title: [Glutamate dysmetabolism in patients with schizophrenia].
abstract: 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.
authors.forename: G Sh
authors.initials: GSh
authors.lastname: Burbaeva
authors.forename: I S
authors.initials: IS
authors.lastname: Boksha
authors.forename: L I
authors.initials: LI
authors.lastname: Starodubtseva
authors.forename: O K
authors.initials: OK
authors.lastname: Savushkina
authors.forename: E B
authors.initials: EB
authors.lastname: Tereshkina
authors.forename: M S
authors.initials: MS
authors.lastname: Turishcheva
authors.forename: T A
authors.initials: TA
authors.lastname: Prokhorova
authors.forename: E A
authors.initials: EA
authors.lastname: Vorob'eva
authors.forename: M A
authors.initials: MA
authors.lastname: Morozova
mesh_terms: D000293:Adolescent; D000328:Adult; D014150:Antipsychotic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001569:Benzodiazepines / Q000008:administration & dosage / Q000627:therapeutic use; D001792:Blood Platelets / Q000201:enzymology; D015153:Blotting, Western; D001921:Brain / Q000201:enzymology / Q000378:metabolism*; D002908:Chronic Disease; D003627:Data Interpretation, Statistical; D005260:Female; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D005970:Glutamate Synthase / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism*; D006801:Humans; D049449:Luminescence; D008297:Male; D008875:Middle Aged; D000077152:Olanzapine; D017397:Prefrontal Cortex / Q000201:enzymology / Q000378:metabolism; D011379:Prognosis; D012559:Schizophrenia / Q000097:blood / Q000188:drug therapy / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D017367:Selective Serotonin Reuptake Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D014150:Antipsychotic Agents; D001569:Benzodiazepines; D005969:Glutamate Dehydrogenase; D005970:Glutamate Synthase; D005971:Glutamates; D000077152:Olanzapine; D017367:Selective Serotonin Reuptake Inhibitors