate NMDA receptors in Alzheimer's disease. The significance of glutamatergic neurotransmission abnormalities to the pathogenesis and clinical progression of the disease remains to be established.