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Alzheimer's disease: Glutamate depletion in the hippocampal perforant pathway zone
Author(s) -
Hyman Bradley T.,
Van Hoesen Gary W.,
Damasio Antonio R.
Publication year - 1987
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410220110
Subject(s) - perforant pathway , glutamate receptor , entorhinal cortex , hippocampal formation , perforant path , neuroscience , hippocampus , alzheimer's disease , neurotransmitter , neurochemical , biology , chemistry , psychology , medicine , disease , central nervous system , dentate gyrus , receptor
The perforant pathway is the primary source of cortical input to the hippocampal formation. Its cells of origin, in the entorhinal cortex, are destroyed in Alzheimer's disease. Because the principal neurotransmitter of the perforant pathway's excitatory action is thought to be glutamate, we microdissected a portion of the pathway's terminal zone and assayed the excised tissue for glutamate. There was an 83% decrease in the level of free glutamate in subjects with Alzheimer's disease as compared to control subjects not affected by dementia ( p < 0.005). We believe that this diminution in the glutamate content is a direct neurochemical correlate of perforant pathway destruction and that disruption of this crucial corticolimbic pathway contributes to the memory dysfunction in Alzheimer's disease.