Endogenous antagonists of N‐methyl‐d‐aspartate receptor in schizophrenia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F21%3A43920568" target="_blank" >RIV/00023752:_____/21:43920568 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11120/21:43920865

Výsledek na webu

<a href="https://alz-journals.onlinelibrary.wiley.com/doi/epdf/10.1002/alz.12244" target="_blank" >https://alz-journals.onlinelibrary.wiley.com/doi/epdf/10.1002/alz.12244</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/alz.12244" target="_blank" >10.1002/alz.12244</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Endogenous antagonists of N‐methyl‐d‐aspartate receptor in schizophrenia

Popis výsledku v původním jazyce

Schizophrenia is a chronic neuropsychiatric brain disorder that has devastating personal impact and rising healthcare costs. Dysregulation of glutamatergic neurotransmission has been implicated in the pathobiology of the disease, attributed largely to the hypofunction of the N‐methyl‐d‐aspartate (NMDA) receptor. Currently, there is a major gap in mechanistic analysis as to how endogenous modulators of the NMDA receptors contribute to the onset and progression of the disease. We present a systematic review of the neurobiology and the role of endogenous NMDA receptor antagonists in animal models of schizophrenia, and in patients. We discuss their neurochemical origin, release from neurons and glia with action mechanisms, and functional effects, which might contribute toward the impairment of neuronal processes underlying this complex pathological state. We consider clinical evidence suggesting dysregulations of endogenous NMDA receptor in schizophrenia, and highlight the pressing need in future studies and emerging directions, to restore the NMDA receptor functions for therapeutic benefits.

Název v anglickém jazyce

Endogenous antagonists of N‐methyl‐d‐aspartate receptor in schizophrenia

Popis výsledku anglicky

Schizophrenia is a chronic neuropsychiatric brain disorder that has devastating personal impact and rising healthcare costs. Dysregulation of glutamatergic neurotransmission has been implicated in the pathobiology of the disease, attributed largely to the hypofunction of the N‐methyl‐d‐aspartate (NMDA) receptor. Currently, there is a major gap in mechanistic analysis as to how endogenous modulators of the NMDA receptors contribute to the onset and progression of the disease. We present a systematic review of the neurobiology and the role of endogenous NMDA receptor antagonists in animal models of schizophrenia, and in patients. We discuss their neurochemical origin, release from neurons and glia with action mechanisms, and functional effects, which might contribute toward the impairment of neuronal processes underlying this complex pathological state. We consider clinical evidence suggesting dysregulations of endogenous NMDA receptor in schizophrenia, and highlight the pressing need in future studies and emerging directions, to restore the NMDA receptor functions for therapeutic benefits.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

<a href="/cs/project/LO1611" target="_blank" >LO1611: Udržitelnost pro Národní ústav duševního zdraví</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Alzheimer`s and Dementia

ISSN

1552-5260

e-ISSN

—

Svazek periodika

17

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

18

Strana od-do

888-905

Kód UT WoS článku

000651096100014

EID výsledku v databázi Scopus

2-s2.0-85097671023