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TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia

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...

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Autores principales: Mori, Yoko, Yoshino, Yuta, Ochi, Shinichiro, Yamazaki, Kiyohiro, Kawabe, Kentaro, Abe, Masao, Kitano, Tomoji, Ozaki, Yuki, Yoshida, Taku, Numata, Shusuke, Mori, Takaaki, Iga, Junichi, Kuroda, Norio, Ohmori, Tetsuro, Ueno, Shu-ichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557831/
https://www.ncbi.nlm.nih.gov/pubmed/26332043
http://dx.doi.org/10.1371/journal.pone.0136835
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author Mori, Yoko
Yoshino, Yuta
Ochi, Shinichiro
Yamazaki, Kiyohiro
Kawabe, Kentaro
Abe, Masao
Kitano, Tomoji
Ozaki, Yuki
Yoshida, Taku
Numata, Shusuke
Mori, Takaaki
Iga, Junichi
Kuroda, Norio
Ohmori, Tetsuro
Ueno, Shu-ichi
author_facet Mori, Yoko
Yoshino, Yuta
Ochi, Shinichiro
Yamazaki, Kiyohiro
Kawabe, Kentaro
Abe, Masao
Kitano, Tomoji
Ozaki, Yuki
Yoshida, Taku
Numata, Shusuke
Mori, Takaaki
Iga, Junichi
Kuroda, Norio
Ohmori, Tetsuro
Ueno, Shu-ichi
author_sort Mori, Yoko
collection PubMed
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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spelling pubmed-45578312015-09-10 TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia Mori, Yoko Yoshino, Yuta Ochi, Shinichiro Yamazaki, Kiyohiro Kawabe, Kentaro Abe, Masao Kitano, Tomoji Ozaki, Yuki Yoshida, Taku Numata, Shusuke Mori, Takaaki Iga, Junichi Kuroda, Norio Ohmori, Tetsuro Ueno, Shu-ichi PLoS One Research Article 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. Public Library of Science 2015-09-02 /pmc/articles/PMC4557831/ /pubmed/26332043 http://dx.doi.org/10.1371/journal.pone.0136835 Text en © 2015 Mori et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Mori, Yoko
Yoshino, Yuta
Ochi, Shinichiro
Yamazaki, Kiyohiro
Kawabe, Kentaro
Abe, Masao
Kitano, Tomoji
Ozaki, Yuki
Yoshida, Taku
Numata, Shusuke
Mori, Takaaki
Iga, Junichi
Kuroda, Norio
Ohmori, Tetsuro
Ueno, Shu-ichi
TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title_full TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title_fullStr TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title_full_unstemmed TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title_short TREM2 mRNA Expression in Leukocytes Is Increased in Alzheimer’s Disease and Schizophrenia
title_sort trem2 mrna expression in leukocytes is increased in alzheimer’s disease and schizophrenia
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557831/
https://www.ncbi.nlm.nih.gov/pubmed/26332043
http://dx.doi.org/10.1371/journal.pone.0136835
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