Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to contemporary views, the glutamatergic system is implicated in the pathogenesis of schizophrenia, and atypical neuroleptics exert their effects (at least partially) through the glutamatergic system. Immunoreactive glutamate-metabolising enzymes, such as glutamine synthetase-like protein (GSLP) and two glutamate dehydrogenase isoenzymes (GDH), have been discovered in human platelets. The amount of GSLP in the platelets of 40 chronic patients with schizophrenia was found to be significantly higher than in 33 controls (consistent with our previous finding of increased amounts of GSLP in the prefrontal cortex of chronic schizophrenia patients). Moreover, survival analysis of the group of patients treated with olanzapine for 28 weeks showed that the larger amount of GSLP measured in platelets before treatment, the shorter the treatment time needed to achieve a positive clinical response (defined a priori as > or = 20% reduction in PANSS total score from the initial level before the treatment). Hence, GSLP level may serve as a predictor of the treatment duration to achieve a positive outcome with olanzapine. Both GSLP and GDH were found significantly changed in the course of treatment; hence, treatment with olanzapine influences the amounts of glutamate-metabolising enzymes in the platelets of chronic schizophrenia patients.
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PMID:Effect of olanzapine treatment on platelet glutamine synthetase-like protein and glutamate dehydrogenase immunoreactivity in schizophrenia. 1668 79

The glutamate-ergic hypothesis of schizophrenia pathogenesis has been substantially expanded due to recent data on changes in glutamate metabolizing enzymes (GME) in the brain of patients with schizophrenia. Significant changes in the amounts of glutamate synthetase (GS), glutamate synthetase-like protein (GSLP), and glutamate dehydrogenase (GDH) have been found. Alterations in the cerebral metabolism of glutamate (together with disturbances in glutamate receptors and transporters) apparently play an important role in the pathogenesis of schizophrenia. Glutamate dysmetabolism has been shown to be of systemic nature, i.e. the amounts of GME (GDH and GSLP) are elevated in platelets of patients with chronic schizophrenia, and these enzymes may be vital markers of glutamate system status. The amounts of GDH and GSLP were monitored in platelets of chronic patients during treatment with olanzapine, an atypical neuroleptic modulating glutamate concentration in the brain and blood of patients. GSLP amount can serve as a predictor of the duration of treatment to achieve a positive outcome. Further studies of GME in blood may result in elaboration of prognostically valuable biological tests not only for schizophrenia treatments, but also for other mental and nervous system diseases in which the glutamate system is substantially implicated.
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PMID:[Glutamate dysmetabolism in patients with schizophrenia]. 1750 Feb 10

Relative amounts of the glutamate metabolizing enzymes - glutamine synthetase, glutamine synthetase-like protein, three isoenzymes of glutamate dehydrogenase as well as creatine phosphokinase (a main astroglial energy metabolism enzyme) and major proteins of astro- and oligodendroglia - a glial fibrillary acidic protein and a myelin basic protein were determined in postmortem brain extracts from three areas - the prefrontal cortex, caudate nucleus and cerebellum - from mentally healthy subjects (n=21) and patients with chronic schizophrenia (n=23). To single out "metabolic types" the data obtained have been subjected to cluster analysis. It has been demonstrated for the first time that the cluster analysis of the biological parameters (enzymes and proteins) with correction for age, gender, postmortem interval and presence/absence of diagnosis, enables to distinguish "mentally healthy" cases and "schizophrenic patients" with a high degree of significance (mean mixing error <20%, small er, Cyrillic>>0,00004). Thus, we suppose that mentally healthy controls and patients with schizophrenia are objectively divided into different "metabolic types".
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PMID:[The complex neurochemical assessment of brain proteins in mentally healthy subjects and schizophrenic patients]. 1842 2