Pyramidal neuron loss and "glycine-site therapy": a need for an animal model and study in late-life depression.
Localization and other studies of glutamatergic receptors are hampered, in part, as pyramidal neurons in the neocortex cannot yet be selectively destroyed in laboratory animals. Demonstration of glutamatergic neuron dysfunction in Alzheimer's disease may allow verification of a technique suitable for the study of these cells in disorders without histopathological hallmarks. This includes Major Depressive Disorder in the elderly which has a poor prognosis.
Bowen
D M
DM
Department of Neurochemistry, National Hospital for Nervous Diseases, University of London, UK.
Francis
P T
PT
Lowe
S L
SL
Pangalos
M N
MN
Procter
A W
AW
Steele
J E
JE
D000367:Age Factors; D000544:Alzheimer Disease / Q000473:pathology*; D000596:Amino Acids / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology*; D003866:Depressive Disorder / Q000473:pathology*; D004195:Disease Models, Animal; D005998:Glycine / Q000378:metabolism*; D006801:Humans
D000596:Amino Acids; D005998:Glycine