Kyselilna chinolinová a peroxidativní poškození mozku: relevance ke schizofrenii

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F07%3A00000750" target="_blank" >RIV/00023752:_____/07:00000750 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Quinolinic acid and peroxidative brain damage: Relevance to schizophrenia

Popis výsledku v původním jazyce

The concept of schizophrenia as a disorder of synapse postulates abnormal development of synaptic connections, their excessive pruning and defective neuronal signaling, possibly as a consequence of interactions of genetic variants and environmental riskfactors, such as prenatal inflammation. Accumulating evidence points to interrelated mechanisms that increase production of highly reactive - and potentially damaging - molecules and/or decrease antioxidant protection in affected individuals. As mitochondria are the main source of reactive oxygen species, a mitochondrial impairment could contribute to the etiology of schizophrenia. Recent studies have suggested an involvement of both candidate genes (e.g. DISCI, Mn-SOD) and infection-induced peroxidants(e.g. quinolinic acid) in mitochondrial dysfunction in brains of patients with schizophrenia. This article reviews several lines of evidence linking mitochondrial dysfunction to abnormal generation of reactive substances and lipid peroxi

Název v anglickém jazyce

Quinolinic acid and peroxidative brain damage: Relevance to schizophrenia

Popis výsledku anglicky

The concept of schizophrenia as a disorder of synapse postulates abnormal development of synaptic connections, their excessive pruning and defective neuronal signaling, possibly as a consequence of interactions of genetic variants and environmental riskfactors, such as prenatal inflammation. Accumulating evidence points to interrelated mechanisms that increase production of highly reactive - and potentially damaging - molecules and/or decrease antioxidant protection in affected individuals. As mitochondria are the main source of reactive oxygen species, a mitochondrial impairment could contribute to the etiology of schizophrenia. Recent studies have suggested an involvement of both candidate genes (e.g. DISCI, Mn-SOD) and infection-induced peroxidants(e.g. quinolinic acid) in mitochondrial dysfunction in brains of patients with schizophrenia. This article reviews several lines of evidence linking mitochondrial dysfunction to abnormal generation of reactive substances and lipid peroxi

Druh

C - Kapitola v odborné knize

CEP obor

FH - Neurologie, neurochirurgie, neurovědy

OECD FORD obor

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Projekt

<a href="/cs/project/1M0517" target="_blank" >1M0517: Centrum neuropsychiatrických studií 2005-2009 (Neurobiologie v klinické aplikaci)</a><br>

Návaznosti

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

Rok uplatnění

2007

Kód důvěrnosti údajů

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

Název knihy nebo sborníku

New Perspectives on Brain Cell Damage, Neurodegeneration and Neuroprotective Strategies

ISBN

81-308-0164-7

Počet stran výsledku

22

Strana od-do

113-134

Počet stran knihy

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Název nakladatele

Research Signpost

Místo vydání

Trivandrum

Kód UT WoS kapitoly

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