kyselina chinolinová, N-methyl-D-aspartatový receptor a schizofrenie: Ověřování integrativní teorie

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F05%3A00000499" target="_blank" >RIV/00023752:_____/05:00000499 - isvavai.cz</a>

Výsledek na webu

—

DOI - Digital Object Identifier

—

Jazyk výsledku

angličtina

Název v původním jazyce

Quinolinic acid, N-methyl-D-aspartate receptor and schizophrenia: Testing an integrative theory

Popis výsledku v původním jazyce

Prenatal inflammations are often mentioned among the most probable environmental factors in the etiology of schizophrenia. Quinolinic acid (QUIN) is potentially neurotoxic and is known to be strongly elevated during brain viral infections. The present review examines the following questions: does an early postnatal neurotoxic damage lead to discrete neuronal and synaptic "pruningů"that could result in delayed changes manifesting as psychosis-like behaviour? In other words, can QUIN belong among main agents of the pruning released by inflammatory processes during the pre- and perinatal period of development that would result in the symptoms of schizophrenia in late adolescence and/or in early adulthood? Critical evaluation of existing experimental and clinical data suggest that this is a realistic possibility: synthesis and release of QUIN can be induced by viral infections (and bacterialt oxins). QUIN acts preferentially on a subset of ionotropic glutamate receptors of NMDA-type contai

Název v anglickém jazyce

Quinolinic acid, N-methyl-D-aspartate receptor and schizophrenia: Testing an integrative theory

Popis výsledku anglicky

Prenatal inflammations are often mentioned among the most probable environmental factors in the etiology of schizophrenia. Quinolinic acid (QUIN) is potentially neurotoxic and is known to be strongly elevated during brain viral infections. The present review examines the following questions: does an early postnatal neurotoxic damage lead to discrete neuronal and synaptic "pruningů"that could result in delayed changes manifesting as psychosis-like behaviour? In other words, can QUIN belong among main agents of the pruning released by inflammatory processes during the pre- and perinatal period of development that would result in the symptoms of schizophrenia in late adolescence and/or in early adulthood? Critical evaluation of existing experimental and clinical data suggest that this is a realistic possibility: synthesis and release of QUIN can be induced by viral infections (and bacterialt oxins). QUIN acts preferentially on a subset of ionotropic glutamate receptors of NMDA-type contai

Druh

C - Kapitola v odborné knize

CEP obor

FH - Neurologie, neurochirurgie, neurovědy

OECD FORD obor

—

Projekt

<a href="/cs/project/NF7626" target="_blank" >NF7626: Hladiny mozkového glutamátu a podjednotková stavba glutamátového receptoru NMDA typu u schizofrenie: experimentálně - klinická studie.</a><br>

Návaznosti

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

Rok uplatnění

2005

Kód důvěrnosti údajů

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

Název knihy nebo sborníku

Amino Acid Signaling 04

ISBN

81-308-0047-0

Počet stran výsledku

16

Strana od-do

68-83

Počet stran knihy

—

Název nakladatele

Research Signpost

Místo vydání

Kerala

Kód UT WoS kapitoly

—