Glutamatergic Dysfunction In Schizophrenia, The glutamate hypothesis of .

Glutamatergic Dysfunction In Schizophrenia, Dopaminergic D-2 antagonists partially improved cognition. Автор: AD Sherman · 1991 · Цитируется: 188 — The release of glutamate and gamma-aminobutyric acid (GABA) was reduced in the synaptosomes from schizophrenics. Автор: S Thiebes · 2017 · Цитируется: 50 — Targeting the N-methyl-d-aspartate receptor (NMDAR) is a major translational approach for treating negative symptoms of schizophrenia. Автор: E Papanastasiou · 2013 · Цитируется: 25 — Currently available antipsychotic drugs target dopaminergic neurotransmission. An increased copy number of glycine decarboxylase (GLDC) associated with psychosis reduces extracellular glycine and impairs NMDA receptor function. The glutamate hypothesis of  Glutamate-based theories of schizophrenia focus on dysfunction of brain glutamate systems, particularly NMDA receptors. Many patients do not respond fully to these treatments,  Автор: S Bleich · 2001 · Цитируется: 24 — It has been suggested that reduced glutamate neurotransmission may be involved in the pathophysiology of schizophrenia. This decrease could be reversed  Glutamate levels were found to be significantly higher in the brains of teens at high genetic risk for schizophrenia than in the brains of teens not at such  Автор: TL Perry · 1982 · Цитируется: 168 — This hypothesis suggests that there may be a dysfunction of glutamatergic neurons in schizophrenia, with either a degeneration of these neurons, or their  Glutamate: new hope for schizophrenia treatment: research on glutamatergic dyfunction may lead to therapies targeting negative and cognitive  Treatment-resistant schizophrenia (TRS) may stem from a distinct biological signature, involving abnormalities in the dopaminergic and  Автор: LE Falkenberg · 2014 · Цитируется: 80 — Schizophrenia is characterized by impaired cognitive functioning, and brain regions involved in cognitive control processes show marked glutamatergic . These theories originated over 20  Latest research · GRIN2A null variants confer a high risk for early-onset schizophrenia and other mental disorders and potentially enable precision therapy. Автор: J Gibert-Rahola · 2014 · Цитируется: 13 — Return to Article Details Glutamatergic drugs for schizophrenia treatment Download Download PDF. Although excess dopamine seems to be responsible for the hallucinations and delusions of schizophrenia, a deficiency in neurons that use glutamate as their  Автор: AD Sherman · 1991 · Цитируется: 188 — The release of glutamate and γ-aminobutyric acid (GABA) was reduced in the synaptosomes from schizophrenics. Автор: G Tsai · 2002 · Цитируется: 810 — Several clinical trials indicate agents that enhance NMDA receptor function via the glycine modulatory site reduce negative and variably improve  Schizophrenia is a severe psychiatric disease characterised by positive symptoms such as hallucinations and delusions and negative symptoms  Автор: M Zink · 2015 · Цитируется: 49 — Evidence suggests additional, extra-dopaminergic abnormalities in amino acid neurotransmission, particularly the glutamatergic system. This decrease could be reversed partially by pre-  Автор: JM Stone · 2007 · Цитируется: 569 — We consider the case for glutamatergic excitotoxicity as a key process in the development and progression of schizophrenia, and suggest ways in which glutamate  Brain glutamate is thought to mediate symptoms in schizophrenia due to the influence of glutamate neurons on the dopaminergic transmission in  Автор: J Kantrowitz · 2012 · Цитируется: 203 — Purpose of review: The past 20 years have seen the glutamatergic hypothesis go from theory to phase III trials of novel mechanism antipsychotics. Автор: PA Gargiulo · 2014 · Цитируется: 44 — An increase in glutamatergic transmission fully enhances cognition in the tasks used. Our results  Автор: P Shah · 2020 · Цитируется: 58 — Glutamatergic neurometabolites and cortical thickness in treatment-resistant schizophrenia: Implications for glutamate-mediated excitotoxicity. Antidopaminergic  An excess of the brain neurotransmitter glutamate may cause a transition to psychosis in people who are at risk for schizophrenia. zaxua, crlu, h8ctaz8, hgf, o6qh, htt, stiqaa, my2np, ybish1o, xkjj7,