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МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ. / Петрова, Н.Н.; Дорофейкова, М. В.

в: ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА, Том 2014, № 11, 2014, стр. 116-123.

Результаты исследований: Научные публикации в периодических изданияхстатьяРецензирование

Harvard

Петрова, НН & Дорофейкова, МВ 2014, 'МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ', ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА, Том. 2014, № 11, стр. 116-123.

APA

Петрова, Н. Н., & Дорофейкова, М. В. (2014). МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ. ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА, 2014(11), 116-123.

Vancouver

Петрова НН, Дорофейкова МВ. МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ. ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА. 2014;2014(11):116-123.

Author

Петрова, Н.Н. ; Дорофейкова, М. В. / МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ. в: ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА. 2014 ; Том 2014, № 11. стр. 116-123.

BibTeX

@article{30c762f0ef284922957820586d7e18f6,
title = "МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ",
abstract = "This article reviews accumulating knowledge on the signs and pathogenesis of cognitive impairment in schizophrenia. The existing data indicate that cognitive disorders, along with positive and negative symptoms, are key symptoms of schizophrenia. Several neurotransmitter systems, including prefrontal dopaminergic transmission, are involved in the pathological process that causes cognitive disorders. GABAergic and glutamatergic pathophysiological models of schizophrenia are discussed. The main subtype of glutamate receptor NMDA receptor hypofunction is one of the causes of cognitive impairment in schizophrenia. Recent studies revealed alterations in gene expression and activity of kynurenine pathway enzymes in patients with schizophrenia. Concentration of kynurenic acid (KYNA) is increased in the prefrontal cortex of schizophrenca patients and correlated with glutamate, dopamine and acetylcholine levels that reflects the pathophysiological mechanism and degree of cognitive impairment. An overview of animal models of schizophrenia, in particular pharmacological models, is presented. Treatment approaches that promote the recovery of cognitive function are described.",
keywords = "Cognitive impairment, Pathophysiology of schizophrenia, Psychopharmacotherapy, Schizophrenia",
author = "Н.Н. Петрова and Дорофейкова, {М. В.}",
note = "Publisher Copyright: {\textcopyright} 2014, Media Sphera. All rights reserved. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.",
year = "2014",
language = "русский",
volume = "2014",
pages = "116--123",
journal = "ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА",
issn = "1997-7298",
publisher = "Медицина",
number = "11",

}

RIS

TY - JOUR

T1 - МЕХАНИЗМЫ РАЗВИТИЯ НЕЙРОКОГНИТИВНОГО ДЕФИЦИТА ПРИ ШИЗОФРЕНИИ И СОВРЕМЕННЫЕ ПОДХОДЫ К ТЕРАПИИ

AU - Петрова, Н.Н.

AU - Дорофейкова, М. В.

N1 - Publisher Copyright: © 2014, Media Sphera. All rights reserved. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.

PY - 2014

Y1 - 2014

N2 - This article reviews accumulating knowledge on the signs and pathogenesis of cognitive impairment in schizophrenia. The existing data indicate that cognitive disorders, along with positive and negative symptoms, are key symptoms of schizophrenia. Several neurotransmitter systems, including prefrontal dopaminergic transmission, are involved in the pathological process that causes cognitive disorders. GABAergic and glutamatergic pathophysiological models of schizophrenia are discussed. The main subtype of glutamate receptor NMDA receptor hypofunction is one of the causes of cognitive impairment in schizophrenia. Recent studies revealed alterations in gene expression and activity of kynurenine pathway enzymes in patients with schizophrenia. Concentration of kynurenic acid (KYNA) is increased in the prefrontal cortex of schizophrenca patients and correlated with glutamate, dopamine and acetylcholine levels that reflects the pathophysiological mechanism and degree of cognitive impairment. An overview of animal models of schizophrenia, in particular pharmacological models, is presented. Treatment approaches that promote the recovery of cognitive function are described.

AB - This article reviews accumulating knowledge on the signs and pathogenesis of cognitive impairment in schizophrenia. The existing data indicate that cognitive disorders, along with positive and negative symptoms, are key symptoms of schizophrenia. Several neurotransmitter systems, including prefrontal dopaminergic transmission, are involved in the pathological process that causes cognitive disorders. GABAergic and glutamatergic pathophysiological models of schizophrenia are discussed. The main subtype of glutamate receptor NMDA receptor hypofunction is one of the causes of cognitive impairment in schizophrenia. Recent studies revealed alterations in gene expression and activity of kynurenine pathway enzymes in patients with schizophrenia. Concentration of kynurenic acid (KYNA) is increased in the prefrontal cortex of schizophrenca patients and correlated with glutamate, dopamine and acetylcholine levels that reflects the pathophysiological mechanism and degree of cognitive impairment. An overview of animal models of schizophrenia, in particular pharmacological models, is presented. Treatment approaches that promote the recovery of cognitive function are described.

KW - Cognitive impairment

KW - Pathophysiology of schizophrenia

KW - Psychopharmacotherapy

KW - Schizophrenia

UR - http://www.scopus.com/inward/record.url?scp=84925028822&partnerID=8YFLogxK

M3 - статья

C2 - 25629134

VL - 2014

SP - 116

EP - 123

JO - ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА

JF - ЖУРНАЛ НЕВРОЛОГИИ И ПСИХИАТРИИ ИМ. C.C. КОРСАКОВА

SN - 1997-7298

IS - 11

ER -

ID: 5759507