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- Uemura Tomihiko
- Tama Hospital Affective Disorders Research Project, Tokyo Metropolitan Institute of Medical Science
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- Tatebayashi Yoshitaka
- Affective Disorders Research Project, Tokyo Metropolitan Institute of Medical Science
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- Mochida Masahiko
- Tama Hospital
Bibliographic Information
- Other Title
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- 統合失調症のキヌレン酸仮説
- トウゴウ シッチョウショウ ノ キヌレンサン カセツ
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Abstract
Besides the positive and negative symptoms, the cognitive deficits are now recognized as a core domain of schizophrenia (SZ). Here, we introduce recent advances in “The kynurenic acid (KYNA)hypothesis of SZ” based especially on the abnormally elevated levels of KYNA, a tryptophan metabolite on the kynurenine pathway, in the SZ prefrontal cortex and the cerebrospinal fluid possibly due to the decreased activity of kynurenine 3 -monooxygenase (KMO) . KYNA modulates glutamate, dopamine, and acetylcholine (Ach) signaling via NMDA- Receptor and α 7nAch-Receptor. The regulation of the kynurenine pathway by inflammatory mediators suggests immunological alterations and neuroinflammation-mediated dysregulation of kynurenine pathway which pertains partly to psychiatric disorders including SZ. Novel therapeutic targets for SZ are discussed according to this hypothesis, regarding especially the cognitive deficits in SZ.
Journal
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- Japanese Journal of Biological Psychiatry
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Japanese Journal of Biological Psychiatry 26 (4), 223-234, 2015
Japanese Society of Biological Psychiatry
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Keywords
Details 詳細情報について
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- CRID
- 1390282680389521792
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- NII Article ID
- 130005395623
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- NII Book ID
- AA12468060
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- ISSN
- 21866465
- 21866619
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- NDL BIB ID
- 027103084
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- Text Lang
- ja
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- Data Source
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- JaLC
- NDL
- CiNii Articles
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- Abstract License Flag
- Disallowed