Updated on 2024/04/12

写真a

 
UEMURA MAIKO
 
Organization
Graduate School of Medicine Department of Basic Medical Science Lecturer
School of Medicine Department of Medical Science
Title
Lecturer
Affiliation
Institute of Medicine
Affiliation campus
Abeno Campus

Position

  • Graduate School of Medicine Department of Basic Medical Science 

    Lecturer  2023.10 - Now

  • School of Medicine Department of Medical Science 

    Lecturer  2023.10 - Now

Degree

  • 博士（医学） （ Kyoto University ） (   Kyoto University )

Research Areas

  • Life Science / Neuroscience-general

  • Life Science / Neuroscience-general  / Tau, α-synuclein, TDP-43, Vascular Dementia

  • Life Science / Neurology

Research Interests

  • Tau

  • α-synuclein

  • TDP-43

  • Alzheimer's Disease

  • Vascular Cognitive Impairment

  • 血管性認知症

  • limbic-predominant age-reoated TDP-43 encephalopathy

  • パーキンソン病

  • アルツハイマー病

Professional Memberships

  • 日本内科学会

      Domestic

  • 日本神経学会

      Domestic

  • 日本神経科学学会

      Domestic

  • 日本認知症学会

      Domestic

  • 日本脳血管・認知症学会

      Domestic

  • 日本神経病理学会

      Domestic

  • 日本老年医学会

      Domestic

  • 日本女性科学者の会

      Domestic

  • THE JAPANESE SOCIETY OF INTERNAL MEDICINE

  • THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

  • JAPANESE SOCIETY OF NEUROLOGY

  • THE JAPANESE SOCIETY OF NEUROPATHOLOGY

  • THE JAPAN NEUROSCIENCE SOCIETY

  • THE JAPAN STROKE SOCIETY

  • JAPAN SOCIETY FOR DEMENTIA RESEARCH

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Awards

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Job Career (off-campus)

  • Kyoto University   Department of Neurology   Researcher

    2023.10 - Now

  • Kyoto University   Department of Neurology, Graduate School of Medicine   Program-specific assistant professor

    2023.04 - 2023.10

  • Otsu Red Cross Hospital   Department of Neurology   Doctor

    2022.10 - 2023.03

  • Kyoto University

    2022.10 - 2023.03

  • University of Pennsylvania   Center for Neurodegenerative Disease Research   Postdoctoral fellow

    2018.07 - 2022.09

  • Japan Society for the Promotion of Science   Overseas Research Fellow-RRA

    2018.07 - 2020.06

  • Kyoto University   Department of Neurology, Graduate School of Medicine   Program-specific Researcher

    2015.04 - 2018.06

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Papers

  • Abundant copathologies of polyglucosan bodies, frontotemporal lobar degeneration with TDP‐43 inclusions and ageing‐related tau astrogliopathy in a family with a GBE1 mutation Reviewed International coauthorship

    Neuropathology and Applied Neurobiology   49 ( 1 )   e12865 - e12865   2023（ ISSN:0305-1846 ）

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Adult polyglucosan body disease (APBD) is a progressive neurogenetic disorder caused by 1,4‐alpha‐glucan branching enzyme 1 (GBE1) mutation with an accumulation of polyglucosan bodies (PBs) in the central and peripheral nervous systems as a pathological hallmark. Here, we report two siblings in a family with a GBE1 mutation with prominent frontotemporal lobar degeneration with TAR DNA‐binding protein 43 (FTLD‐TDP) and ageing‐related tau astrogliopathy (ARTAG) copathologies with PBs in the central nervous system. Whole‐genome sequencing (WGS) followed by Sanger sequencing (SS) was performed on three affected and two unaffected siblings in a pedigree diagnosed with familial frontotemporal dementia. Out of the affected siblings, autopsies were conducted on two cases, and brain samples were used for biochemical and histological analyses. Brain sections were stained with haematoxylin and eosin and immunostained with antibodies against ubiquitin, tau, amyloid β, α‐synuclein, TDP‐43 and fused in sarcoma (FUS). A novel single nucleotide deletion in GBE1, c.1280delG, was identified, which is predicted to result in a reading frameshift, p.Gly427Glufs*9. This variant segregated with disease in the family, is absent from population databases and is predicted to cause loss of function, a known genetic mechanism for APBD. The affected siblings showed a greater than 50\% decrease in GBE protein levels. Immunohistochemical analysis revealed widespread FTLD‐TDP (type A) and ARTAG pathologies as well as PBs in the brains of two affected siblings for whom an autopsy was performed. This is the first report of a family with several individuals with a FTD clinical phenotype and underlying copathologies of APBD, FTLD‐TDP and ARTAG with a segregating GBE1 loss‐of‐function mutation in affected siblings. The finding of copathologies of APBD and FTLD‐TDP suggests these processes may share a disease mechanism resulting from this GBE1 mutation. A family with FTD clinical phenotype with a novel GBE1 mutation c.1280delG was identified, which is predicted to result in a reading frameshift, p.Gly427Glufs*9. Two of the affected siblings showed a reduction in GBE protein expression levels with abundant FTLD‐TDP Type A pathology in the grey matter, abundant PBs, and ARTAG in the subpial matter and the white matter. The finding of copathologies of APBD and FTLD‐TDP suggest these processes may share a disease mechanism resulting from this GBE1 loss‐of‐function mutation.

    DOI： 10.1111/nan.12865

  • Hemosiderin Detection inside the Mammillary Bodies Using Quantitative Susceptibility Mapping on Patients with Wernicke-Korsakoff Syndrome. Reviewed International coauthorship

    Nakamura, Yuri and Fushimi, Yasutaka and Hinoda, Takuya and Nakajima, Satoshi and Sakata, Akihiko and Okuchi, Sachi and Otani, Sayo and Tagawa, Hiroshi and Wang, Yang and Ikeda, Satoshi and Kawashima, Hirotsugu and Uemura, Maiko T and Nakamoto, Yuji

    Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine   23 ( 1 )   14 - 17   2022（ ISSN:1347-3182 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Hemorrhage inside the mammillary bodies (MMBs) is known to be one of the findings of Wernicke encephalopathy. Brain MRI of two patients with Wernicke-Korsakoff syndrome (WKS) demonstrated high susceptibility values representing hemosiderin deposition in MMBs by using quantitative susceptibility mapping (QSM). QSM provided additional information of susceptibility values to susceptibility-weighted imaging in diagnosis of WKS.

    DOI： 10.2463/mrms.ici.2022-0109

    PubMed

  • Failure of DNA double-strand break repair by tau mediates Alzheimer's disease pathology in vitro. Reviewed

    Megumi Asada-Utsugi, Kengo Uemura, Takashi Ayaki, Maiko T. Uemura, Sumio Minamiyama, Ryota Hikiami, Toshifumi Morimura, Akemi Shodai, Takatoshi Ueki, Ryosuke Takahashi, Ayae Kinoshita, Makoto Urushitani

    Communications biology   5 ( 1 )   358 - 358   2022

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    DNA double-strand break (DSB) is the most severe form of DNA damage and accumulates with age, in which cytoskeletal proteins are polymerized to repair DSB in dividing cells. Since tau is a microtubule-associated protein, we investigate whether DSB is involved in tau pathologies in Alzheimer's disease (AD). First, immunohistochemistry reveals the frequent coexistence of DSB and phosphorylated tau in the cortex of AD patients. In vitro studies using primary mouse cortical neurons show that non-p-tau accumulates perinuclearly together with the tubulin after DSB induction with etoposide, followed by the accumulation of phosphorylated tau. Moreover, the knockdown of endogenous tau exacerbates DSB in neurons, suggesting the protective role of tau on DNA repair. Interestingly, synergistic exposure of neurons to microtubule disassembly and the DSB strikingly augments aberrant p-tau aggregation and apoptosis. These data suggest that DSB plays a pivotal role in AD-tau pathology and that the failure of DSB repair leads to tauopathy.

    DOI： 10.1038/s42003-022-03312-0

    Other URL： https://www.nature.com/articles/s42003-022-03312-0

  • Rapid Induction of Dopaminergic Neuron Loss Accompanied by Lewy Body-Like Inclusions in A53T BAC-SNCA Transgenic Mice. Reviewed

    Shinya Okuda, Norihito Uemura, Masanori Sawamura, Tomoyuki Taguchi, Masashi Ikuno, Maiko T Uemura, Hodaka Yamakado, Ryosuke Takahashi

    Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics   19 ( 1 )   289 - 289   2022（ ISSN:1933-7213 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Parkinson's disease (PD), the most common neurodegenerative movement disorder, is characterized by dopaminergic neuron loss in the substantia nigra pars compacta (SNpc) and intraneuronal α-synuclein (α-syn) inclusions. It is highly needed to establish a rodent model that recapitulates the clinicopathological features of PD within a short period to efficiently investigate the pathological mechanisms and test disease-modifying therapies. To this end, we analyzed three mouse lines, i.e., wild-type mice, wild-type human α-syn bacterial artificial chromosome (BAC) transgenic (BAC-SNCA Tg) mice, and A53T human α-syn BAC transgenic (A53T BAC-SNCA Tg) mice, receiving dorsal striatum injections of human and mouse α-syn preformed fibrils (hPFFs and mPFFs, respectively). mPFF injections induced more severe α-syn pathology in most brain regions, including the ipsilateral SNpc, than hPFF injections in all genotypes at 1-month post-injection. Although these Tg mouse lines expressed a comparable amount of α-syn in the brains, the mPFF-injected A53T BAC-SNCA Tg mice exhibited the most severe α-syn pathology as early as 0.5-month post-injection. The mPFF-injected A53T BAC-SNCA Tg mice showed a 38\% reduction in tyrosine hydroxylase (TH)-positive neurons in the ipsilateral SNpc, apomorphine-induced rotational behavior, and motor dysfunction at 2 months post-injection. These data indicate that the extent of α-syn pathology induced by α-syn PFF injection depends on the types of α-syn PFFs and exogenously expressed α-syn in Tg mice. The mPFF-injected A53T BAC-SNCA Tg mice recapitulate the key features of PD more rapidly than previously reported mouse models, suggesting their usefulness for testing disease-modifying therapies as well as analyzing the pathological mechanisms.

    DOI： 10.1007/s13311-021-01169-5

    PubMed

    Other URL： https://www.researchsquare.com/article/rs-355605/v1.html

  • α-Synuclein Spread from Olfactory Bulb Causes Hyposmia, Anxiety, and Memory Loss in BAC-SNCA Mice. Reviewed International coauthorship

    Norihito Uemura, Jun Ueda, Toru Yoshihara, Masashi Ikuno, Maiko T Uemura, Hodaka Yamakado, Masahide Asano, John Q Trojanowski, Ryosuke Takahashi

    Movement disorders : official journal of the Movement Disorder Society   36 ( 9 )   2036 - 2036   2021（ ISSN:0885-3185 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    BACKGROUND: Patients with Parkinson's disease (PD) show motor symptoms as well as various non-motor symptoms. Postmortem studies of PD have suggested that initial alpha-synuclein (α-Syn) pathology develops independently in the olfactory bulb and lower brainstem, spreading from there stereotypically. However, it remains unclear how these two pathological pathways contribute to the clinicopathological progression of PD. OBJECTIVE: The objective of this study was to examine the clinicopathological contribution of α-Syn spread from the olfactory bulb. METHODS: We conducted pathological and behavioral analyses of human α-Syn bacterial artificial chromosome transgenic mice injected with α-Syn preformed fibrils into the bilateral olfactory bulb up to 10 months postinjection. RESULTS: α-Syn preformed fibril injections induced more widespread α-Syn pathology in the transgenic mice than that in wild-type mice. Severe α-Syn pathology in the transgenic mice injected with α-Syn preformed fibrils was initially observed along the olfactory pathway and later in the brain regions that are included in the limbic system and have connections with it. The α-Syn pathology was accompanied by regional atrophy, neuron loss, reactive astrogliosis, and microglial activation, which were remarkable in the hippocampus. Behavioral analyses revealed hyposmia, followed by anxiety-like behavior and memory impairment, but not motor dysfunction, depression-like behavior, or circadian rhythm disturbance. CONCLUSION: Our data suggest that α-Syn spread from the olfactory bulb mainly affects the olfactory pathway and limbic system as well as its related regions, leading to the development of hyposmia, anxiety, and memory loss in PD. © 2021 International Parkinson and Movement Disorder Society.

    DOI： 10.1002/mds.28512

    PubMed

    Other URL： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/mds.28512

  • Distinct characteristics of limbic-predominant age-related TDP-43 encephalopathy in Lewy body disease Reviewed International coauthorship

    Acta Neuropathologica   1 - 1   2021（ ISSN:0001-6322 ）

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    Authorship：Lead author,　Corresponding author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Limbic-predominant age-related TDP-43 encephalopathy (LATE) is characterized by the accumulation of TAR-DNA-binding protein 43 (TDP-43) aggregates in older adults. LATE coexists with Lewy body disease (LBD) as well as other neuropathological changes including Alzheimer’s disease (AD). We aimed to identify the pathological, clinical, and genetic characteristics of LATE in LBD (LATE-LBD) by comparing it with LATE in AD (LATE-AD), LATE with mixed pathology of LBD and AD (LATE-LBD + AD), and LATE alone (Pure LATE). We analyzed four cohorts of autopsy-confirmed LBD (n = 313), AD (n = 282), LBD + AD (n = 355), and aging (n = 111). We assessed the association of LATE with patient profiles including LBD subtype and AD neuropathologic change (ADNC). We studied the morphological and distributional differences between LATE-LBD and LATE-AD. By frequency analysis, we staged LATE-LBD and examined the association with cognitive impairment and genetic risk factors. Demographic analysis showed LATE associated with age in all four cohorts and the frequency of LATE was the highest in LBD + AD followed by AD, LBD, and Aging. LBD subtype and ADNC associated with LATE in LBD or AD but not in LBD + AD. Pathological analysis revealed that the hippocampal distribution of LATE was different between LATE-LBD and LATE-AD: neuronal cytoplasmic inclusions were more frequent in cornu ammonis 3 (CA3) in LATE-LBD compared to LATE-AD and abundant fine neurites composed of C-terminal truncated TDP-43 were found mainly in CA2 to subiculum in LATE-LBD, which were not as numerous in LATE-AD. Some of these fine neurites colocalized with phosphorylated α-synuclein. LATE-LBD staging showed LATE neuropathological changes spread in the dentate gyrus and brainstem earlier than in LATE-AD. The presence and prevalence of LATE in LBD associated with cognitive impairment independent of either LBD subtype or ADNC; LATE-LBD stage also associated with the genetic risk variants of TMEM106B rs1990622 and GRN rs5848. These data highlight clinicopathological and genetic features of LATE-LBD.

    DOI： 10.1007/s00401-021-02383-3

  • α-Synuclein BAC transgenic mice exhibit RBD-like behaviour and hyposmia: a prodromal Parkinson's disease model. Reviewed International coauthorship

    Tomoyuki Taguchi, Masashi Ikuno, Mari Hondo, Laxmi Kumar Parajuli, Katsutoshi Taguchi, Jun Ueda, Masanori Sawamura, Shinya Okuda, Etsuro Nakanishi, Junko Hara, Norihito Uemura, Yusuke Hatanaka, Takashi Ayaki, Shuichi Matsuzawa, Masaki Tanaka, Omar M A El-Agnaf, Masato Koike, Masashi Yanagisawa, Maiko T Uemura, Hodaka Yamakado, Ryosuke Takahashi

    Brain : a journal of neurology   143 ( 1 )   249 - 249   2020（ ISSN:0006-8950 ）

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    Authorship：Corresponding author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Parkinson's disease is one of the most common movement disorders and is characterized by dopaminergic cell loss and the accumulation of pathological α-synuclein, but its precise pathogenetic mechanisms remain elusive. To develop disease-modifying therapies for Parkinson's disease, an animal model that recapitulates the pathology and symptoms of the disease, especially in the prodromal stage, is indispensable. As subjects with α-synuclein gene (SNCA) multiplication as well as point mutations develop familial Parkinson's disease and a genome-wide association study in Parkinson's disease has identified SNCA as a risk gene for Parkinson's disease, the increased expression of α-synuclein is closely associated with the aetiology of Parkinson's disease. In this study we generated bacterial artificial chromosome transgenic mice harbouring SNCA and its gene expression regulatory regions in order to maintain the native expression pattern of α-synuclein. Furthermore, to enhance the pathological properties of α-synuclein, we inserted into SNCA an A53T mutation, two single-nucleotide polymorphisms identified in a genome-wide association study in Parkinson's disease and a Rep1 polymorphism, all of which are causal of familial Parkinson's disease or increase the risk of sporadic Parkinson's disease. These A53T SNCA bacterial artificial chromosome transgenic mice showed an expression pattern of human α-synuclein very similar to that of endogenous mouse α-synuclein. They expressed truncated, oligomeric and proteinase K-resistant phosphorylated forms of α-synuclein in the regions that are specifically affected in Parkinson's disease and/or dementia with Lewy bodies, including the olfactory bulb, cerebral cortex, striatum and substantia nigra. Surprisingly, these mice exhibited rapid eye movement (REM) sleep without atonia, which is a key feature of REM sleep behaviour disorder, at as early as 5 months of age. Consistent with this observation, the REM sleep-regulating neuronal populations in the lower brainstem, including the sublaterodorsal tegmental nucleus, nuclei in the ventromedial medullary reticular formation and the pedunculopontine nuclei, expressed phosphorylated α-synuclein. In addition, they also showed hyposmia at 9 months of age, which is consistent with the significant accumulation of phosphorylated α-synuclein in the olfactory bulb. The dopaminergic neurons in the substantia nigra pars compacta degenerated, and their number was decreased in an age-dependent manner by up to 17.1\% at 18 months of age compared to wild-type, although the mice did not show any related locomotor dysfunction. In conclusion, we created a novel mouse model of prodromal Parkinson's disease that showed RBD-like behaviour and hyposmia without motor symptoms.

    DOI： 10.1093/brain/awz380

    PubMed

  • Limited spread of pathology within the brainstem of α-synuclein BAC transgenic mice inoculated with preformed fibrils into the gastrointestinal tract. Reviewed International coauthorship

    Norihito Uemura, Hisashi Yagi, Maiko T Uemura, Hodaka Yamakado, Ryosuke Takahashi

    Neuroscience letters   716   134651 - 134651   2020（ ISSN:0304-3940 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Parkinson's disease (PD) is pathologically characterized by intraneuronal α-synuclein (α-Syn) aggregates called Lewy bodies (LBs) as well as the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). On the basis of autopsy studies, Braak et al. hypothesized that Lewy pathology initially occurs in the enteric nervous system, subsequently spreading to the dorsal motor nucleus of the vagus nerve (dmX) and then ascending in the brainstem to the SNpc. However, this hypothetical progression lacks adequate experimental evidence. We previously reported that inoculation of α-Syn preformed fibrils (PFFs) into the gastric wall of wild-type (WT) mice induced LB-like α-Syn aggregates in the dmX via the vagus nerve. However, α-Syn pathology did not spread beyond the dmX up to 12 months postinoculation. In the present study, we inoculated α-Syn PFFs into the gastric wall of bacterial artificial chromosome (BAC) transgenic mice harboring the human α-Syn gene with an A53 T mutation and analyzed the pathology. The transgenic mice had ∼1.5-fold overexpression of α-Syn in the brains and ∼6-fold overexpression of α-Syn in the stomach compared with WT mice. After inoculation of α-Syn PFFs, the transgenic mice developed a higher number of phosphorylated α-Syn (p-α-Syn)-positive neurons in the dmX compared with similarly inoculated WT mice. However, the number of p-α-Syn-positive neurons in the dmX decreased over time, and α-Syn pathology was not observed in other brain regions except in the ambiguous nucleus up to 8 months postinoculation. Taken together, BAC transgenic expression of α-Syn facilitated induction of α-Syn pathology in the brainstem, but not subsequent caudo-rostral spread in accordance with Braak's hypothesis.

    DOI： 10.1016/j.neulet.2019.134651

    PubMed

  • Cell-to-Cell Transmission of Tau and α-Synuclein. Reviewed International coauthorship

    Trends in molecular medicine   26   936 - 936   2020（ ISSN:1471-4914 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    The stereotypical spread of pathological protein inclusions and clinicopathological heterogeneity are well described in neurodegenerative diseases. Accumulating evidence suggests that the former can be attributed to consecutive cell-to-cell transmission of pathological proteins between anatomically connected brain regions, while the latter has been hypothesized to result from the spread of conformationally distinct pathological protein aggregates, or strains. These emerging concepts have dramatically changed our understanding of neurodegenerative diseases. In this review, we first summarize the background and recent findings underpinning these concepts with a focus on two major pathological proteins: tau and α-synuclein. We then discuss their clinical implications for tauopathies and synucleinopathies and propose a working hypothesis for future research.

    DOI： 10.1016/j.molmed.2020.03.012

  • Brain Microvascular Pericytes in Vascular Cognitive Impairment and Dementia. Reviewed International coauthorship

    Frontiers in aging neuroscience   12   80 - 80   2020（ ISSN:1663-4365 ）

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    Authorship：Lead author,　Corresponding author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Pericytes are unique, multi-functional mural cells localized at the abluminal side of the perivascular space in microvessels. Originally discovered in 19th century, pericytes had drawn less attention until decades ago mainly due to lack of specific markers. Recently, however, a growing body of evidence has revealed that pericytes play various important roles: development and maintenance of blood-brain barrier (BBB), regulation of the neurovascular system (e.g., vascular stability, vessel formation, cerebral blood flow, etc.), trafficking of inflammatory cells, clearance of toxic waste products from the brain, and acquisition of stem cell-like properties. In the neurovascular unit, pericytes perform these functions through coordinated crosstalk with neighboring cells including endothelial, glial, and neuronal cells. Dysfunction of pericytes contribute to a wide variety of diseases that lead to cognitive impairments such as cerebral small vessel disease (SVD), acute stroke, Alzheimer's disease (AD), and other neurological disorders. For instance, in SVDs, pericyte degeneration leads to microvessel instability and demyelination while in stroke, pericyte constriction after ischemia causes a no-reflow phenomenon in brain capillaries. In AD, which shares some common risk factors with vascular dementia, reduction in pericyte coverage and subsequent microvascular impairments are observed in association with white matter attenuation and contribute to impaired cognition. Pericyte loss causes BBB-breakdown, which stagnates amyloid β clearance and the leakage of neurotoxic molecules into the brain parenchyma. In this review, we first summarize the characteristics of brain microvessel pericytes, and their roles in the central nervous system. Then, we focus on how dysfunctional pericytes contribute to the pathogenesis of vascular cognitive impairment including cerebral 'small vessel' and 'large vessel' diseases, as well as AD. Finally, we discuss therapeutic implications for these disorders by targeting pericytes.

    DOI： 10.3389/fnagi.2020.00080

  • Correction to: Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve. Reviewed

    Molecular neurodegeneration   14 ( 1 )   31 - 31   2019

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    The original article [1] mistakenly omitted essential information regarding Fig. 1c; thus, the authors would like to note that Fig. 1c describes transmission electron microscopy of α-Syn PFFs before sonication.

    DOI： 10.1186/s13024-019-0331-7

  • Slow Progressive Accumulation of Oligodendroglial Alpha-Synuclein (α-Syn) Pathology in Synthetic α-Syn Fibril-Induced Mouse Models of Synucleinopathy. Reviewed International coauthorship

    Norihito Uemura, Maiko T Uemura, Angela Lo, Fares Bassil, Bin Zhang, Kelvin C Luk, Virginia M-Y Lee, Ryosuke Takahashi, John Q Trojanowski

    Journal of neuropathology and experimental neurology   78 ( 10 )   877 - 877   2019（ ISSN:0022-3069 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Synucleinopathies are composed of Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Alpha-synuclein (α-Syn) forms aggregates mainly in neurons in PD and DLB, while oligodendroglial α-Syn aggregates are characteristic of MSA. Recent studies have demonstrated that injections of synthetic α-Syn preformed fibrils (PFFs) into the brains of wild-type (WT) animals induce intraneuronal α-Syn aggregates and the subsequent interneuronal transmission of α-Syn aggregates. However, injections of α-Syn PFFs or even brain lysates of patients with MSA have not been reported to induce oligodendroglial α-Syn aggregates, raising questions about the pathogenesis of oligodendroglial α-Syn aggregates in MSA. Here, we report that WT mice injected with mouse α-Syn (m-α-Syn) PFFs develop neuronal α-Syn pathology after short postinjection (PI) intervals on the scale of weeks, while oligodendroglial α-Syn pathology emerges after longer PI intervals of several months. Abundant oligodendroglial α-Syn pathology in white matter at later time points is reminiscent of MSA. Furthermore, comparison between young and aged mice injected with m-α-Syn PFFs revealed that PI intervals rather than aging correlate with oligodendroglial α-Syn aggregation. These results provide novel insights into the pathological mechanisms of oligodendroglial α-Syn aggregation in MSA.

    DOI： 10.1093/jnen/nlz070

    PubMed

  • Prolonged sensory impairment in the perineal region after painless delivery through lumbar epidural anesthesia Reviewed

    Maiko T Uemura, Takahiro Mezaki, Hiroshi Shibasaki, Ryosuke Takahashi

    Neurology and Clinical Neuroscience   7 ( 1 )   43 - 43   2018（ ISSN:2049-4173 ）

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    Authorship：Lead author,　Corresponding author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    In the painless delivery, the neuronal injury caused by regional anesthesia sometimes causes diagnostic difficulty because of the common findings with lumbosacral injury due to vaginal delivery. We herein report a 36‐year‐old woman presenting with long‐standing cauda equina syndrome due to neurotoxicity of regional anesthetic. Neurological examination revealed the almost symmetrical, heterogeneous sensory deficit mainly in the perineal region, hypoactive quadriceps femoris reflex, decreased anal sphincter reflex, and dermographia. The correct diagnosis is important to support the quality of life of patients.

    DOI： 10.1111/ncn3.12245

    Other URL： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/ncn3.12245

  • Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve. Reviewed

    Molecular neurodegeneration   13 ( 1 )   21 - 21   2018（ ISSN:1750-1326 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    BACKGROUND: Intraneuronal α-synuclein (α-Syn) aggregates known as Lewy bodies (LBs) and the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) are the pathological hallmarks of Parkinson's disease (PD). Braak's hypothesis based on autopsy studies suggests that Lewy pathology initially occurs in the enteric nervous system (ENS) and then travels retrogradely to the dorsal motor nucleus of the vagus nerve (dmX), proceeding from there in a caudo-rostral direction. Recent evidence that α-Syn aggregates propagate between interconnected neurons supports this hypothesis. However, there is no direct evidence demonstrating this transmission from the ENS to the dmX and then to the SNpc. METHODS: We inoculated α-Syn preformed fibrils (PFFs) or phosphate-buffered saline (PBS) into the mouse gastric wall and analyzed the progression of the pathology. RESULTS: The mice inoculated with α-Syn PFFs, but not with PBS, developed phosphorylated α-Syn (p-α-Syn)-positive LB-like aggregates in the dmX at 45 days postinoculation. This aggregate formation was completely abolished when vagotomy was performed prior to inoculation of α-Syn PFFs, suggesting that the aggregates in the dmX were retrogradely induced via the vagus nerve. Unexpectedly, the number of neurons containing p-α-Syn-positive aggregates in the dmX decreased over time, and no further caudo-rostral propagation beyond the dmX was observed up to 12 months postinoculation. P-α-Syn-positive aggregates were also present in the myenteric plexus at 12 months postinoculation. However, unlike in patients with PD, there was no cell-type specificity in neurons containing those aggregates in this model. CONCLUSIONS: These results indicate that α-Syn PFF inoculation into the mouse gastrointestinal tract can induce α-Syn pathology resembling that of very early PD, but other factors are apparently required if further progression of PD pathology is to be replicated in this animal model.

    DOI： 10.1186/s13024-018-0257-5

    PubMed

  • Zonisamide inhibits monoamine oxidase and enhances motor performance and social activity. Reviewed

    Neuroscience research   124   25 - 25   2017（ ISSN:0168-0102 ）

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Zonisamide (ZNS) is an effective drug for not only motor symptoms but also non-motor symptoms in Parkinson's disease. However, the actions of ZNS as an anti-Parkinsonian drug are not well understood. To clarify the actions of ZNS in vivo, we administered ZNS to mice and examined the effects on neurotransmitter metabolism and behaviors, focusing on motor and non-motor symptoms. Administration of ZNS decreased dopamine (DA) turnover in various brain regions, including the striatum. In behavioral tests, ZNS enhanced locomotor activity and novelty seeking in the open field test, light-dark transition test, and the social interaction test. Consistent with these results of DA metabolism in ZNS-treated mice, monoamine oxidase activity was significantly inhibited by ZNS in primary neurons and astrocytes. Collectively, these data suggest that ZNS inhibits monoamine oxidase activity and decreases DA turnover, which increases locomotor activity and novelty seeking in mice. ZNS is potentially useful to improve not only motor symptoms but also neuropsychiatric non-motor symptoms such as apathy in PD.

    DOI： 10.1016/j.neures.2017.05.008

    PubMed

  • Pericyte-derived bone morphogenetic protein 4 underlies white matter damage after chronic hypoperfusion. Reviewed International coauthorship

    Brain pathology (Zurich, Switzerland)   28 ( 4 )   521 - 535   2017（ ISSN:1750-3639 ）

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Subcortical small vessel disease (SVD) is characterized by white matter damage resulting from arteriolosclerosis and chronic hypoperfusion. Transforming growth factor beta 1 (TGFB1) is dysregulated in the hereditary SVD, CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy). However, very little is known about the role of the largest group in the TGFB superfamily - the bone morphogenetic proteins (BMPs) - in SVD pathogenesis. The aim of this study was to characterize signaling abnormalities of BMPs in sporadic SVD. We examined immunostaining of TGFB1 and BMPs (BMP2/BMP4/BMP6/BMP7/BMP9) in a total of 19 post-mortem human brain samples as follows: 7 SVD patients (4 males, 76-90 years old); 6 Alzheimer's disease (AD) patients (2 males, 67-93 years old) and 6 age-matched disease controls (3 males, 68-78 years old). We subsequently investigated the effects of oxygen-glucose deprivation and BMP4 addition on cultured cells. Furthermore, adult mice were subjected to chronic cerebral hypoperfusion using bilateral common carotid artery stenosis, followed by continuous intracerebroventricular infusion of the BMP antagonist, noggin. In the SVD cases, BMP4 was highly expressed in white matter pericytes. Oxygen-glucose deprivation induced BMP4 expression in cultured pericytes in vitro. Recombinant BMP4 increased the number of cultured endothelial cells and pericytes and converted oligodendrocyte precursor cells into astrocytes. Chronic cerebral hypoperfusion in vivo also upregulated BMP4 with concomitant white matter astrogliogenesis and reduced oligodendrocyte lineage cells, both of which were suppressed by intracerebroventricular noggin infusion. Our findings suggest ischemic white matter damage evolves in parallel with BMP4 upregulation in pericytes. BMP4 promotes angiogenesis, but induces astrogliogenesis at the expense of oligodendrocyte precursor cell proliferation and maturation, thereby aggravating white matter damage. This may explain white matter vulnerability to chronic hypoperfusion. The regulation of BMP4 signaling is a potential therapeutic strategy for treating SVD.

    DOI： 10.1111/bpa.12523

    PubMed

  • High Fat Diet Enhances β-Site Cleavage of Amyloid Precursor Protein (APP) via Promoting β-Site APP Cleaving Enzyme 1/Adaptor Protein 2/Clathrin Complex Formation Reviewed

    PLOS ONE   10 ( 9 )   e0131199 - e0131199   2015（ ISSN:1932-6203 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Obesity and type 2 diabetes are risk factors of Alzheimer’s disease (AD). We reported that a high fat diet (HFD) promotes amyloid precursor protein (APP) cleavage by β-site APP cleaving enzyme 1 (BACE1) without increasing BACE1 levels in APP transgenic mice. However, the detailed mechanism had remained unclear. Here we demonstrate that HFD promotes BACE1/Adaptor protein-2 (AP-2)/clathrin complex formation by increasing AP-2 levels in APP transgenic mice. In Swedish APP overexpressing Chinese hamster ovary (CHO) cells as well as in SH-SY5Y cells, overexpression of AP-2 promoted the formation of BACE1/AP-2/clathrin complex, increasing the level of the soluble form of APP β (sAPPβ). On the other hand, mutant D495R BACE1, which inhibits formation of this trimeric complex, was shown to decrease the level of sAPPβ. Overexpression of AP-2 promoted the internalization of BACE1 from the cell surface, thus reducing the cell surface BACE1 level. As such, we concluded that HFD may induce the formation of the BACE1/AP-2/clathrin complex, which is followed by its transport of BACE1 from the cell surface to the intracellular compartments. These events might be associated with the enhancement of β-site cleavage of APP in APP transgenic mice. Here we present evidence that HFD, by regulation of subcellular trafficking of BACE1, promotes APP cleavage.

    DOI： 10.1371/journal.pone.0131199

    PubMed

  • Potential interactions between pericytes and oligodendrocyte precursor cells in perivascular regions of cerebral white matter. Reviewed International coauthorship

    Neuroscience letters   597 ( 29 )   164 - 164   2015（ ISSN:0304-3940 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Pericytes are embedded within basal lamina and play multiple roles in the perivascular niche in brain. Recently, oligodendrocyte precursor cells (OPCs) have also been reported to associate with cerebral endothelium. Is it possible that within this gliovascular locus, there may also exist potential spatial and functional interactions between pericytes and OPCs? Here, we demonstrated that in the perivascular region of cerebral white matter, pericytes and OPCs may attach and support each other. Immunostaining showed that pericytes and OPCs are localized in close contact with each other in mouse white matter at postnatal days 0, 60 and 240. Electron microscopic analysis confirmed that pericytes attached to OPCs via basal lamina in the perivascular region. The close proximity between these two cell types was also observed in postmortem human brains. Functional interaction between pericytes and OPCs was assessed by in vitro media transfer experiments. When OPC cultures were treated with pericyte-conditioned media, OPC number increased. Similarly, pericyte number increased when pericytes were maintained in OPC-conditioned media. Taken together, our data suggest a potential anatomical and functional interaction between pericytes and OPCs in cerebral white matter.

    DOI： 10.1016/j.neulet.2015.04.047

    PubMed

  • Copper enhances APP dimerization and promotes Aβ production. Reviewed

    Neuroscience letters   547   10 - 10   2013（ ISSN:0304-3940 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Alzheimer's disease (AD) is characterized by the deposition of amyloid-β (Aβ) plaques, senile plaque. The Aβ peptide is cleaved from amyloid precursor protein (APP) by β-secretase and γ-secretase. Until now, many literatures have documented that the high concentration of copper is present in Aβ plaques and enhances aggregation of. The APP copper binding domain (CuBD) is located in the N-terminal next to the growth factor-like domain that gets involved in APP homodimerization. Importantly, dimerization of APP has profound effect on Aβ production. We investigated whether copper alters the state of APP dimerization and how it affects APP metabolism. Here, we demonstrate that copper enhanced APP dimerization and increased extracellular release of Aβ. Moreover, copper chelator, D-penicillamine, suppressed APP dimerization and decreased extracellular release of Aβ. These results suggest that the action of copper may be profoundly associated with the pathway of Aβ production in AD pathogenesis.

    DOI： 10.1016/j.neulet.2013.04.057

    PubMed

  • Continuation of exercise is necessary to inhibit high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice. Reviewed

    PloS one   8 ( 9 )   e72796 - e72796   2013

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    High fat diet (HFD) is prevalent in many modern societies and HFD-induced metabolic condition is a growing concern worldwide. It has been previously reported that HFD clearly worsens cognitive function in amyloid precursor protein (APP) transgenic mice. On the other hand, we have demonstrated that voluntary exercise in an enriched environment is an effective intervention to rescue HFD-induced β-amyloid (Aβ) deposition and memory deficit. However, it had been unclear whether consumption of HFD after exercising abolished the beneficial effect of exercise on the inhibition of Alzheimer's disease (AD) pathology. To examine this question, we exposed wild type (WT) and APP mice fed with HFD to exercise conditions at different time periods. In our previous experiment, we gave HFD to mice for 20 weeks and subjected them to exercise during weeks 10-20. In the present study, mice were subjected to exercise conditions during weeks 0-10 or weeks 5-15 while being on HFD. Interestingly, we found that the effect of exercise during weeks 0-10 or weeks 5-15 on memory function was not abolished in WT mice even if they kept having HFD after finishing exercise. However, in APP transgenic mice, HFD clearly disrupted the effect of exercise during weeks 0-10 or weeks 5-15 on memory function. Importantly, we observed that the level of Aβ oligomer was significantly elevated in the APP mice that exercised during weeks 0-10: this might have been caused by the up-regulation of Aβ production. These results provide solid evidence that continuation of exercise is necessary to rescue HFD-induced aggravation of cognitive decline in the pathological setting of AD.

    DOI： 10.1371/journal.pone.0072796

    PubMed

  • Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice. Reviewed

    Maesako, Masato and Uemura, Kengo and Kubota, Masakazu and Kuzuya, Akira and Sasaki, Kazuki and Hayashida, Naoko and Asada-Utsugi, Megumi and Watanabe, Kiwamu and Uemura, Maiko and Kihara, Takeshi and Takahashi, Ryosuke and Shimohama, Shun and Kinoshita, Ayae

    The Journal of biological chemistry   287 ( 27 )   23024 - 23024   2012（ ISSN:0021-9258 ）

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    Publishing type：Research paper (scientific journal)   Kind of work：Joint Work   International / domestic magazine：International journal  

    Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD). Thus, interventions targeting HFD-induced metabolic dysfunctions may be effective in preventing the development of AD. We previously demonstrated that amyloid precursor protein (APP)-overexpressing transgenic mice fed HFD showed worsening of cognitive function when compared with control APP mice on normal diet. Moreover, we reported that voluntary exercise ameliorates HFD-induced memory impairment and β-amyloid (Aβ) deposition. In the present study, we conducted diet control to ameliorate the metabolic abnormality caused by HFD on APP transgenic mice and compared the effect of diet control on cognitive function with that of voluntary exercise as well as that of combined (diet control plus exercise) treatment. Surprisingly, we found that exercise was more effective than diet control, although both exercise and diet control ameliorated HFD-induced memory deficit and Aβ deposition. The production of Aβ was not different between the exercise- and the diet control-treated mice. On the other hand, exercise specifically strengthened the activity of neprilysin, the Aβ-degrading enzyme, the level of which was significantly correlated with that of deposited Aβ in our mice. Notably, the effect of the combination treatment (exercise and diet control) on memory and amyloid pathology was not significantly different from that of exercise alone. These studies provide solid evidence that exercise is a useful intervention to rescue HFD-induced aggravation of cognitive decline in transgenic model mice of AD.

    DOI： 10.1074/jbc.m112.367011

    PubMed

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MISC

  • レヴィ小体病及びアルツハイマー病に合併する辺縁系優位型加齢性TDP-43脳症(LATE)の臨床病理学的特徴

    上村 麻衣子

    日本女性科学者の会学術誌   24   17 - 23   2024（ ISSN:1349-4449 ）

  • Correction to: Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve (Mol Neurodegener DOI: 10.1186/s13024-018-0257-5)

    Uemura N.

    Molecular Neurodegeneration   14 ( 1 )   31   2019.07

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  • αシヌクレイントランスジェニックマウスへのフィブリル脳内接種によるパーキンソン病動物モデル作製

    11th   98 - 98   2017.10

  • BMP-4 expression by pericytes after ischemia aggravates white matter damage

    UEMURA Maiko,IHARA Masafumi,NAKAGOMI Takayuki,MAKI Takakuni,KAJI Seiji,UEMURA Kengo,NAGATSUKA Kazuyuki,MATSUYAMA Tomohiro,KALARIA Raj,KINOSHITA Ayae,TAKAHASHI Ryosuke

    57th   471   2016.01

  • ApoE Isoforms Differentially Affect Amyloid beta-Induced Synaptic Toxocity

    UEMURA MAIKO,NODA YASUHA,TASHIRO YOSHITAKA,ASADA MEGUMI,UEMURA KENGO,KINOSHITA AYAE,TAKAHASHI RYOSUKE

    56th   466   2015.01

  • アストロサイトから放出されるIGFBP‐3とアルツハイマー病の病態生理の関連

    WATANABE KIWAMU,ASADA MEGUMI,MAESAKO MASATO,UEMURA MAIKO,KUBOTA MASAKAZU,KIHARA TAKESHI,AKIYAMA HARUHIKO,SHIMOHAMA SHUN,UEMURA KENGO,TAKAHASHI RYOSUKE,KINOSHITA AYAE

    55th   617   2014.01

  • BMP-4 expression by immature pericytes correlates with white matter damage.

    UEMURA MAIKO,IHARA MASAFUMI,NAKAGOMI TAKAYUKI,MATSUYAMA TOMOHIRO,KINOSHITA AYAE,TAKAHASHI RYOSUKE

    55th   461   2014.01

  • BMP-4 expression by immature pericytes correlates with white matter damage.

    UEMURA MAIKO,IHARA MASAFUMI,NAKAGOMI TAKAYUKI,MATSUYAMA TOMOHIRO,KINOSHITA AYAE,TAKAHASHI RYOSUKE

    55th   704   2014.01

  • 運動は食事制限よりも高脂肪食によるアルツハイマー病症状の悪化を改善する

    MAESAKO MASATO,SASAKI KAZUKI,KUBOTA MASAKAZU,KUZUYA AKIRA,HAYASHIDA NAOKO,ASADA MEGUMI,WATANABE KIWAMU,UEMURA MAIKO,KIHARA TAKESHI,TAKAHASHI RYOSUKE,SHIMOHAMA SHUN,UEMURA KENGO,KINOSHITA AYAE

    35th   1P-0564 (WEB ONLY)   2012.01

  • アルツハイマー病モデルマウスにおける糖尿病関連シグナル伝達の変化について

    UEMURA MAIKO,MAESAKO MASATO,WATANABE KIWAMU,ASADA MEGUMI,KUBOTA MASAKAZU,UEMURA KENGO,TAKAHASHI RYOSUKE,KINOSHITA AYAE

    53rd   423   2012.01

  • 銅はAPPダイマー化を促進し,アミロイド産生に影響する

    UEMURA KENGO,ASADA MEGUMI,NODA YASUHA,WATANABE KIWAMU,UEMURA MAIKO,MAESAKO MASATO,KUBOTA MASAKAZU,TAKAHASHI RYOSUKE,KINOSHITA AYAE

    53rd   258   2012.01

  • アルツハイマー病と皮質下血管性認知症において炎症性マーカーの発現局在性は異なる

    UEMURA MAIKO,YAMADA MASATO,OKAMOTO YOKO,IHARA TADAFUMI,ITO HIDEFUMI,TOMIMOTO HIDEKAZU,TAKAHASHI RYOSUKE

    25 ( 3 )   365   2011.10

  • A 25-Year-Old Woman with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

    OZAKI MOE,MASUDA HIROAKI,TODA MAIKO,KITAGUCHI HIROSHI,OI TAKEKAZU

    73   161 - 166   2011.03

  • 全身性の疼痛が先行し,両眼のかすみが発現したIgG4関連肥厚性硬膜炎の一症例

    MASUDA HIROAKI,OSAKI YUSUKE,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 10 )   752 - 752   2010.10

  • 頚髄のTIAを繰り返した後に頚髄梗塞を発症した1症例

    GOTO KAZUYA,OSAKI HIROAKI,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 9 )   671 - 671   2010.09

  • 筋皮弁術後に発現した脊髄性ミオクローヌスの1症例

    SATO AKIRA,OSAKI HIROAKI,GOTO KAZUYA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 9 )   676 - 676   2010.09

  • 特発性分節型無汗症の1症例

    GOTO KAZUYA,OSAKI YUSUKE,NAMBA AKIKO,MASUDA HIROAKI,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,UEMURA MAIKO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 7 )   510 - 510   2010.07

  • 一過性全健忘を示した脳梁膝部及び脳弓前部梗塞の一症例

    NAMBA AKIKO,OSAKI YUSUKE,GOTO KAZUYA,SATO AKIRA,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,SHOZAKI TAISAKU,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 7 )   521 - 521   2010.07

  • チョウセンアサガオによる食中毒の1症例

    GOTO KAZUYA,OSAKI YUSUKE,NAMBA AKIKO,MASUDA HIROAKI,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,UEMURA MAIKO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 7 )   512 - 512   2010.07

  • 抗N‐methyl‐D‐aspartate受容体(NMDA‐R)抗体陽性脳炎における呼吸異常について

    TODA MAIKO,OSAKI YUSUKE,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,DALMAU JOSEPH

    50 ( 7 )   507 - 507   2010.07

  • 多発性神経線維腫を合併した固定性内斜視の一例

    TANNO YUHEI,SATO SHIN'YA,GOTO KAZUYA,OSAKI YUSUKE,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,TODA MAIKO,UEMURA NORIHITO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 7 )   501 - 501   2010.07

  • 眼咽頭型筋ジストロフィーの一症例

    UEMURA NORIHITO,OSAKI HIROYOSHI,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,MINAMI NARIHIRO,NISHINO ICHIZO

    50 ( 5 )   348 - 348   2010.05

  • バンコマイシン(VCM)の髄注療法が奏効したMRSA髄膜脳炎の1症例

    GOTO KAZUYA,NAMBA AKIKO,OSAKI HIROAKI,MASUDA HIROAKI,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 5 )   358 - 358   2010.05

  • 側頭葉てんかんを初発徴候としたCADASILの一例

    OSAKI HIROAKI,GOTO KAZUYA,NAMBA AKIKO,SATO AKIRA,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,TODA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,SAIGO KAZUHIRO,MIZUNO TOSHIKI

    50 ( 5 )   358 - 358   2010.05

  • 頸髄梗塞を認めたシェーグレン症候群の一例

    TANNO YUHEI,GOTO KAZUYA,OSAKI HIROAKI,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,TODA MAIKO,UEMURA NORIHITO,MASAZAKI TAISAKU,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 5 )   346 - 346   2010.05

  • 橋本脳症の治療中に後天性血友病を発症した1症例

    MASAZAKI TAISAKU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,ONISHI TATSUHITO,UEDA YASUNORI

    50 ( 4 )   272 - 272   2010.04

  • Gitelman's Syndrome Presenting Hypokalemic Myopathy

    TODA MAIKO,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,KATAYAMA NAOKO,SHOZAKI TAISAKU,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI TAKEKAZU,NOZU KANDAI

    72   59 - 63   2010.03

  • CNS‐SLEによる両側基底核梗塞の一例

    UEMURA NORIHITO,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MIYAGI AI,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 3 )   180 - 180   2010.03

  • 難治性てんかん重積を呈した非ヘルペス性辺縁系脳炎の1例

    MIYAGI AI,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 3 )   184 - 184   2010.03

  • 磁気刺激で幻視の抑制を認めた1症例

    TODA MAIKO,OSAKI HIROAKI,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 3 )   194 - 194   2010.03

  • Gradenigo症候群を示したWegener肉芽腫症の1症例

    SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,MORI HITOSHI,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,NAKAZAWA TAKASHI,YOKOTA TOSHIHIKO

    50 ( 3 )   198   2010.03

  • インフルエンザワクチン接種後に急性散在性脳脊髄炎(ADEM)をきたした1症例

    SATO SHIN'YA,MIZUNO KEI,TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,MORI HITOSHI,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50 ( 3 )   198   2010.03

  • 明確な外傷の受傷歴の無い破傷風症例の臨床像について

    OSAKI HIROAKI,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    51st   387   2010.01

  • 当院での卵円孔開存を伴った脳梗塞の臨床的検討

    KITAGUCHI HIROFUMI,NAMBA AKIKO,SATO AKIRA,OSAKI YUSUKE,MASUDA HIROAKI,GOTO KAZUYA,SATO SHIN'YA,TANNO YUHEI,UEMURA MAIKO,UEMURA NORIHITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    51st   348   2010.01

  • 道順障害の責任病巣はどこか?

    OI NAGAKAZU,GOTO KAZUYA,OSAKI HIROAKI,MASUDA HIROAKI,NAMBA AKIKO,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,UEMURA MAIKO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE

    51st   273   2010.01

  • 一過性全健忘における記憶障害時間と脳MRI所見の関係

    GOTO KAZUYA,OSAKI HIROAKI,MASUDA HIROAKI,NAMBA AKIKO,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,UEMURA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    51st   249   2010.01

  • てんかん重積状態(SE)に対する治療法の検討

    SATO SHIN'YA,OSAKI HIROAKI,GOTO KAZUYA,SATO AKIRA,MASUDA HIROAKI,NAMBA AKIKO,TANNO YUHEI,UEMURA MAIKO,UEMURA NORIHITO,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    51st   391   2010.01

  • 一側性中脳病変は両眼の垂直性眼球運動障害をきたすか?

    OI TAKEKAZU,SATO SHIN'YA,OSAKI YUSUKE,GOTO KAZUYA,SATO KEI,NAMBA AKIKO,MASUDA HIROAKI,TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,MORI HITOSHI,KITAGUCHI TAKEKAZU,SHINDO KATSURO,YAMAO FUSAE

    26 ( 増補1 )   56 - 56   2009.11

  • MRIで脊髄梗塞を認めたintravascular large B‐cell lymphomatosis(IVL)の1例

    MASUDA HIROAKI,OSAKI YUSUKE,GOTO KAZUYA,NAMBA AKIKO,SATO AKIRA,SATO SHIN'YA,UEMURA NORIHITO,TODA MAIKO,TANNO YUHEI,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 10 )   686 - 686   2009.10

  • 痙攣で発症し陰性myoclonusを示Lた傍腫瘍性脳症疑いの一例

    UEMURA NORIHITO,OSAKI HIROAKI,GOTO KAZUYA,SATO AKIRA,NAMBA AKIKO,MASUDA HIROAKI,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,MORI HITOSHI,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,TAKAHASHI YUKITOSHI

    49 ( 10 )   683 - 683   2009.10

  • 上部頸髄と左延髄の梗塞を示した一症例

    SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,KATAYAMA NAOKO,HATTORI YORITO,MASAZAKI TAISAKU,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,KAWAMURA YOICHIRO,YOSHIDA KAZUMICHI,YAMAGATA SEN

    49 ( 7 )   441 - 441   2009.07

  • 発作性運動誘発性舞踏アテトーゼの一例

    UEMURA NORIHITO,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 7 )   442 - 442   2009.07

  • 四肢の筋力低下をきたしたGitelman症候群の一症例

    TODA MAIKO,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 5 )   294   2009.05

  • 横断性脊髄障害を来たした出血性脊髄梗塞の1例

    MASAZAKI TAISAKU,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 5 )   305 - 305   2009.05

  • Mirror movementを認めた大脳皮質基底核変性症の一例

    UEMURA NORIHITO,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 5 )   306 - 306   2009.05

  • 大脳皮質基底核変性症(CBD)の手の運動の解析

    OI NAGAKAZU,UEMURA NORIHITO,TODA MAIKO,KITAGUCHI HIROSHI,SHINDO KATSURO

    50th   224   2009.04

  • 遺伝性海綿状血管腫の一家系

    OTA KENTARO,SATO SHIN'YA,UEMURA NORIHITO,TODA MAIKO,TANNO YUHEI,KATAYAMA NAOKO,MIYAGI AI,HATTORI YORITO,MASAZAKI TAISAKU,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49 ( 4 )   204 - 204   2009.04

  • ビタミンB6の投与により血中CKが正常化したMcArdle病の1症例

    SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,KATAYAMA NAOKO,HATTORI YORITO,MASAZAKI TAISAKU,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,SHIMADA NORIAKI,FUKUSHIMA MASAKI,NISHINO ICHIZO,FUKUDA TOKIKO,SUGIE HIDEO

    49 ( 4 )   208 - 208   2009.04

  • 睡眠時無呼吸・低呼吸症候群患者の頭痛

    YAMAO FUSAE,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,OI NAGAKAZU

    50th ( 12 )   131 - 978   2009.04

  • 特発性脊髄梗塞の自験10例の臨床的検討

    TANNO YUHEI,SATO SHIN'YA,TODA MAIKO,UEMURA NORIHITO,KATAYAMA NAOKO,HATTORI YORITO,MASAZAKI TAISAKU,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50th   206   2009.04

  • 成人発症Reye症候群に対する血漿交換療法の有効性の検討

    HATTORI YORITO,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    50th   243   2009.04

  • 難聴を伴うBickerstaff脳炎に認めた眼球運動障害について

    OI NAGATOSHI,UEMURA NORIHITO,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,SHOZAKI YASUSAKU,HATTORI YORIKUNI,MORI HITOSHI,OTA KENTARO,KITAKUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,KUSUNOKI SUSUMU

    25 ( 増補1 )   95 - 95   2008.10

  • 異食症を示したPick病の1症例

    KATAYAMA NAOKO,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 10 )   775 - 775   2008.10

  • 脳波で周期性同期性放電(PSD)を示した間歇型一酸化炭素中毒の1症例

    TODA MAIKO,SATO SHIN'YA,UEMURA NORIHITO,TANNO YUHEI,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,OTA KENTARO,KITAGUCHI HIROSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 10 )   773 - 773   2008.10

  • 眼球運動障害と難聴を示したBickerstaff脳炎の一例

    UEMURA NORIHITO,SATO SHIN'YA,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MIYAGI AI,HATTORI YORITO,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,KUSUNOKI SUSUMU

    48 ( 9 )   698 - 698   2008.09

  • GQ1b抗体陽性を示したpharyngeal‐cervical‐brachial(PCB)variant of GBSの一症例

    TANNO YUHEI,TODA MAIKO,UEMURA NORIHITO,KATAYAMA NAOKO,HATTORI YORITO,MIYAGI AI,MASAZAKI TAISAKU,MORI HITOSHI,OTA KENTARO,KITAGUCHI HIROFUMI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,KUSUNOKI SUSUMU

    48 ( 9 )   698 - 698   2008.09

  • 成人発症のReye症候群と考えた一剖検例

    HATTORI YORITO,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,OI NAGAKAZU,UCHINO KAORI,NOTOHARA KENJI,YAMASHITA SHIGEKI

    48 ( 8 )   612 - 612   2008.08

  • 頭痛後に片麻痺と一側性の感覚障害をきたした1症例

    MIYAGI AI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,KATAYAMA NAOKO,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 8 )   607 - 607   2008.08

  • 起立性ミオクローヌスによる歩行障害を示した1例

    KATAYAMA NAOKO,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,HATTORI YORITO,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 7 )   528 - 528   2008.07

  • 左手のavoiding reactionと右手の優位使用を示した大脳皮質基底核変性症(CBD)の一症例

    TODA MAIKO,UEMURA NORIHITO,TANNO YUHEI,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 6 )   450   2008.06

  • 3回の再燃を示した左腰椎神経根炎の一例

    UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MIYAGI AI,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 4 )   298 - 298   2008.04

  • 発作性に歩行障害が増強した1症例

    MIYAGI AI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,ISHIKAWA KIN'YA,MIZUSAWA HIDEHIRO

    48 ( 4 )   298 - 298   2008.04

  • A Case of Guillain Barre Syndrome with Anti-Ganglioside Complex Antibodies Effectively Treated with Plasmapheresis Inspite of Intravenous Immunoglobulin

    SHOZAKI TAISAKU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MIYASHIRO AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI TAKEKAZU,KUSUNOKI SUSUMU

    70   85 - 89   2008.03

  • possible ALSに両側中小脳脚病変を認めた1症例

    UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,MIYAGI AI,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,KODAMA TAKAO

    48 ( 3 )   221 - 221   2008.03

  • 右大腿四頭筋の限局性筋萎縮と筋力低下を示したneurofibromatosis type1(NF1)の1症例

    MIYAGI AI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 1 )   79 - 79   2008.01

  • 難治性てんかん重積に対するイソフルレンの有用性の検討

    OI NAGAKAZU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,HATTORI YORITO,KATAYAMA NAOKO,MIYAGI AI,MASAZAKI TAISAKU,SHINDO KATSURO,YAMAO FUSAE,YAMASHITA SHIGEKI

    49th   284   2008.01

  • 神経変性疾患の起立性低血圧に対するピリドスチグミンの効果

    HATTORI YORITO,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MASAZAKI TAISAKU,KATAYAMA NAOKO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49th   249   2008.01

  • 重症破傷風患者へのイソフルランの有用性の検討

    MASAZAKI TAISAKU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49th   293   2008.01

  • マーカー酵素は正常であったがムコ多糖症3型が疑われた一例

    MORI HITOSHI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MIYAGI AI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    49th   186   2008.01

  • 一過性の眩暈を初発症状とした脳底動脈閉塞症の検討

    MIYAGI AI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,YOSHIDA KAZUMICHI,YAMAGATA MAKOTO

    49th   267   2008.01

  • 難治性の吃逆と嘔吐を呈した一症例

    MASAZAKI TAISAKU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 1 )   66 - 66   2008.01

  • 複合ガングリオシド抗体陽性を示し,血漿交換療怯が有効であったGBSの一症例

    MASAZAKI TAISAKU,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MIYAGI AI,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU,KUSUNOKI SUSUMU

    48 ( 1 )   70 - 70   2008.01

  • 一側の舌下神経麻痺を示した2症例

    KATAYAMA NAOKO,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,MIYAGI AI,MASAZAKI TAISAKU,HATTORI YORITO,MORI HITOSHI,MORI ATSUKO,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    48 ( 1 )   80 - 80   2008.01

  • 一側性緩徐衝動性眼球運動を認めた症例について

    OI NAGATOSHI,MIYAGI AI,UEMURA NORIHITO,TANNO YUHEI,TODA MAIKO,KATAYAMA NAOKO,HATTORI YORITO,MASAZAKI YASUSAKU,MORI HITOSHI,SHINDO KATSURO,YAMAO FUSAE

    24   46   2007.11

  • 脳梁膨大部病変を認めた脳炎の2症例

    MORI HITOSHI,MIYAGI AI,TODA MAIKO,UEMURA NORIHITO,TANNO YUHEI,KATAYAMA NAOKO,MASAZAKI TAISAKU,HATTORI YORITO,SHINDO KATSURO,YAMAO FUSAE,OI NAGAKAZU

    47 ( 9 )   620 - 620   2007.09

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Presentations

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Grant-in-Aid for Scientific Research

  • The development of biomarkers for prodromal Parkinson disease using a novel rat model.

    Grant-in-Aid for Early-Career Scientists  2018.05

  • Drug screening for suppression of alpha-synulcein expression

    Grant-in-Aid for Young Scientists(B)  2016.05

Incentive donations / subsidies

  • Exploring the Mechanism of Tau Clearance in Cerebrovascular Pericytes

    Japan Brain Foundation  Research Funding  2024.04

  • Elucidation of the Pathomechanism of Dementia Targeting Cerebrovascular and Cellular Senescence

    Health Science Center  Research Funding  2024.02

  • 微小脳血管障害及び慢性脳低灌流が及ぼす、タウ凝集体形成伝播メカニズムの解明

    公益財団法人武田科学振興財団  医学系研究助成   2023.10

  • タウ凝集体のクリアランス及び脳内伝播に及ぼす、脳血管障害の影響

    公益財団法人京都大学教育研究振興財団  研究活動推進助成   2023.04

Other subsidies, etc.

  • 認知症におけるARTAGの病態メカニズムの解明

    公益財団法人上原記念生命科学財団  外留学助成リサーチフェローシップ   2020.07

  • 疾患特異的なフィブリルコアに着目したタウ抗体の開発―診断・治療への新規アプローチ

    日本学術振興会  海外特別研究員ーRRA  2018.07

Media Coverage

  • 京大、パーキンソン病前駆期の動物モデルを作製 Internet

    日経BP  日経バイオテク  2019.12

  • パーキンソン病前駆期のモデル動物を作製、新規治療法開発に期待－京大ほか Internet

    医療NEWS  QLifePro  2019.12

  • 京大、パーキンソン病前駆期の動物モデルを作製　筑波大・順天堂大・京都府立医科大と共同で Newspaper, magazine

    日本経済新聞  日本経済新聞  2019.12

  • パーキンソン病前駆期の動物モデルを作製～発症予防や進行抑制に向けた治療法開発の貢献に期待～ Internet

    Tii生命科学  Tii生命科学  2019.12

  • パーキンソン病前駆期の動物モデルを作製 - AMED Internet

    国立研究開発法人日本医療研究開発機構  2019.12

  • パーキンソン病前駆期の動物モデルを作製―発症予防や進行抑制に向けた治療法開発の貢献に期待―」 Promotional material

    京都大学産学連携  2019.12

  • 孤発性小血管性認知症の発症機序の一部を解明 －認知症の治療に向けての新たなアプローチ、マウスで効果を確認－ Promotional material

    京都大学産学連携  2017.06

  • 血管性認知症　脳障害を改善 Newspaper, magazine

    朝日新聞  2017.06

  • 血管性認知症の一端解明 Newspaper, magazine

    京都新聞  2017.06

  • 小血管性認知症　脳内に特定タンパク質 Newspaper, magazine

    産経新聞  2017.06

  • 「血管性認知症」特定たんぱく増 Newspaper, magazine

    毎日新聞  2017.06

  • 脳に特定タンパク質多発＝小血管性認知症の患者 Newspaper, magazine

    時事通信  2017.06

  • 血管性認知症の関連物質発見、京大チーム、脳内で増加 Newspaper, magazine

    宮崎日日新聞  2017.06

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