Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Nutritional ketosis, induced via either the classical ketogenic diet or the use of emulsified medium-chain triglycerides, is an established treatment for pharmaceutical resistant epilepsy in children and more recently in adults. In addition, the use of oral ketogenic compounds, fractionated coconut oil, very low carbohydrate intake, or ketone monoester supplementation has been reported to be potentially helpful in mild cognitive impairment, Parkinson's disease, schizophrenia, bipolar disorder, and autistic spectrum disorder. In these and other neurodegenerative and neuroprogressive disorders, there are detrimental effects of oxidative stress, mitochondrial dysfunction, and neuroinflammation on neuronal function. However, they also adversely impact on neurone-glia interactions, disrupting the role of microglia and astrocytes in central nervous system (CNS) homeostasis. Astrocytes are the main site of CNS fatty acid oxidation; the resulting ketone bodies constitute an important source of oxidative fuel for neurones in an environment of glucose restriction. Importantly, the lactate shuttle between astrocytes and neurones is dependent on glycogenolysis and glycolysis, resulting from the fact that the astrocytic filopodia responsible for lactate release are too narrow to accommodate mitochondria. The entry into the CNS of ketone bodies and fatty acids, as a result of nutritional ketosis, has effects on the astrocytic glutamate-glutamine cycle, glutamate synthase activity, and on the function of vesicular glutamate transporters, EAAT, Na+, K+-ATPase, Kir4.1, aquaporin-4, Cx34 and KATP channels, as well as on astrogliosis. These mechanisms are detailed and it is suggested that they would tend to mitigate the changes seen in many neurodegenerative and neuroprogressive disorders. Hence, it is hypothesized that nutritional ketosis may have therapeutic applications in such disorders.
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PMID:Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders. 3209 91