Excitatory dicarboxylic amino acid and pyramidal neurone neurotransmission of the cerebral cortex in Alzheimer’s disease

Drug development for Alzheimer’s disease has so far had little success, possibly due to failure to correct abnormalities of neurones other than the corticopetal. Most enquiries indicate that cortical inhibitory neurotransmitters are neither selectively nor critically affected. It is highly probable that shrinkage or loss of corticocortical association fibres occurs. This change appears to be circumscribed, clinically relevant and to involve neurotransmitter glutamate. Modulatory domains of the N-methyl-D-aspartate receptor complex are identified as sites at which potential therapeutic agents might be safely directed.