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  1. Article ; Online: Neuroinflammation in neurodegenerative disease.

    Yamanaka, Koji

    Nagoya journal of medical science

    2023  Volume 85, Issue 1, Page(s) 30–32

    Language English
    Publishing date 2023-04-19
    Publishing country Japan
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 193148-9
    ISSN 2186-3326 ; 0027-7622
    ISSN (online) 2186-3326
    ISSN 0027-7622
    DOI 10.18999/nagjms.85.1.30
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.181: Show issues Location:
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  2. Article ; Online: An open chat with… Koji Yamanaka.

    Tsagakis, Ioannis / Yamanaka, Koji

    FEBS open bio

    2024  Volume 14, Issue 2, Page(s) 162–164

    Abstract: Koji Yamanaka is a Professor at the Research Institute of Environmental Medicine at Nagoya University of Japan. His research interests lie in understanding the mechanism of onset and progression of motor neuron disease as well as the role of glial cells ... ...

    Abstract Koji Yamanaka is a Professor at the Research Institute of Environmental Medicine at Nagoya University of Japan. His research interests lie in understanding the mechanism of onset and progression of motor neuron disease as well as the role of glial cells in Alzheimer's disease neuroinflammation. Koji has been serving on the FEBS Open Bio Editorial Board since 2013. In this interview, he explains the implications of recent findings in neurobiology for amyotrophic lateral sclerosis, provides updates on the research environment in Japan and discusses how editors might use their position to positively influence academic culture.
    MeSH term(s) Humans ; Male ; Amyotrophic Lateral Sclerosis/genetics
    Language English
    Publishing date 2024-01-12
    Publishing country England
    Document type Interview
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13763
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Novel insights into brain lipid metabolism in Alzheimer's disease: Oligodendrocytes and white matter abnormalities.

    Kawade, Noe / Yamanaka, Koji

    FEBS open bio

    2023  Volume 14, Issue 2, Page(s) 194–216

    Abstract: Alzheimer's disease (AD) is the most common cause of dementia. A genome-wide association study has shown that several AD risk genes are involved in lipid metabolism. Additionally, epidemiological studies have indicated that the levels of several lipid ... ...

    Abstract Alzheimer's disease (AD) is the most common cause of dementia. A genome-wide association study has shown that several AD risk genes are involved in lipid metabolism. Additionally, epidemiological studies have indicated that the levels of several lipid species are altered in the AD brain. Therefore, lipid metabolism is likely changed in the AD brain, and these alterations might be associated with an exacerbation of AD pathology. Oligodendrocytes are glial cells that produce the myelin sheath, which is a lipid-rich insulator. Dysfunctions of the myelin sheath have been linked to white matter abnormalities observed in the AD brain. Here, we review the lipid composition and metabolism in the brain and myelin and the association between lipidic alterations and AD pathology. We also present the abnormalities in oligodendrocyte lineage cells and white matter observed in AD. Additionally, we discuss metabolic disorders, including obesity, as AD risk factors and the effects of obesity and dietary intake of lipids on the brain.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; White Matter/metabolism ; White Matter/pathology ; Lipid Metabolism ; Genome-Wide Association Study ; Oligodendroglia ; Brain/metabolism ; Lipids ; Obesity/metabolism
    Chemical Substances Lipids
    Language English
    Publishing date 2023-06-26
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13661
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: [Roles of Microglia in Neurodegenerative Diseases].

    Yamanaka, Koji

    Brain and nerve = Shinkei kenkyu no shinpo

    2017  Volume 69, Issue 9, Page(s) 999–1005

    Abstract: Recent advances in glial research have elucidated the roles of microglia under various contexts in health and disease. Microglial activation used to be considered only as a consequence of neuronal damage. However, a series of studies using mouse models ... ...

    Abstract Recent advances in glial research have elucidated the roles of microglia under various contexts in health and disease. Microglial activation used to be considered only as a consequence of neuronal damage. However, a series of studies using mouse models of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease selectively affecting motor neurons, indicated that microglia actively influence the disease course. In this review, we summarize the growing evidence that microglia play a critical role in the survival and demise of motor neurons in ALS. These observations suggest microglia as a promising therapeutic target of neurodegenerative diseases.
    Language Japanese
    Publishing date 2017-09
    Publishing country Japan
    Document type English Abstract ; Journal Article
    ZDB-ID 390389-8
    ISSN 1344-8129 ; 1881-6096 ; 0006-8969
    ISSN (online) 1344-8129
    ISSN 1881-6096 ; 0006-8969
    DOI 10.11477/mf.1416200859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 398: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Neuroinflammation in Alzheimer's disease: microglial signature and their relevance to disease.

    Sobue, Akira / Komine, Okiru / Yamanaka, Koji

    Inflammation and regeneration

    2023  Volume 43, Issue 1, Page(s) 26

    Abstract: Alzheimer's disease (AD) is the most common form of dementia, pathologically characterized by senile plaques and neurofibrillary tangles (NFTs), resulting in neurodegeneration. Neuroinflammation, defined as the activation of glial cells such as microglia ...

    Abstract Alzheimer's disease (AD) is the most common form of dementia, pathologically characterized by senile plaques and neurofibrillary tangles (NFTs), resulting in neurodegeneration. Neuroinflammation, defined as the activation of glial cells such as microglia and astrocytes, is observed surrounding senile plaques and affected neurons in AD. Recently conducted genome-wide association studies (GWAS) indicate that a large section of identified AD risk genes are involved in immune responses and are enriched in microglia. Microglia are innate immune cells in the central nervous system (CNS), which are involved in immune surveillance and maintenance of homeostasis in the CNS. Recently, a novel subpopulation of activated microglia named as disease-associated microglia (DAM), also known as activated response microglia (ARM) or microglial neurodegenerative phenotype (MGnD), was identified in AD model mice. These microglia closely associate with β-amyloid (Aβ) plaques and exhibit characteristic gene expression profiles accompanied with reduced expressions of homeostatic microglial genes. However, it remains unclear whether decreased homeostatic microglia functions or increased DAM/ARM/MGnD functions correlate with the degree of neuronal loss in AD. To translate the results of rodent studies to human AD, precuneus, the brain region vulnerable to β-amyloid accumulation in preclinical AD, is of high interest, as it can provide novel insights into the mechanisms of microglia response to Aβ in early AD. In this study, we performed comparative analyses of gene expression profiles of microglia among three representative neurodegenerative mouse models and the human precunei with early AD pathology. We proceeded to evaluate the identified genes as potential therapeutic targets for AD. We believe that our findings will provide important resources to better understand the role of glial dysfunction in AD.
    Language English
    Publishing date 2023-05-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2051471-2
    ISSN 1880-9693 ; 0389-4290
    ISSN 1880-9693 ; 0389-4290
    DOI 10.1186/s41232-023-00277-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 2929: Show issues Location:
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  6. Article: Comprehensive expression analysis with cell-type-specific transcriptome in ALS-linked mutant SOD1 mice: Revisiting the active role of glial cells in disease.

    Yamashita, Hirofumi / Komine, Okiru / Fujimori-Tonou, Noriko / Yamanaka, Koji

    Frontiers in cellular neuroscience

    2023  Volume 16, Page(s) 1045647

    Abstract: Non-cell autonomous mechanisms are involved in the pathogenesis of amyotrophic lateral sclerosis (ALS), an adult neurodegenerative disease characterized by selective motor neuron loss. While the emerging role of glial cells in ALS has been noted, the ... ...

    Abstract Non-cell autonomous mechanisms are involved in the pathogenesis of amyotrophic lateral sclerosis (ALS), an adult neurodegenerative disease characterized by selective motor neuron loss. While the emerging role of glial cells in ALS has been noted, the detailed cell-type-specific role of glial cells has not been clarified. Here, we examined mRNA expression changes using microarrays of the spinal cords of three distinct lines of mutant superoxide dismutase (SOD) 1 transgenic mice, an established ALS model. Our analysis used a transcriptome database of component cell types in the central nervous system (CNS), as well as SOD1
    Language English
    Publishing date 2023-01-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2022.1045647
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Corrigendum: Comprehensive expression analysis with cell-type-specific transcriptome in ALS-linked mutant SOD1 mice: Revisiting the active role of glial cells in disease.

    Yamashita, Hirofumi / Komine, Okiru / Fujimori-Tonou, Noriko / Yamanaka, Koji

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1160444

    Abstract: This corrects the article DOI: 10.3389/fncel.2022.1045647.]. ...

    Abstract [This corrects the article DOI: 10.3389/fncel.2022.1045647.].
    Language English
    Publishing date 2023-03-03
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1160444
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: [Biochemical abnormality of mutant TDP-43 protein].

    Yamanaka, Koji

    Rinsho shinkeigaku = Clinical neurology

    2014  Volume 54, Issue 12, Page(s) 1148–1150

    Abstract: Dominant mutations in the TDP-43 gene are causative for familial ALS, however, the relationship between mutant protein biochemical phenotypes and disease course and their significance to disease pathomechanism are unclarified. We found that longer half- ... ...

    Abstract Dominant mutations in the TDP-43 gene are causative for familial ALS, however, the relationship between mutant protein biochemical phenotypes and disease course and their significance to disease pathomechanism are unclarified. We found that longer half-lives of mutant proteins correlated with accelerated disease onset. Increased stability of TDP-43 protein was also observed in ALS/FTLD linked mutations in RNA recognition motif of TDP-43. Based on our findings, we established a cell model in which chronic stabilization of wild-type TDP-43 protein provoked cytotoxicity and recapitulated pathogenic protein cleavage and insolubility to the detergent sarkosyl, TDP-43 properties that have been observed in the lesions of sporadic ALS. Moreover, these cells expressing stabilized TDP-43 showed proteasomal impairment and dysregulation of their own mRNA levels. These results suggest that chronically increased stability of mutant or wild-type TDP-43 proteins results in a gain of toxicity through abnormal proteostasis.
    MeSH term(s) Amyotrophic Lateral Sclerosis/genetics ; Animals ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/toxicity ; Humans ; Mice ; Mutation ; Protein Stability ; Proteostasis Deficiencies/genetics ; RNA, Messenger
    Chemical Substances DNA-Binding Proteins ; RNA, Messenger ; TARDBP protein, human
    Language Japanese
    Publishing date 2014-12-14
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 604200-4
    ISSN 1882-0654 ; 0009-918X
    ISSN (online) 1882-0654
    ISSN 0009-918X
    DOI 10.5692/clinicalneurol.54.1148
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 1455: Show issues Location:
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    Zs.MO 223: Show issues

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  9. Article ; Online: Dimethyl fumarate improves cognitive impairment and neuroinflammation in mice with Alzheimer's disease.

    Wang, Ting / Sobue, Akira / Watanabe, Seiji / Komine, Okiru / Saido, Takaomi C / Saito, Takashi / Yamanaka, Koji

    Journal of neuroinflammation

    2024  Volume 21, Issue 1, Page(s) 55

    Abstract: Background: Neuroinflammation substantially contributes to the pathology of Alzheimer's disease (AD), the most common form of dementia. Studies have reported that nuclear factor erythroid 2-related factor 2 (Nrf2) attenuates neuroinflammation in the ... ...

    Abstract Background: Neuroinflammation substantially contributes to the pathology of Alzheimer's disease (AD), the most common form of dementia. Studies have reported that nuclear factor erythroid 2-related factor 2 (Nrf2) attenuates neuroinflammation in the mouse models of neurodegenerative diseases, however, the detailed mechanism remains unclear.
    Methods: The effects of dimethyl fumarate (DMF), a clinically used drug to activate the Nrf2 pathway, on neuroinflammation were analyzed in primary astrocytes and App
    Results: DMF treatment activated some Nrf2 target genes and inhibited the expression of proinflammatory markers in primary astrocytes. Moreover, chronic oral administration of DMF attenuated neuroinflammation, particularly in astrocytes, and reversed cognitive dysfunction presumably by activating the Nrf2-dependent pathway in App-KI mice. Furthermore, DMF administration inhibited the expression of STAT3/C3 and C3 receptor in astrocytes and microglia isolated from App-KI mice, respectively, suggesting that the astrocyte-microglia crosstalk is involved in neuroinflammation in mice with AD.
    Conclusion: The activation of astrocytic Nrf2 signaling confers neuroprotection in mice with AD by controlling neuroinflammation, particularly by regulating astrocytic C3-STAT3 signaling. Furthermore, our study has implications for the repositioning of DMF as a drug for AD treatment.
    MeSH term(s) Mice ; Animals ; Alzheimer Disease/complications ; Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Dimethyl Fumarate/pharmacology ; Dimethyl Fumarate/therapeutic use ; Mice, Transgenic ; Neuroinflammatory Diseases ; NF-E2-Related Factor 2/metabolism ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Disease Models, Animal
    Chemical Substances Dimethyl Fumarate (FO2303MNI2) ; NF-E2-Related Factor 2
    Language English
    Publishing date 2024-02-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-024-03046-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Depletion of perivascular macrophages delays ALS disease progression by ameliorating blood-spinal cord barrier impairment in SOD1

    Adachi, Kazuki / Miyata, Kota / Chida, Yukino / Hirose, Mikako / Morisaki, Yuta / Yamanaka, Koji / Misawa, Hidemi

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1291673

    Abstract: Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which non-cell-autonomous processes have been proposed as its cause. Non-neuronal cells that constitute the environment around motor neurons are known to mediate the pathogenesis of ... ...

    Abstract Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which non-cell-autonomous processes have been proposed as its cause. Non-neuronal cells that constitute the environment around motor neurons are known to mediate the pathogenesis of ALS. Perivascular macrophages (PVM) are immune cells that reside between the blood vessels of the central nervous system and the brain parenchyma; PVM are components of the neurovascular unit and regulate the integrity of the blood-spinal cord barrier (BSCB). However, it is not known whether regulation of BSCB function by PVM is involved in the pathogenesis of ALS. Here, we used SOD1
    Language English
    Publishing date 2023-11-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1291673
    Database MEDical Literature Analysis and Retrieval System OnLINE

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