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  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0964-2633</Issn>
      <Volume>70</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Prevalence and Modifiable Risk Factors of Dementia in People With Down Syndrome: Cross‐Sectional Study of Japan in Collaboration With the Intellectual Diversity for Goodness Research Consortium (INDIGO‐2019)</ArticleTitle>
    <FirstPage LZero="delete">329</FirstPage>
    <LastPage>336</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomokazu</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation>Asahigawaso Research Institute, Social Welfare Corporation Asahigawaso</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Taku</FirstName>
        <LastName>Kurozumi</LastName>
        <Affiliation>Asahigawaso Research Institute, Social Welfare Corporation Asahigawaso</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Takaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryozo</FirstName>
        <LastName>Kuwano</LastName>
        <Affiliation>Asahigawaso Research Institute, Social Welfare Corporation Asahigawaso</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shigeru</FirstName>
        <LastName>Suemitsu</LastName>
        <Affiliation>Asahigawaso Research Institute, Social Welfare Corporation Asahigawaso</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract>Background: People with Down syndrome (DS) have a strong genetic predisposition to Alzheimer's disease (AD). However, the clinical burden and associated risk factors in diverse, non-Western populations remain less understood. This study aimed to investigate the prevalence of dementia in Japanese adults with DS and to identify modifiable clinical factors associated with dementia.&lt;br&gt;
Methods: This cross-sectional multicentre study surveyed 133 adults with DS (mean age 50.1&#8201;years) residing in 45 welfare facilities across Japan in 2019. Dementia was diagnosed by a consensus panel of physicians using established criteria (DSM-5, ICD-10, DC-LD) after comprehensive assessments, including the Japanese version of the Dementia Screening Questionnaire for Individuals with Intellectual Disabilities (DSQIID-J). Logistic regression analysis was performed to identify factors independently associated with dementia.&lt;br&gt;
Results: Forty-six participants (34.6%) were diagnosed with dementia. The prevalence rose sharply with age: 0% in their 30s, 30.8% in their 40s, 31.6% in their 50s and 65.5% in their 60s. After adjusting for covariates, older age, female sex, dyslipidaemia and visual impairment were independently associated with dementia.&lt;br&gt;
Conclusions: This study, the largest of its kind in Asia, confirms a high prevalence of dementia in institutionalized Japanese adults with DS. Crucially, this study is the first to identify dyslipidaemia and visual impairment as independent and potentially modifiable risk factors in this population. These findings highlight tangible targets for clinical interventions aimed at mitigating dementia risk in people with DS.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1432-0533</Issn>
      <Volume>149</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Cerebral Braak stage and amygdala granular fuzzy astrocyte status have independent effects on neuronal 3R-tau and 4R-tau accumulations in the olfactory bulb, respectively, in cases with low to intermediate AD neuropathologic change</ArticleTitle>
    <FirstPage LZero="delete">36</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hanae</FirstName>
        <LastName>Nakashima-Yasuda</LastName>
        <Affiliation>Okayama University Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideki</FirstName>
        <LastName>Ishizu</LastName>
        <Affiliation>Okayama University Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Haraguchi</LastName>
        <Affiliation>Department of Neurology, National Hospital Organization Minami-Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akinori</FirstName>
        <LastName>Miyashita</LastName>
        <Affiliation>Department of Molecular Genetics, Brain Research Institute, Niigata University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Ikeuchi</LastName>
        <Affiliation>Department of Molecular Genetics, Brain Research Institute, Niigata University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masato</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Dementia Research Project, Tokyo Metropolitan Institute of Medical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoto</FirstName>
        <LastName>Nishikawa</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Takaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1432-0533</Issn>
      <Volume>150</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Biallelic variants in DNAJC7 cause familial amyotrophic lateral sclerosis with the TDP-43 pathology</ArticleTitle>
    <FirstPage LZero="delete">19</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Yamashita</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daiki</FirstName>
        <LastName>Ousaka</LastName>
        <Affiliation>Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hongming</FirstName>
        <LastName>Sun</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Haraguchi</LastName>
        <Affiliation>Department of Neurology, National Hospital Organisation Minami-Okayama Medical Centre</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ricardo Satoshi</FirstName>
        <LastName>Ota-Elliott</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chika</FirstName>
        <LastName>Matsuoka</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomohito</FirstName>
        <LastName>Kawano</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hanae</FirstName>
        <LastName>Nakashima-Yasuda</LastName>
        <Affiliation>Department of Psychiatry, Zikei Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yusuke</FirstName>
        <LastName>Fukui</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yumiko</FirstName>
        <LastName>Nakano</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryuta</FirstName>
        <LastName>Morihara</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masato</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Hosono</LastName>
        <Affiliation>Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Takaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Ishiura</LastName>
        <Affiliation>Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
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      <ArticleId IdType="doi"/>
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    <Abstract>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive degeneration of motor neurons. ALS pathology primarily involves the failure of protein quality control mechanisms, leading to the accumulation of misfolded proteins, particularly TAR DNA-binding protein 43 (TDP-43). TDP-43 aggregation is a central pathological feature of ALS. Maintaining protein homeostasis is critical and facilitated by heat shock proteins (HSPs), particularly the HSP40 family, which includes co-chaperones such as DNAJC7. Here, we report a family with three siblings affected by ALS who carry a homozygous c.518dupC frameshift variant in DNAJC7, a member of the HSP40 family. All three patients exhibited progressive muscle weakness, limb atrophy, bulbar palsy, and respiratory failure. Pathological examination revealed degeneration of both upper and lower motor neurons, with phosphorylated TDP-43-positive neuronal cytoplasmic inclusions in the frontal and temporal cortices. Immunoblot analysis were consistent with a type B pattern of phosphorylated TDP-43 in the precentral gyrus. Immunohistochemistry and RNA sequencing analyses demonstrated a substantial reduction in DNAJC7 expression at both the protein and RNA levels in affected brain regions. In a TDP-43 cell model, DNAJC7 knockdown impaired the disassembly of TDP-43 following arsenite-induced stress, whereas DNAJC7 overexpression suppressed the assembly and promoted the disassembly of arsenite-induced TDP-43 condensates. Furthermore, in a zebrafish ALS model, dnajc7 knockdown resulted in increased TDP-43 aggregation in motor neurons and reduced survival. To the best of our knowledge, this study provides the first evidence linking biallelic loss-of-function variants in DNAJC7 to familial ALS with TDP-43 pathology.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Amyotrophic lateral sclerosis</Param>
      </Object>
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        <Param Name="value">Heat shock protein</Param>
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      <Object Type="keyword">
        <Param Name="value">DNAJC7</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">TDP-43</Param>
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      <Object Type="keyword">
        <Param Name="value">Live-cell imaging</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Zebrafish disease model</Param>
      </Object>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>137</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>認知症治療</ArticleTitle>
    <FirstPage LZero="delete">33</FirstPage>
    <LastPage>35</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>BMJ Publishing Group</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2755-9734</Issn>
      <Volume>27</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Potential dopaminergic deficit in patients with geriatric psychiatric disorders as revealed by DAT-SPECT: a cross-sectional study</ArticleTitle>
    <FirstPage LZero="delete">1</FirstPage>
    <LastPage>9</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Faculty of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhide</FirstName>
        <LastName>Kojima</LastName>
        <Affiliation>Department of Radiology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoto</FirstName>
        <LastName>Nishikawa</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Faculty of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaki</FirstName>
        <LastName>Fujiwara</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Takaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Faculty of Medicine Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background It has been reported that patients with geriatric psychiatric disorders include many cases of the prodromal stages of neurodegenerative diseases. Abnormal I-123-2 beta-carbomethoxy-3 beta-(4-iodophenyl)-N-(3-fluoropropyl) nortropane dopamine transporter single-photon emission computed tomography (DAT-SPECT) reveals a nigrostriatal dopaminergic deficit and is considered useful to detect dementia with Lewy bodies and Parkinson's disease as well as progressive supranuclear palsy and corticobasal degeneration. We aimed to determine the proportion of cases that are abnormal on DAT-SPECT in patients with geriatric psychiatric disorders and to identify their clinical profile. &lt;br&gt;
Methods The design is a cross-sectional study. Clinical findings of 61 inpatients aged 60 years or older who underwent DAT-SPECT and had been diagnosed with psychiatric disorders, but not neurodegenerative disease or dementia were analysed. &lt;br&gt;
Results 36 of 61 (59%) had abnormal results on DAT-SPECT. 54 of 61 patients who had DAT-SPECT (89%) had undergone I-123-metaiodobenzylguanidine myocardial scintigraphy (I-123-MIBG scintigraphy); 12 of the 54 patients (22.2%) had abnormal findings on I-123-MIBG scintigraphy. There were no cases that were normal on DAT-SPECT and abnormal on I-123-MIBG scintigraphy. DAT-SPECT abnormalities were more frequent in patients with late-onset (55 years and older) psychiatric disorders (69.0%) and depressive disorder (75.7%), especially late-onset depressive disorder (79.3%). &lt;br&gt;
Conclusion Patients with geriatric psychiatric disorders include many cases showing abnormalities on DAT-SPECT. It is suggested that these cases are at high risk of developing neurodegenerative diseases characterised by a dopaminergic deficit. It is possible that patients with geriatric psychiatric disorders with abnormal findings on DAT-SPECT tend to show abnormalities on DAT-SPECT first rather than on I-123-MIBG scintigraphy.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>BMC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2051-5960</Issn>
      <Volume>12</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Pure argyrophilic grain disease revisited: independent effects on limbic, neocortical, and striato-pallido-nigral degeneration and the development of dementia in a series with a low to moderate Braak stage</ArticleTitle>
    <FirstPage LZero="delete">121</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hanae</FirstName>
        <LastName>Nakashima-Yasuda</LastName>
        <Affiliation>Okayama University Medical School </Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideki</FirstName>
        <LastName>Ishizu</LastName>
        <Affiliation>Okayama University Medical School </Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Haraguchi</LastName>
        <Affiliation>Department of Neurology, National Hospital Organization Minami Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chikako</FirstName>
        <LastName>Ikeda</LastName>
        <Affiliation>Okayama University Medical School </Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masato</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Dementia Research Project, Tokyo Metropolitan Institute of Medical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akinori</FirstName>
        <LastName>Miyashita</LastName>
        <Affiliation>Department of Molecular Genetics, Brain Research Institute, Niigata University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Ikeuchi</LastName>
        <Affiliation>Department of Molecular Genetics, Brain Research Institute, Niigata University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoto</FirstName>
        <LastName>Nishikawa</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Sudo</LastName>
        <Affiliation>Department of Psychiatry, Tosa Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Takaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
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    <Abstract>Agyrophilic grains (AGs) are age-related limbic-predominant lesions in which four-repeat tau is selectively accumulated. Because previous methodologically heterogeneous studies have demonstrated inconsistent findings on the relationship between AGs and dementia, whether AGs affect cognitive function remains unclear. To address this question, we first comprehensively evaluated the distribution and quantity of Gallyas-positive AGs and the severity of neuronal loss in the limbic, neocortical, and subcortical regions in 30 cases of pure argyrophilic grain disease (pAGD) in Braak stages I-IV and without other degenerative diseases, and 34 control cases that had only neurofibrillary tangles with Braak stages I-IV and no or minimal A beta deposits. Then, we examined whether AGs have independent effects on neuronal loss and dementia by employing multivariate ordered logistic regression and binomial logistic regression. Of 30 pAGD cases, three were classified in diffuse form pAGD, which had evident neuronal loss not only in the limbic region but also in the neocortex and subcortical nuclei. In all 30 pAGD cases, neuronal loss developed first in the amygdala, followed by temporo-frontal cortex, hippocampal CA1, substantia nigra, and finally, the striatum and globus pallidus with the progression of Saito AG stage. In multivariate analyses of 30 pAGD and 34 control cases, the Saito AG stage affected neuronal loss in the amygdala, hippocampal CA1, temporo-frontal cortex, striatum, globus pallidus, and substantia nigra independent of the age, Braak stage, and limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) stage. In multivariate analyses of 23 pAGD and 28 control cases that lacked two or more lacunae and/or one or more large infarctions, 100 or more AGs per x 400 visual field in the amygdala (OR 10.02, 95% CI 1.12-89.43) and hippocampal CA1 (OR 12.22, 95% CI 1.70-87.81), and the presence of AGs in the inferior temporal cortex (OR 8.18, 95% CI 1.03-65.13) affected dementia independent of age, moderate Braak stages (III-IV), and LATE-NC. Given these findings, the high density of limbic AGs and the increase of AGs in the inferior temporal gyrus may contribute to the occurrence of dementia through neuronal loss, at least in cases in a low to moderate Braak stage.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Substantia nigra</Param>
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        <Param Name="value">Subthalamic nucleus</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>77</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Venous Thromboembolism in Eating Disorders: A Retrospective Observational Study</ArticleTitle>
    <FirstPage LZero="delete">131</FirstPage>
    <LastPage>137</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Mayuko</FirstName>
        <LastName>Senda</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaki</FirstName>
        <LastName>Fujiwara</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/65142</ArticleId>
    </ArticleIdList>
    <Abstract>Eating disorders (EDs) are associated with a high mortality rate. Patients with EDs often experience severe dehydration due to food restriction and/or vomiting. Severely underweight patients are often prescribed bed rest during inpatient care to reduce their energy consumption, and they may thus develop multiple risk factors for venous thromboembolism (VTE). We compared the clinical features of ED inpatients with VTE to those of ED inpatients without VTE. Seventy-one inpatients with ED were treated at Okayama University Hospital’s psychiatric ward in 2016-2020; five were experienced a VTE. Compared to the non-VTE group, the VTE group’s median age and disease duration were greater and the median body mass index (BMI) was lower. The VTE group’s D-dimer peak values were &gt; 5 mg/L. Physical restraint and central venous catheter use were associated with VTE. Longer ED duration and lower BMI might be risk factors for VTE. To make inpatient treatment for ED safer, it is important to avoid the use of physical restraints and central venous catheters. Continuous D-dimer monitoring is necessary for the early detection of VTE in ED patients at high risk of VTE.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">eating disorder</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">anorexia nervosa</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">venous thromboembolism</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">deep vein thrombosis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>BMC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1471-2377</Issn>
      <Volume>22</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Secondary autoimmune hypothalamitis with severe memory impairment 7 years after the onset of diabetes insipidus due to lymphocytic hypophysitis: a case report</ArticleTitle>
    <FirstPage LZero="delete">371</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takahiro</FirstName>
        <LastName>Asada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mayuko</FirstName>
        <LastName>Senda</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation>Department of General Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryo</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation>Department of Neurology, Faculty of Medicine,  Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumio</FirstName>
        <LastName>Otsuka</LastName>
        <Affiliation>Department of General Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background Autoimmune hypothalamitis is a very rare neuroendocrine disorder that causes central diabetes insipidus, headache, visual impairment, and sometimes cognitive impairment. Autoimmune hypothalamitis may occur in association with autoimmune hypophysitis, including lymphocytic hypophysitis, or in isolation. It is not known whether autoimmune hypothalamitis and autoimmune hypophysitis are consecutive diseases. Case presentation A 52-year-old woman developed autoimmune hypothalamitis 7 years after developing central diabetes insipidus due to lymphocytic hypophysitis, resulting in severe memory impairment. High-dose intravenous methylprednisolone therapy improved her cognitive function and decreased the size of the lesion. Conclusion This case presented a unique clinical course, with a long period of time between the onset of autoimmune hypopituitaritis and the development of autoimmune hypothalamitis.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Lymphocytic hypophysitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Autoimmune hypophysitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Autoimmune hypothalamitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cognitive dysfunction</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Memory impairment</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1015-6305</Issn>
      <Volume>30</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Factors associated with development and distribution of granular/fuzzy astrocytes in neurodegenerative diseases</ArticleTitle>
    <FirstPage LZero="delete">811</FirstPage>
    <LastPage>830</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Haraguchi</LastName>
        <Affiliation>Department of Neurology, National Hospital Organization Minami‐Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideki</FirstName>
        <LastName>Ishizu</LastName>
        <Affiliation>Department of Laboratory Medicine and Pathology, Zikei Institute of Psychiatry</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masato</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Dementia Research Project, Tokyo Metropolitan Institute of Medical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Ishihara</LastName>
        <Affiliation>Department of Psychiatry, Kawasaki Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shu‐ichi</FirstName>
        <LastName>Ueno</LastName>
        <Affiliation>Department of Neuropsychiatry, Ehime University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Granular/fuzzy astrocytes (GFAs), a subtype of “aging‐related tau astrogliopathy,” are noted in cases bearing various neurodegenerative diseases. However, the pathogenic significance of GFAs remains unclear. We immunohistochemically examined the frontal cortex, caudate nucleus, putamen and amygdala in 105 cases composed of argyrophilic grain disease cases (AGD, N = 26), and progressive supranuclear palsy (PSP, N = 10), Alzheimer’s disease (AD, N = 20) and primary age‐related tauopathy cases (PART, N = 18) lacking AGD, as well as 31 cases bearing other various neurodegenerative diseases to clarify (i) the distribution patterns of GFAs in AGD, and PSP, AD and PART lacking AGD, (ii) the impacts of major pathological factors and age on GFA formation and (iii) immunohistochemical features useful to understand the formation process of GFAs. In AGD cases, GFAs consistently occurred in the amygdala (100%), followed by the putamen (69.2%) and caudate nucleus and frontal cortex (57.7%, respectively). In PSP cases without AGD, GFAs were almost consistently noted in all regions examined (90&#8211;100%). In AD cases without AGD, GFAs were less frequent, developing preferably in the putamen (35.0%) and caudate nucleus (30.0%). PART cases without AGD had GFAs most frequently in the amygdala (35.3%), being more similar to AGD than to AD cases. Ordered logistic regression analyses using all cases demonstrated that the strongest independent factor of GFA formation in the frontal cortex and striatum was the diagnosis of PSP, while that in the amygdala was AGD. The age was not significantly associated with GFA formation in any region. In GFAs in AGD cases, phosphorylation and conformational change of tau, Gallyas‐positive glial threads indistinguishable from those in tufted astrocytes, and the activation of autophagy occurred sequentially. Given these findings, AGD, PSP, AD and PART cases may show distinct distributions of GFAs, which may provide clues to predict the underlying processes of primary tauopathies.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">aging‐related tau astrogliopathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">argyrophilic grain</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">granular/fuzzy astrocyte</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">primary age‐related tauopathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tau</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tufted astrocyte</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>08856230</Issn>
      <Volume>35</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Prevalence of dementia in people with intellectual disabilities: Cross‐sectional study</ArticleTitle>
    <FirstPage LZero="delete">414</FirstPage>
    <LastPage>422</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryozo</FirstName>
        <LastName>Kuwano</LastName>
        <Affiliation>Asahigawaso Research Institute, Asahigawa Medical Welfare Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomokazu</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation>Asahigawaso Research Institute, Asahigawa Medical Welfare Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Atsushi</FirstName>
        <LastName>Cyoju</LastName>
        <Affiliation>Asahigawaso Research Institute, Asahigawa Medical Welfare Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shigeru</FirstName>
        <LastName>Suemitsu</LastName>
        <Affiliation>Asahigawaso Research Institute, Asahigawa Medical Welfare Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background
There are only a few studies of the prevalence of dementia in people with intellectual disability (ID) without Down syndrome (DS), and there is a large difference in the prevalences between reported studies. Moreover, the prevalence of mild cognitive impairment (MCI) in ID has not been reported. We aimed to evaluate the prevalence of dementia in adults of all ages and the prevalence of MCI in people with ID. Furthermore, we tried to clarify the differences depending on the various diagnostic criteria.

Methods
The survey included 493 adults with ID at 28 facilities in Japan. The caregivers answered a questionnaire, and physicians directly examined the participants who were suspected of cognitive decline. Dementia and MCI were diagnosed according to ICD‐10, DC‐LD, and DSM‐5 criteria.

Results
The prevalence of dementia was 0.8% for the 45 to 54&#8201;years old group, 3.5% for the 55 to 64&#8201;years old group, and 13.9% for the 65 to 74&#8201;years old group in people with ID without DS. The prevalence of MCI was 3.1% for patients 45 to 54, 3.5% for patients 55 to 64, and 2.8% for patients 65 to 74 with ID without DS. DSM‐5 was the most inclusive in diagnosing dementia and MCI in people with ID.

Conclusions
People with ID without DS may develop dementia and MCI at an earlier age and higher rate than the general population. Among the diagnostic criteria, DSM‐5 was the most useful for diagnosing their cognitive impairment.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">dementia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">intellectual disability</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">mental retardation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">mild cognitive impairment</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">prevalence of dementia</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1346-3500</Issn>
      <Volume>19</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2019</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Clinical characteristics of elderly depressive patients with low metaiodobenzylguanidine uptake</ArticleTitle>
    <FirstPage LZero="delete">566</FirstPage>
    <LastPage>573</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Etsuko</FirstName>
        <LastName>Oshima</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Megumi</FirstName>
        <LastName>Yamaguchi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Hayashi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Hinotsu</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoru</FirstName>
        <LastName>Esumi</LastName>
        <Affiliation>Department of Pharmacy, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takayoshi</FirstName>
        <LastName>Shinya</LastName>
        <Affiliation>Department of Pediatric Radiology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>BACKGROUND:&lt;br/&gt;
Recently, depression with Lewy body pathology before the appearance of parkinsonism and cognitive dysfunction has been drawing attention. Low cardiac metaiodobenzylguanidine (MIBG) uptake is helpful for early differentiation of Lewy body disease (LBD) from late-onset psychiatric disorders even before parkinsonism or dementia appears. In this study, we used MIBG uptake as a tool in suspected LBD, and evaluated the relationship of MIBG results to clinical characteristics and depressive symptoms.&lt;br/&gt;
METHODS:&lt;br/&gt;
Fifty-two elderly inpatients with depression were included in this study. The Hamilton Depression Rating Scale (HDRS) was administered at admission, and 123 I-MIBG cardiac scintigraphy was performed. Of 52 patients, 38 had normal and 14 had reduced MIBG uptake.&lt;br/&gt;
RESULTS:&lt;br/&gt;
Correlation analyses of the late phase heart-to-mediastinum (H/M) ratio on the MIBG test and each item of the HDRS revealed that the H/M ratio was significantly correlated with scores of 'agitation', 'anxiety-somatic', and 'retardation' on the HDRS. Mean HDRS composite scores of 'somatic and psychic anxiety (Marcos)' and 'somatic anxiety/somatization factor (Pancheri)' were higher in the low uptake group than in the normal uptake group.&lt;br/&gt;
CONCLUSION:&lt;br/&gt;
Elderly patients with depression who manifested an obvious somatic anxiety tend to show low MIBG uptake, and are more likely to have Lewy body pathology.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">depression</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">elderly</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Lewy body disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">metaiodobenzylguanidine</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">somatic anxiety</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1444-1586</Issn>
      <Volume>19</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2018</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Social problems in daily life of patients with dementia</ArticleTitle>
    <FirstPage LZero="delete">113</FirstPage>
    <LastPage>118</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation>Department of Psychiatry, Okayama Red Cross Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Wakutani</LastName>
        <Affiliation>Department of Neurology, Kurashiki Heisei Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Nakata</LastName>
        <Affiliation>Department of Psychiatry, Taiyo Hills Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yumiko</FirstName>
        <LastName>Kutoku</LastName>
        <Affiliation> Department of Neurology, Kawasaki Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihide</FirstName>
        <LastName>Sunada</LastName>
        <Affiliation> Department of Neurology, Kawasaki Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Kondo</LastName>
        <Affiliation>Department of Psychiatry, Sekizen Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideki</FirstName>
        <LastName>Ishizu</LastName>
        <Affiliation>Department of Psychiatry, Zikei Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yohko</FirstName>
        <LastName>Maki</LastName>
        <Affiliation>Center for Comprehensive Care and Research on Memory Disorders, National Center for Geriatrics and Gerontology</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hideyuki</FirstName>
        <LastName>Hattori</LastName>
        <Affiliation>Department of Psychiatry, National Hospital for Geriatric Medicine, NCGG</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>AIM:&lt;br/&gt;
Most patients with dementia frequently encounter various problems in their daily lives. Those troubles embarrass both the patients and their families, and cause problems for society. However, there have been few scientific reports on the difficulties in the daily life of patients with dementia. Therefore, we tried to clarify the frequency and characteristics of troubles experienced by patients with dementia.&lt;br/&gt;
METHODS:&lt;br/&gt;
Seven medical centers treating dementia patients in Okayama Prefecture, Japan, participated in this survey. A total of 737 patients were placed in one of the three groups: a dementia group (n = 478), a mild cognitive impairment group (n = 199) and a control group (n = 60). The frequency of 13 difficulties was scored for each patient.&lt;br/&gt;
RESULTS:&lt;br/&gt;
Among normal participants, no person caused these problems once a year or more frequently. "Massive, recurrent buying" and "acts that risk causing a fire" were reported once a year or more for &gt;10% of mild cognitive impairment patients. "Troubles with wealth management" and "troubles with money management" were the most frequent problems of dementia patients.&lt;br/&gt;
CONCLUSIONS:&lt;br/&gt;
Several problems are already sometimes encountered in patients with mild cognitive impairment. It would be useful to know which social difficulties are often seen in dementia patients in order to protect the safety of the patients. It is always difficult to balance respecting the autonomy of dementia patients and ensuring their safely. </Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">mild cognitive impairment</Param>
      </Object>
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        <Param Name="value">sex</Param>
      </Object>
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        <Param Name="value">trouble</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>13463500</Issn>
      <Volume>20</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2019</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Patient affect and caregiver burden in dementia</ArticleTitle>
    <FirstPage LZero="delete">189</FirstPage>
    <LastPage>195</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yoshiko</FirstName>
        <LastName>Kawano</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Hayashi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshitaka</FirstName>
        <LastName>Oshima</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
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    <Abstract>BACKGROUND:&lt;br/&gt;
Numerous studies focusing on the burden of caregivers of dementia patients have been published. However, there have been few studies focusing on positive affect as an important factor affecting the caregiver burden, and only a few studies comparing the caregiver burden between different dementia diseases have been reported.&lt;br/&gt;
METHODS:&lt;br/&gt;
Three hundred and thirty-seven consecutive caregivers of people with dementia participated in this study. The caregiver burden was evaluated by the short version of the Japanese version of the Zarit Burden Interview.&lt;br/&gt;
RESULTS:&lt;br/&gt;
Positive affect scores had a significant relationship with the scores of the short version of the Zarit Burden Interview. Caregivers for patients with dementia with Lewy bodies or frontotemporal dementia suffered from a greater burden than those for patients with Alzheimer's disease dementia.&lt;br/&gt;
CONCLUSIONS:&lt;br/&gt;
The caregiver burden differed between people caring for patients with different dementia diseases. Positive affect of dementia patients has a significant relationship with caregiver burden, independently from neuropsychiatric symptoms of patients.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Alzheimer's disease</Param>
      </Object>
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      </Object>
      <Object Type="keyword">
        <Param Name="value">dementia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">dementia with Lewy bodies</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">frontotemporal dementia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">positive affect</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>BMC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>14712318</Issn>
      <Volume>19</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2019</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Validation of Addenbrooke's cognitive examination III for detecting mild cognitive impairment and dementia in Japan</ArticleTitle>
    <FirstPage LZero="delete">123</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shintaro</FirstName>
        <LastName>Takenoshita</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidenori</FirstName>
        <LastName>Yoshida</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Megumi</FirstName>
        <LastName>Yamaguchi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mayumi</FirstName>
        <LastName>Yabe</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nao</FirstName>
        <LastName>Imai</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makiko</FirstName>
        <LastName>Horiuchi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Yokota</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract>BACKGROUND:Early detection of mild cognitive impairment (MCI) and dementia is very important to begin appropriate treatment promptly and to prevent disease exacerbation. We investigated the screening accuracy of the Japanese version of Addenbrooke's Cognitive Examination III (ACE-III) to diagnose MCI and dementia.&lt;/br&gt;
METHODS:The original ACE-III was translated and adapted to Japanese. It was then administered to a Japanese population. The Hasegawa Dementia Scale-revised (HDS-R) and Mini-mental State Examination (MMSE) were also applied to evaluate cognitive dysfunction. In total, 389 subjects (dementia&#8201;=&#8201;178, MCI&#8201;=&#8201;137, controls&#8201;=&#8201;73) took part in our study.&lt;/br&gt;
RESULTS:The optimal ACE-III cut-off scores to detect MCI and dementia were 88/89 (sensitivity 0.77, specificity 0.92) and 75/76 (sensitivity 0.82, specificity 0.90), respectively. ACE-III was superior to HDS-R and MMSE in the detection of MCI or dementia. The internal consistency, test-retest reliability, and inter-rater reliability of ACE-III were excellent.&lt;/br&gt;
CONCLUSIONS:ACE-III is a useful cognitive test to detect MCI and dementia. ACE-III may be widely useful in clinical practice.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      </Object>
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        <Param Name="value">Cognitive screening</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Diagnosis dementia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Diagnosis mild cognitive impairment</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Mild cognitive impairment</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>70</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2016</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>An Open-Label Feasibility Trial of Repetitive Transcranial Magnetic Stimulation for Treatment-Resistant Major Depressive Episodes</ArticleTitle>
    <FirstPage LZero="delete">307</FirstPage>
    <LastPage>311</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masaki</FirstName>
        <LastName>Fujiwara</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masatoshi</FirstName>
        <LastName>Inagaki</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuji</FirstName>
        <LastName>Higuchi</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Uchitomi</LastName>
        <Affiliation>Innovation Center for Supportive, Palliative and Psychosocial Care, National Cancer Center Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>Terada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masafumi</FirstName>
        <LastName>Kodama</LastName>
        <Affiliation>Okayama Psychiatric Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiki</FirstName>
        <LastName>Kishi</LastName>
        <Affiliation>Okayama Psychiatric Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihito</FirstName>
        <LastName>Yamada</LastName>
        <Affiliation>Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Clinical Study Protocols</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/54510</ArticleId>
    </ArticleIdList>
    <Abstract>Repetitive transcranial magnetic stimulation (rTMS) has been reported to be a new treatment option for treatment-resistant depression. In Japan, there has been limited research into its feasibility, efficacy, and tolerability. We have launched a trial of rTMS for treating medication-resistant major depressive disorder and bipolar depression. We are investigating low-frequency rTMS to the right dorsolateral prefrontal cortex and traditional high-frequency rTMS to the left dorsolateral prefrontal cortex, in 20 patients. The primary outcome of the study is the treatment completion rate. This study will provide new data on the usefulness of rTMS for treatment-resistant depression in Japan.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">repetitive transcranial magnetic stimulation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">depression</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">treatment resistance</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">low frequency</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>116</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2004</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>石灰沈着を伴うび漫性神経原線維変化病における α-Synuclein 陽性病変から分かること―岡山大学医学賞（新見賞）を受賞して―</ArticleTitle>
    <FirstPage LZero="delete">89</FirstPage>
    <LastPage>96</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">α-synuclein</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diffuse neurofibrillary tangles with calcification</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">NAC</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">synucleinopathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tauopathy</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>118</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2007</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>モデル動物を用いたタウオパシーの病態解明と有効な薬剤同定：αトコフェロールの効果について</ArticleTitle>
    <FirstPage LZero="delete">193</FirstPage>
    <LastPage>198</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
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        <Param Name="value">タウオパシー</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">認知症</Param>
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      <Object Type="keyword">
        <Param Name="value">神経変性疾患</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">酸化ストレス</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">α トコフェロール</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2001</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Tau-negative astrocytic star-like inclusions and coiled bodies in dementia with Lewy bodies</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
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    <PublicationType/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
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