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Dorothy P Schafer PhD

TitleAssistant Professor
InstitutionUniversity of Massachusetts Medical School
DepartmentNeurobiology
AddressUniversity of Massachusetts Medical School
55 Lake Ave North
Worcester MA 01605
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    Other Positions
    InstitutionUMMS - School of Medicine
    DepartmentNeurobiology

    InstitutionUMMS - School of Medicine
    DepartmentNeuroNexus Neuroscience Institute

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentImmunology and Microbiology Program

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentMD/PhD Program

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentNeuroscience


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    Collapse education and training
    Mount Holyoke College, South Hadley, MA, United StatesBANeuroscience
    University of Connecticut, Storrs, CT, United StatesPHDNeuroscience
    Collapse awards and honors
    2017 - 2019Young Investigator Grant, NARSAD
    2016 - 2018Child Health Research Award, Charles H. Hood Foundation
    2016 - 2017Biomedical Research Award, Worcester Foundation
    2014 - 2018K99/R00 Career Transition Award, NIMH
    2012 - 2013Postdoctoral Fellowship Award, Nancy Lurie Marks
    2010 - 2011Bok Center distinction for excellence in teaching, Harvard University
    2010 - 2012NRSA F32 Postdoctoral Fellowship, NINDS
    2010 - 2011Marian Keyes Award for outstanding graduate work, American Society for Neurochemistry
    2007 - 2007Lepow Award for outstanding graduate work, University of Connecticut Health Center

    Collapse Overview 
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    Biography


    Dori Schafer earned her Bachelor’s degree in Neuroscience and Behaviour from Mount Holyoke College in 2001. She attended graduate school at the University of Connecticut Health Center in Matthew Rasband’s lab where she used rodent models to study neuron-glia interactions regulating assembly and maintenance of functional, polarized domains along the axon, nodes of Ranvier and axon initial segments. Upon completion of her PhD in 2008, she began her postdoctoral training in the laboratory of Beth Stevens at Boston Children’s Hospital. While in the Stevens lab (2008-2014), she studied the role of microglia, the resident CNS myeloid-derived cell, in mammalian synapse development and plasticity.  She was hired in 2015 as a tenure-track Assistant Professor in the Department of Neurobiology at The University of Massachusetts Medical School. Her laboratory utilizes a combination of molecular biology and high resolution static and live imaging to understand how neurons and glia communicate with one another to regulating synapse development and plasticity.


    Microglia-Synapse Interactions Regulating Neural Circuit Development, Plasticity, and Dysfunction. The nervous and immune systems are comprised of vastly different cell types long thought to perform separable and distinct physiological functions. Unexpectedly, these seemingly disparate systems are, in fact, working in concert. At the center are microglia, the resident central nervous system (CNS) macrophages, which were recently identified by us and others as key regulators of synapse number in the developing brain. Specifically, we identified that microglia regulate the elimination of excess synaptic connections that form in the developing rodent visual system by engulfing a subset of less active synapses. These results have changed how we think about microglia function (~5-10% of brain cells) and the importance is emphasized in devastating neuropsychiatric disorders (e.g. autism and schizophrenia) as well as neurodegenerative diseases (Alzheimer's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis, etc.) where to few or too many synaptic connections coupled with abnormally reactive microglia are characteristic features and, perhaps, causative in disease. The overall goal of my research is to achieve a deep understanding of how microglia regulate synapse development, maintenance, and plasticity in the healthy brain and determine whether these mechanisms are dysregulated in disorders of the nervous system. The primary disorders we are currently focused on include autism, schizophrenia, ALS, and multiple sclerosis. We are now focused on the following main questions:


    1) How do microglia respond on a cellular and molecular level to changes in neural activity and sensory experience ?


    2) Are microglial necessary for remodeling of neural circuits in response to changes in sensory experience?


    3) Do microglia regulate abnormal synaptic connectivity in neurological disease?


    To address these questions, the lab has developed novel strategies to image glia-synaptic circuit interactions by high resolution static imaging as well as 2-photon in vivo live imaging in behaving mice. In addition, we have implemented cutting-edge molecular genetic techniques to dissect microglia-specific mechanisms underlying synapse development, plasticity, and function.


     For more information please visit our website: https://www.schaferlabumms.com


     



    Collapse Rotation Projects

    There are a variety of rotation projects that use a variety of imaging and biochemical techniques to assess microglial function in the CNS. The main projects are highlighted below.


    1.  Dissecting novel molecular mechanisms underlying microglial function at synapses.


    2. Exploring new roles for microglia in the spread of neuroinflammation in neurological disease.


    3. Identifying novel ways microglia regulate other glial cell populations (astrocytes and oligodendrocytes) in the CNS.




    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    List All   |   Timeline
    1. Schafer DP, Heller CT, Gunner G, Heller M, Gordon C, Hammond T, Wolf Y, Jung S, Stevens B. Microglia contribute to circuit defects in Mecp2 null mice independent of microglia-specific loss of Mecp2 expression. Elife. 2016 Jul 26; 5. PMID: 27458802.
      View in: PubMed
    2. Frost JL, Schafer DP. Microglia: Architects of the Developing Nervous System. Trends Cell Biol. 2016 Aug; 26(8):587-97. PMID: 27004698.
      View in: PubMed
    3. Schafer DP, Stevens B. Microglia Function in Central Nervous System Development and Plasticity. Cold Spring Harb Perspect Biol. 2015 Oct; 7(10):a020545. PMID: 26187728.
      View in: PubMed
    4. Schafer DP, Stevens B. Brains, Blood, and Guts: MeCP2 Regulates Microglia, Monocytes, and Peripheral Macrophages. Immunity. 2015 Apr 21; 42(4):600-2. PMID: 25902477.
      View in: PubMed
    5. Goldey GJ, Roumis DK, Glickfeld LL, Kerlin AM, Reid RC, Bonin V, Schafer DP, Andermann ML. Removable cranial windows for long-term imaging in awake mice. Nat Protoc. 2014 Nov; 9(11):2515-38. PMID: 25275789.
      View in: PubMed
    6. Schafer DP, Lehrman EK, Heller CT, Stevens B. An engulfment assay: a protocol to assess interactions between CNS phagocytes and neurons. J Vis Exp. 2014 Jun 08; (88). PMID: 24962472.
      View in: PubMed
    7. Schafer DP, Stevens B. Phagocytic glial cells: sculpting synaptic circuits in the developing nervous system. Curr Opin Neurobiol. 2013 Dec; 23(6):1034-40. PMID: 24157239.
      View in: PubMed
    8. Schafer DP, Lehrman EK, Stevens B. The "quad-partite" synapse: microglia-synapse interactions in the developing and mature CNS. Glia. 2013 Jan; 61(1):24-36. PMID: 22829357.
      View in: PubMed
    9. Schafer DP, Lehrman EK, Kautzman AG, Koyama R, Mardinly AR, Yamasaki R, Ransohoff RM, Greenberg ME, Barres BA, Stevens B. Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner. Neuron. 2012 May 24; 74(4):691-705. PMID: 22632727.
      View in: PubMed
    10. Susuki K, Yuki N, Schafer DP, Hirata K, Zhang G, Funakoshi K, Rasband MN. Dysfunction of nodes of Ranvier: a mechanism for anti-ganglioside antibody-mediated neuropathies. Exp Neurol. 2012 Jan; 233(1):534-42. PMID: 22178332.
      View in: PubMed
    11. Schafer DP, Stevens B. Synapse elimination during development and disease: immune molecules take centre stage. Biochem Soc Trans. 2010 Apr; 38(2):476-81. PMID: 20298206.
      View in: PubMed
    12. Schafer DP, Jha S, Liu F, Akella T, McCullough LD, Rasband MN. Disruption of the axon initial segment cytoskeleton is a new mechanism for neuronal injury. J Neurosci. 2009 Oct 21; 29(42):13242-54. PMID: 19846712.
      View in: PubMed
    13. Liu F, Schafer DP, McCullough LD. TTC, fluoro-Jade B and NeuN staining confirm evolving phases of infarction induced by middle cerebral artery occlusion. J Neurosci Methods. 2009 Apr 30; 179(1):1-8. PMID: 19167427.
      View in: PubMed
    14. Schafer DP, Rasband MN. Glial regulation of the axonal membrane at nodes of Ranvier. Curr Opin Neurobiol. 2006 Oct; 16(5):508-14. PMID: 16945520.
      View in: PubMed
    15. Ogawa Y, Schafer DP, Horresh I, Bar V, Hales K, Yang Y, Susuki K, Peles E, Stankewich MC, Rasband MN. Spectrins and ankyrinB constitute a specialized paranodal cytoskeleton. J Neurosci. 2006 May 10; 26(19):5230-9. PMID: 16687515.
      View in: PubMed
    16. Schafer DP, Custer AW, Shrager P, Rasband MN. Early events in node of Ranvier formation during myelination and remyelination in the PNS. Neuron Glia Biol. 2006 May; 2(2):69-79. PMID: 16652168.
      View in: PubMed
    17. Schafer DP, Bansal R, Hedstrom KL, Pfeiffer SE, Rasband MN. Does paranode formation and maintenance require partitioning of neurofascin 155 into lipid rafts? J Neurosci. 2004 Mar 31; 24(13):3176-85. PMID: 15056697.
      View in: PubMed
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