ID | 114922 |
Title Alternative | TREM2 Expression in Schizophrenia
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Author |
Mori, Yoko
Ehime University
Yoshino, Yuta
Ehime University
Ochi, Shinichiro
Ehime University
Yamazaki, Kiyohiro
Ehime University
Kawabe, Kentaro
Ehime University
Abe, Masao
Ehime University
Kitano, Tomoji
Ehime University
Ozaki, Yuki
Ehime University
Yoshida, Taku
Ehime University
Numata, Shusuke
The University of Tokushima
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Mori, Takaaki
Ehime University
Kuroda, Norio
Kuroda Hospital
Ohmori, Tetsuro
The University of Tokushima
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Ueno, Shu-ichi
Ehime University
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Content Type |
Journal Article
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Description | TREM2 and TYROBP are causal genes for Nasu–Hakola disease (NHD), a rare autosomal recessive disease characterized by bone lesions and early-onset progressive dementia. TREM2 forms a receptor signaling complex with TYROBP, which triggers the activation of immune responses in macrophages and dendritic cells, and the functional polymorphism of TREM2 is reported to be associated with neurodegenerative disorders such as Alzheimer’s disease (AD). The objective of this study was to reveal the involvement of TYROBP and TREM2 in the pathophysiology of AD and schizophrenia. Methods: We investigated the mRNA expression level of the 2 genes in leukocytes of 26 patients with AD and 24 with schizophrenia in comparison with age-matched controls. Moreover, we performed gene association analysis between these 2 genes and schizophrenia. Results: No differences were found in TYROBP mRNA expression in patients with AD and schizophrenia; however, TREM2 mRNA expression was increased in patients with AD and schizophrenia compared with controls (P < 0.001). There were no genetic associations of either gene with schizophrenia in Japanese patients. Conclusion: TREM2 expression in leukocytes is elevated not only in AD but also in schizophrenia. Inflammatory processes involving TREM2 may occur in schizophrenia, as observed in neurocognitive disorders such as AD. TREM2 expression in leukocytes may be a novel biomarker for neurological and psychiatric disorders.
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Journal Title |
PLOS ONE
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ISSN | 19326203
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Publisher | PLOS
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Volume | 10
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Issue | 9
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Start Page | e0136835
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Published Date | 2015-09-02
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Rights | © 2015 Mori et al. This is an open access article distributed under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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language |
eng
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departments |
Medical Sciences
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