Does modulation of glutamatergic function represent a viable therapeutic strategy in Alzheimer's disease?
- 1 February 1992
- journal article
- review article
- Published by Elsevier in Biological Psychiatry
- Vol. 31 (4) , 337-350
- https://doi.org/10.1016/0006-3223(92)90227-q
Abstract
No abstract availableKeywords
This publication has 63 references indexed in Scilit:
- NMDA receptors - their role in long-term potentiationPublished by Elsevier ,2003
- Glutamate Neurotoxicity, Calcium, and ZincaAnnals of the New York Academy of Sciences, 1989
- Pyramidal neuron loss and “glycine-site therapy”: A need for an animal model and study in late-life depressionNeurobiology of Aging, 1989
- Characterisation, Density, and Distribution of Kainate Receptors in Normal and Alzheimer's Diseased Human BrainJournal of Neurochemistry, 1989
- Regional distribution of pre- and postsynaptic glutamatergic function in Alzheimer's diseaseBrain Research, 1988
- Stimulation of the receptor has a trophic effect on differentiating cerebellar granule cellsNeuroscience Letters, 1988
- Presynaptic and postsynaptic glutamatergic function in Alzheimer's diseaseNeuroscience Letters, 1988
- Selective Sparing of a Class of Striatal Neurons in Huntington's DiseaseScience, 1985
- Controlled induction of paired helical filaments of the Alzheimer type in cultured human neurons, by glutamate and aspartateJournal of the Neurological Sciences, 1985
- Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral MicrodialysisJournal of Neurochemistry, 1984