Title Associate Professor of Neurology Institution Brigham and Women's Hospital Address Dr. Butovsky Lab, BTM Lab 10032A 60 Fenwood Rd Boston MA 02115
|
|
Biography
Tel Aviv University, Israel | B.Sc. cum laude | 09/1995 | Biology Science |
The Weizmann Institute of Science, Israel | M.Sc. magna cum laude | 09/2000 | Neurobiology Science |
The Weizmann Institute of Science, Israel | Ph.D. summa cum laude | 09/2005 | Neuroimmunology |
BWH/Harvard Medical School, USA | Postdoctoral Training | 2012 | Center for Neurologic Diseases |
BWH/Harvard Medical School, USA | Instructor in Neurology | 2014 | Center for Neurologic Diseases |
BWH/Harvard Medical School, USA | Assistant Professor | 2018 | Center for Neurologic Diseases |
BWH/Harvard Medical School, USA | Associate Professor | Present | Center for Neurologic Diseases |
2012
Translational Research Advancing Therapies for ALS award
2014
The Race to Erase MS – Faculty Award
2016
Commitment to Innovation Discovery
Updated Awards: https://orcid.org/0000-0003-0186-8867
Overview
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.
Research
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.
-
R41AG073059
(BUTOVSKY, OLEG ;ILIN, ILYA)
Sep 30, 2021 - Feb 28, 2023
Xenon gas treatment to modulate microglia in neurodegenerative diseases
Role: Co-Principal Investigator
-
R21NS104609
(BUTOVSKY, OLEG)
Jul 1, 2018 - Dec 31, 2020
Identification of exosome signature in serum from ALS patients
Role: Principal Investigator
-
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
-
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
-
R01AG054672
(BUTOVSKY, OLEG)
Aug 15, 2017 - Apr 30, 2022
Targeting the miR-155 and APOE-TREM2 pathways to restore dysfunctional microglia in Alzheimerâs 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
-
APOE:Butovsky
(Butovsky, Oleg)
Jul 1, 2017 - Jun 1, 2019
The role of APOE in microglia regulation in neurodegeneration
Role Description: We hypothesize that danger signals (dead neurons, dystrophic axons and amyloid-ß peptides) induce APOE signaling, which alters functional phenotype of microglia from the homeostatic (M0) to neurodegenerative MGnD) phenotype in a gender-dependent manner. We will address the hypothesis in the following aims: 1) determine the role of human APOE isoforms in microglia regulation in a gender-dependent manner in aging and mouse models of neurodegeneration (Holtzman/Greengard collaboration); 2) investigate how APOE isoforms affect phenotype and function of recruited human inflammatory monocytes (Bu/Wellington collaboration).
Role: Principal Investigator
-
R21NS101673
(BUTOVSKY, OLEG)
Apr 1, 2017 - Mar 31, 2019
Identification of MicroRNA and Proteomics in immune cells and plasma in ALS
Role Description: NIH/NINDS R21 NS101673 (Butovsky)
Role: PI.
We hypothesize that abnormalities in miRNA and proteomic signatures in ALS may serve as immune-based biomarkers of disease progression and may reveal new targets for immune-modulation to slow ALS. Our objective will be addressed in aims 1) identification of miRNA and proteomic signature in sALS and fALS progression; and 2) replication and validation of the identified hits.
Role: Principal Investigator
-
R01AG051812
(CROSBY, GREGORY)
Sep 15, 2016 - May 30, 2021
Microglial mechanisms of postoperative CNS inflammation and cognitive decline
Role Description: Microglial mechanisms of postoperative cognitive decline
NIH/NIA R01 AG051812-02 (PI: Crosby/Co-PI: Butovsky)
Role: MPI.
The goal of this project is to investigate microglial involvement in the cognitive after-effects of general anesthesia and surgery in old subjects.
Role: Principal Investigator
-
R01NS088137
(BUTOVSKY, OLEG)
Sep 30, 2014 - Jun 30, 2024
Restoration of homeostatic microglia in CNS inflammation
Role Description: Mechanism of regulation of CNS inflammation by microglia
NIH/NINDS R01 NS088137-02 (Butovsky)
Role: PI.
The goals of this project are 1) to determine the specific molecular and functional properties of microglia during processes of tissue injury and repair that characterizes MS; and 2) to define a strategy whereby specific targeting of microglia can be used to reduce compartment-specific immune injury and promote repair in MS by restoring microglial unique molecular signature and function.
Role: Principal Investigator
-
https://orcid.org/0000-0003-0186-8867
Featured Content
Bibliographic
Local representatives can answer questions about the Profiles website or help with editing a profile or issues with profile data. For assistance with this profile: HMS/HSDM faculty should contact contactcatalyst.harvard.edu. For faculty or fellow appointment updates and changes, please ask your appointing department to contact HMS. For fellow personal and demographic information, contact HMS Human Resources at human_resourceshms.harvard.edu. For faculty personal and demographic information, contact HMS Office for Faculty Affairs at facappthms.harvard.edu.