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  1. AU="Udeochu, Joe C"
  2. AU="Osoba, Osonde A." AU="Osoba, Osonde A."
  3. AU="Palani, Sowmiya"
  4. AU="Manfred Frick"
  5. AU="Jensen, Leonard"
  6. AU="Pakhomov, Evgeny A."
  7. AU="Subramanyam, Chithirala Bala"
  8. AU=Petrek J A
  9. AU="Thomson-Baker, B"
  10. AU=Shahidi Shahrzad
  11. AU="Taylor, Holly A"
  12. AU="Yeong Jeong Jeon"
  13. AU="Bueno-Cavanillas, Aurora"
  14. AU="Kavčič, Tina"
  15. AU="Arias-Jiménez, José Luís"
  16. AU="Tünçok, Ekin"
  17. AU="Roberto Toro"
  18. AU="Bharti Sahu"
  19. AU="Soo-Yeon Choi"
  20. AU="Nono, Sandra"
  21. AU="Diepens, Robin J W"
  22. AU="Baselga-Garriga, Clara"

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  1. Artikel: Microglia communication: Parallels between aging and Alzheimer's disease.

    Udeochu, Joe C / Shea, Jeremy M / Villeda, Saul A

    Clinical & experimental neuroimmunology

    2016  Band 7, Heft 2, Seite(n) 114–125

    Abstract: Aging alters the functional integrity of the adult brain, driving cognitive impairments and susceptibility to neurodegenerative disorders in healthy individuals. In fact, aging remains the most dominant risk factor for Alzheimer's disease (AD). Recent ... ...

    Abstract Aging alters the functional integrity of the adult brain, driving cognitive impairments and susceptibility to neurodegenerative disorders in healthy individuals. In fact, aging remains the most dominant risk factor for Alzheimer's disease (AD). Recent findings have expanded our understanding of microglia function in the normal aging and AD brain, provoking an appreciation for microglia involvement in remodeling neuronal connections and maintaining brain integrity. This homeostatic function of microglia is achieved in part through the ability of microglia to interact extensively with and rapidly respond to changes in the brain microenvironment to enable adequate phenotypic transformations. Here, we discuss pro-inflammatory drivers of microglia transformation in aging and AD by focusing on the immune-modulatory functions of secreted factors, such as cytokines, complement factors and extracellular vesicles. We highlight the involvement of these secreted factors in aging and AD-associated cellular changes in microglia immune activation, surveillance function, and phagocytosis. Finally, we discuss how pro-inflammatory phenotypic changes associated with altered immune communication could both facilitate and exacerbate impairments in synaptic plasticity and cognitive function observed in the aged and AD brain.
    Sprache Englisch
    Erscheinungsdatum 2016-05-03
    Erscheinungsland United States
    Dokumenttyp Review ; Journal Article
    ISSN 1759-1961
    ISSN 1759-1961
    DOI 10.1111/cen3.12307
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: A CRISPRi/a platform in human iPSC-derived microglia uncovers regulators of disease states.

    Dräger, Nina M / Sattler, Sydney M / Huang, Cindy Tzu-Ling / Teter, Olivia M / Leng, Kun / Hashemi, Sayed Hadi / Hong, Jason / Aviles, Giovanni / Clelland, Claire D / Zhan, Lihong / Udeochu, Joe C / Kodama, Lay / Singleton, Andrew B / Nalls, Mike A / Ichida, Justin / Ward, Michael E / Faghri, Faraz / Gan, Li / Kampmann, Martin

    Nature neuroscience

    2022  Band 25, Heft 9, Seite(n) 1149–1162

    Abstract: Microglia are emerging as key drivers of neurological diseases. However, we lack a systematic understanding of the underlying mechanisms. Here, we present a screening platform to systematically elucidate functional consequences of genetic perturbations ... ...

    Abstract Microglia are emerging as key drivers of neurological diseases. However, we lack a systematic understanding of the underlying mechanisms. Here, we present a screening platform to systematically elucidate functional consequences of genetic perturbations in human induced pluripotent stem cell-derived microglia. We developed an efficient 8-day protocol for the generation of microglia-like cells based on the inducible expression of six transcription factors. We established inducible CRISPR interference and activation in this system and conducted three screens targeting the 'druggable genome'. These screens uncovered genes controlling microglia survival, activation and phagocytosis, including neurodegeneration-associated genes. A screen with single-cell RNA sequencing as the readout revealed that these microglia adopt a spectrum of states mirroring those observed in human brains and identified regulators of these states. A disease-associated state characterized by osteopontin (SPP1) expression was selectively depleted by colony-stimulating factor-1 (CSF1R) inhibition. Thus, our platform can systematically uncover regulators of microglial states, enabling their functional characterization and therapeutic targeting.
    Mesh-Begriff(e) Brain/metabolism ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Microglia/metabolism ; Phagocytosis/genetics
    Sprache Englisch
    Erscheinungsdatum 2022-08-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/s41593-022-01131-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Tau activation of microglial cGAS-IFN reduces MEF2C-mediated cognitive resilience.

    Udeochu, Joe C / Amin, Sadaf / Huang, Yige / Fan, Li / Torres, Eileen Ruth S / Carling, Gillian K / Liu, Bangyan / McGurran, Hugo / Coronas-Samano, Guillermo / Kauwe, Grant / Mousa, Gergey Alzaem / Wong, Man Ying / Ye, Pearly / Nagiri, Ravi Kumar / Lo, Iris / Holtzman, Julia / Corona, Carlo / Yarahmady, Allan / Gill, Michael T /
    Raju, Ravikiran M / Mok, Sue-Ann / Gong, Shiaoching / Luo, Wenjie / Zhao, Mingrui / Tracy, Tara E / Ratan, Rajiv R / Tsai, Li-Huei / Sinha, Subhash C / Gan, Li

    Nature neuroscience

    2023  Band 26, Heft 5, Seite(n) 737–750

    Abstract: Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. Here, we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive ... ...

    Abstract Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. Here, we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling. Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA. Genetic ablation of Cgas in mice with tauopathy diminished the microglial IFN-I response, preserved synapse integrity and plasticity and protected against cognitive impairment without affecting the pathogenic tau load. cGAS ablation increased, while activation of IFN-I decreased, the neuronal MEF2C expression network linked to cognitive resilience in AD. Pharmacological inhibition of cGAS in mice with tauopathy enhanced the neuronal MEF2C transcriptional network and restored synaptic integrity, plasticity and memory, supporting the therapeutic potential of targeting the cGAS-IFN-MEF2C axis to improve resilience against AD-related pathological insults.
    Mesh-Begriff(e) Animals ; Mice ; Cognition ; Immunity, Innate ; Interferons ; MEF2 Transcription Factors/genetics ; Microglia/metabolism ; Nucleotidyltransferases/genetics ; Nucleotidyltransferases/metabolism ; tau Proteins
    Chemische Substanzen Interferons (9008-11-1) ; MEF2 Transcription Factors ; Mef2c protein, mouse ; Nucleotidyltransferases (EC 2.7.7.-) ; tau Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-04-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/s41593-023-01315-6
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Disabled-1 dorsal horn spinal cord neurons co-express Lmx1b and function in nociceptive circuits.

    Yvone, Griselda M / Zhao-Fleming, Hannah H / Udeochu, Joe C / Chavez-Martinez, Carmine L / Wang, Austin / Hirose-Ikeda, Megumi / Phelps, Patricia E

    The European journal of neuroscience

    2017  Band 45, Heft 5, Seite(n) 733–747

    Abstract: The Reelin-signaling pathway is essential for correct neuronal positioning within the central nervous system. Mutant mice with a deletion of Reelin, its lipoprotein receptors, or its intracellular adaptor protein Disabled-1 (Dab1), exhibit nociceptive ... ...

    Abstract The Reelin-signaling pathway is essential for correct neuronal positioning within the central nervous system. Mutant mice with a deletion of Reelin, its lipoprotein receptors, or its intracellular adaptor protein Disabled-1 (Dab1), exhibit nociceptive abnormalities: thermal (heat) hyperalgesia and reduced mechanical sensitivity. To determine dorsal horn alterations associated with these nociceptive abnormalities, we first characterized the correctly positioned Dab1 neurons in wild-type and mispositioned neurons in Reelin-signaling pathway mutant lumbar spinal cord. Using immunofluorescence, we found that 70% of the numerous Dab1 neurons in Reln
    Mesh-Begriff(e) Animals ; Cell Adhesion Molecules, Neuronal/genetics ; Cell Adhesion Molecules, Neuronal/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; LIM-Homeodomain Proteins/genetics ; LIM-Homeodomain Proteins/metabolism ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nociception ; Posterior Horn Cells/metabolism ; Posterior Horn Cells/physiology ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemische Substanzen Cell Adhesion Molecules, Neuronal ; Dab1 protein, mouse ; Extracellular Matrix Proteins ; LIM homeobox transcription factor 1 beta ; LIM-Homeodomain Proteins ; Nerve Tissue Proteins ; Transcription Factors ; Serine Endopeptidases (EC 3.4.21.-) ; reelin protein (EC 3.4.21.-)
    Sprache Englisch
    Erscheinungsdatum 2017
    Erscheinungsland France
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1111/ejn.13520
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Microglial microRNAs mediate sex-specific responses to tau pathology.

    Kodama, Lay / Guzman, Elmer / Etchegaray, Jon I / Li, Yaqiao / Sayed, Faten A / Zhou, Lu / Zhou, Yungui / Zhan, Lihong / Le, David / Udeochu, Joe C / Clelland, Claire D / Cheng, Zuolin / Yu, Guoqiang / Li, Qingyun / Kosik, Kenneth S / Gan, Li

    Nature neuroscience

    2019  Band 23, Heft 2, Seite(n) 167–171

    Abstract: Sex is a key modifier of neurological disease outcomes. Microglia are implicated in neurological diseases and modulated by microRNAs, but it is unknown whether microglial microRNAs have sex-specific influences on disease. We show in mice that microglial ... ...

    Abstract Sex is a key modifier of neurological disease outcomes. Microglia are implicated in neurological diseases and modulated by microRNAs, but it is unknown whether microglial microRNAs have sex-specific influences on disease. We show in mice that microglial microRNA expression differs in males and females and that loss of microRNAs leads to sex-specific changes in the microglial transcriptome and tau pathology. These findings suggest that microglial microRNAs influence tau pathogenesis in a sex-specific manner.
    Mesh-Begriff(e) Animals ; Brain/metabolism ; Brain/pathology ; Female ; Male ; Mice ; MicroRNAs/metabolism ; Microglia/metabolism ; Microglia/pathology ; Sex Characteristics ; Tauopathies/metabolism ; Tauopathies/pathology ; Transcriptome ; tau Proteins/metabolism
    Chemische Substanzen MicroRNAs ; tau Proteins
    Sprache Englisch
    Erscheinungsdatum 2019-12-23
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/s41593-019-0560-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: AD-linked R47H-

    Sayed, Faten A / Kodama, Lay / Fan, Li / Carling, Gillian K / Udeochu, Joe C / Le, David / Li, Qingyun / Zhou, Lu / Wong, Man Ying / Horowitz, Rose / Ye, Pearly / Mathys, Hansruedi / Wang, Minghui / Niu, Xiang / Mazutis, Linas / Jiang, Xueqiao / Wang, Xueting / Gao, Fuying / Brendel, Matthew /
    Telpoukhovskaia, Maria / Tracy, Tara E / Frost, Georgia / Zhou, Yungui / Li, Yaqiao / Qiu, Yue / Cheng, Zuolin / Yu, Guoqiang / Hardy, John / Coppola, Giovanni / Wang, Fei / DeTure, Michael A / Zhang, Bin / Xie, Lei / Trajnowski, John Q / Lee, Virginia M Y / Gong, Shiaoching / Sinha, Subhash C / Dickson, Dennis W / Luo, Wenjie / Gan, Li

    Science translational medicine

    2021  Band 13, Heft 622, Seite(n) eabe3947

    Abstract: The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( ...

    Abstract The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 (
    Mesh-Begriff(e) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Female ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Microglia/metabolism ; Mutation/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Immunologic/metabolism
    Chemische Substanzen Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human ; Trem2 protein, mouse ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2021-12-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abe3947
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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