ID | 57755 |
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Author |
Shi, Xiaowen
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Liu, Xia
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Shang, Jingwei
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Morihara, Ryuta
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Nakano, Yumiko
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Feng, Tian
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Huang, Yong
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Sato, Kota
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
ORCID
Takemoto, Mami
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
ORCID
Kaken ID
Hishikawa, Nozomi
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kaken ID
Yamashita, Toru
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
ORCID
Kaken ID
researchmap
Abe, Koji
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kaken ID
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Abstract | Alzheimer's disease (AD) is the most common dementia and a progressive neurodegenerative disorder aggravated by chronic hypoperfusion (HP). Since numerous evidence suggests that inflammation is related with AD pathology, we investigated the expression change of two anti-inflammatory markers, inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4) and alpha-2-HS-glycoprotein (AHSG), in a novel AD model (APP23) with HP at 12 month of age. As compared with wild type (WT, n = 10), immunohistochemical analysis showed a higher ITIH4 and a lower AHSG expressions in the cerebral cortex, hippocampus, and thalamus of the APP23 + HP group (n = 12) than the simple APP23 (n = 10) group (*p < 0.05 and **p < 0.01 versus WT; #p < 0.05 and # #p < 0.01 versus APP23). The present study provides an upregulation of anti-inflammatory ITIH4 and a downregulation of pro-inflammatory TNFα-dependent AHSG in a novel AD plus HP mice model.
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Keywords | AHSG
APP23 mice
ITIH4
alzheimer’s disease
hypoperfusion
inflammation
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Published Date | 2019-04-23
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Publication Title |
Journal of Alzheimer's Disease
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Volume | volume68
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Issue | issue4
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Publisher | IOS Press
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Start Page | 1667
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End Page | 1675
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ISSN | 1387-2877
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NCID | AA11545428
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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File Version | author
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PubMed ID | |
DOI | |
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Related Url | isVersionOf https://doi.org/10.3233/JAD-181218
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Funder Name |
Japan Agency for Medical Research and Development
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助成番号 | 7211700176
7211700180
7211700095
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