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Oleg Butovsky, Ph.D.

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Tel Aviv University, IsraelB.Sc. cum laude09/1995Biology Science
The Weizmann Institute of Science, IsraelM.Sc. magna cum laude09/2000Neurobiology Science
The Weizmann Institute of Science, IsraelPh.D. summa cum laude09/2005Neuroimmunology
BWH/Harvard Medical School, USAPostdoctoral Training2012Center for Neurologic Diseases
BWH/Harvard Medical School, USAInstructor in Neurology2014Center for Neurologic Diseases
BWH/Harvard Medical School, USAAssistant Professor2018Center for Neurologic Diseases
BWH/Harvard Medical School, USAAssociate ProfessorPresentCenter for Neurologic Diseases
Translational Research Advancing Therapies for ALS award
The Race to Erase MS – Faculty Award
Commitment to Innovation Discovery
Updated Awards: https://orcid.org/0000-0003-0186-8867

My laboratory focuses on basic fundamental questions of microglia biology and developing novel microglia-targeting therapies. One of the important new areas in neuroimmunology is the emerging field of the innate immune system and the interface between microglia and the peripheral innate immune system. Our novel tools and therapeutic approaches are applicable to neurological diseases including Multiple sclerosis, Amyotrophic lateral sclerosis and Alzheimer’s disease that currently lack therapy.

Available: 01/01/23, Expires: 01/01/24

The Butovsky lab is looking for HMS medical students to study mechanisms of microglia regulation in neurodegenerative diseases. Our laboratory focuses on microglial perturbations and their interactions with immune cells regulating brain function such microglia-astrocytes and peripheral immunity, applying novel approaches including microglia spatial interactions, gene-specific targeting and microglia replacement in neurodegenerative disease including Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and glaucoma. We are broadly interested in how immune mechanisms regulate microglial functions and how they malfunction in neurodegenerative diseases, carrying major genetic risk factors such as APOE4 utilizing iPSCs, reprogramming human blood monocytes into microglia-like cells to replenish and restore microglial functions. Our laboratory is located in the Center of Neurologic Disease, in the Hale Building for Transformative Medicine, BWH and Harvard Medical School. Our Center is a collegial and highly collaborative biomedical research institution with world-class investigators in neurology and immunology. We are collaborating with a diverse scientific community including MIT, Broad Institute and top-ranked biotechnology companies, and other leading labs at Harvard.

The research activities and funding listed below are automatically derived from NIH ExPORTER and other sources, which might result in incorrect or missing items. Faculty can login to make corrections and additions.
  1. R41AG073059 (ILIN, ILYA) Sep 30, 2021 - Aug 31, 2022
    Xenon gas treatment to modulate microglia in neurodegenerative diseases
    Role: Co-Principal Investigator
  2. R21NS104609 (BUTOVSKY, OLEG) Jul 1, 2018 - Dec 31, 2020
    Identification of exosome signature in serum from ALS patients
    Role: Principal Investigator
  3. A222469 (Butovsky, Oleg) Apr 1, 2018 - Mar 1, 2019
    Evaluate the effect of CFMS antagonist on microglia cell phenotypes and gene signatures
    Role Description: The goal of this project is to determine the contribution of CSF1R in microglia modulation of functional properties during processes of tissue injury, neuroinflammation and neurodegeneration.
    Role: Principal Investigator
  4. R01EY027921 (WEINER, HOWARD L) Sep 30, 2017 - Dec 31, 2020
    Role of Microglia in Retinitis Pigementosa
    Role Description: NIH R01EY027921 (PI:Weiner/Co-PI: Butovsky) Role: Co-PI. The focus of this grant proposal is to characterize retinal microglia and how they regulate and/or participate in retinal damage in both animal models of retinitis pigmentosa and in eyes from human subjects. We will investigate whether retinitis pigmentosa in animal models can be treated by specifically targeting and modulating microglia. We will use new technology and approaches to understand features of microglia cells that can then be exploited to develop novel microglia-targeting therapies to treat humans with retinitis pigmentosa.
    Role: Principal Investigator
  5. R01AG054672 (BUTOVSKY, OLEG) Aug 15, 2017 - Apr 30, 2022
    Targeting the miR-155 and APOE-TREM2 pathways to restore dysfunctional microglia in Alzheimer’s disease
    Role Description: Targeting the miR-155 and APOE-TREM2 pathways to restore dysfunctional microglia in Alzheimer’s disease NIH/NIA R01 AG054672-01 (Butovsky) Role: PI. We hypothesize that danger signals (dead neurons and amyloid-ß peptides) alter functional phenotype of innate immune cells from the homeostatic (M0) to newly discovered neurodegenerative (MGnD) phenotype. We will address our hypothesis in the following aims: 1) targeting Trem2-induced Apoe/miR155 pathway to restore M0-homeostatic microglia in AD mouse models. We will specifically delete miR-155, Apoe and Trem2 in microglia of AD mouse models; 2) restoration of M0-homeostatic microglia via Mertk pathway in humanized APOE4 and AD mice. We will specifically over-express Mertk in microglia of APOE4 humanized mice and AD mouse models. We will validate our findings by investigating AD brains from prodromal to advanced stages. The goal of our investigations is to define new molecular mechanisms of immune and inflammatory processes that contribute to the development and progression of AD, which in turn will provide a basis for new approaches for immune based therapy of the disease.
    Role: Principal Investigator

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Funded by the NIH National Center for Advancing Translational Sciences through its Clinical and Translational Science Awards Program, grant number UL1TR002541.