Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.4 (glutamate dehydrogenase)
 4,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the activity of the cerebral form of glutamate dehydrogenase (GDH) in 59 patients suffering from vegetative paroxysms (VP), 8 patients with multiple sclerosis and 15 normal test subjects. As compared to the normal test subjects, the patients with VP manifested higher activity and lability of the enzyme. The patients with VP demonstrating the "labile" and "stable" enzyme were subjected to a clinicopsychological analysis which revealed a graver disease course and more pronounced anxiety in the group with the "stable" enzyme. The role of GDH in the pathogenesis of VP is under discussion.
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PMID:[Cerebral form of glutamate dehydrogenase activity in autonomic paroxysms (attacks of panic)]. 196 77

Glutamate excitotoxicity, recently demonstrated in an animal model of multiple sclerosis (MS), is evoked by altered glutamate homeostasis. In the present study, we investigated the major regulating factors in glutamate excitotoxicity by immunohistochemistry in MS and control white matter with markers for glutamate production (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamate dehydrogenase [GDH] and glutamine synthetase [GS]), axonal damage (SMI 32) and CNS cell types. Active MS lesions showed high-level glutaminase expression in macrophages and microglia in close proximity to dystrophic axons. Correlation between glutaminase expression and axonal damage was confirmed experimentally in animals. White matter from other inflammatory neurologic diseases displayed glutaminase reactivity, whereas normals and noninflammatory conditions showed none. All three glutamate transporters were expressed robustly, mainly on oligodendrocytes, in normal, control and MS white matter, except for GLT-1, which showed low-level expression around active MS lesions. GS and GDH were present in oligodendrocytes in normal and non-MS white matter but were absent from both active and chronic silent MS lesions, suggesting lasting metabolic impediments. Thus, imbalanced glutamate homeostasis contributes to axonal and oligodendroglial pathology in MS. Manipulation of this imbalance may have therapeutic import.
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PMID:Multiple sclerosis: altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage. 1150 99