Treatment of Alzheimer's disease. Molecular pathology versus neurotransmitter-based therapy.
Cortical inhibitory neurotransmitters, neuropeptides, dopamine and noradrenaline are probably either not selectively or not critically affected in AD. It is, however, likely that a key change is shrinkage or loss of corticocortical pyramidal neurones, which probably use glutamate as their transmitter. This depletion appears to be circumscribed and clinically relevant.
Bowen
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Miriam Marks Department of Neurochemistry, Institute of Neurology, London.
D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D016229:Amyloid beta-Peptides / Q000235:genetics*; D016564:Amyloid beta-Protein Precursor; D002540:Cerebral Cortex / Q000473:pathology; D002891:Chromosomes, Human, Pair 21; D003001:Cloning, Molecular; D003523:Cycloserine / Q000008:administration & dosage; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D006801:Humans; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011480:Protease Inhibitors; D011498:Protein Precursors / Q000235:genetics*; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D005971:Glutamates; D018377:Neurotransmitter Agents; D011480:Protease Inhibitors; D011498:Protein Precursors; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D003523:Cycloserine