
Oleg
Butovsky
PhD
Location
Boston, MA, USA
Current Organization
Brigham and Women’s Hospital
Biography
Dr. Butovsky’s laboratory is recognized for redefining microglia and their interplay with peripheral innate immunity in homeostasis, aging and neurodegeneration. Dr. Butovsky’s group identified a unique microglial signature and the mechanism of regulation in mice and humans and are elucidating the relationship of microglia to CNS disease including AD, multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS). Recent discoveries include the identification of the TGFß-dependent homeostatic M0-microglia and the second major microglia phenotype, neurodegenerative MGnD-microglia which is regulated by TREM2-APOE pathway. These series of investigations led to the generation of novel tools to study microglial biology in health and disease and prompted investigate the crosstalk between microglia and peripheral innate immunity in AD. These findings led to the establishment of national and international collaborations to develop microglial targets to treat neurodegenerative diseases. This has led to the investigation of APOE in microglia regulation during disease progression in AD and TAU mice in collaboration with leading experts in the field. Dr. Butovsky’s interest and expertise in APOE signaling in microglia regulation subsequently led his laboratory to extensive investigations of APOE in AD models and the preliminary data pointing to a new role of APOE in regulation of peripheral innate immunity which are part of this application, both in animals’ models and subjects with AD.
News Featuring This Grantee

Research News
Why APOE4 Makes Women More Susceptible to Alzheimer’s
The Alzheimer’s risk gene APOE4 puts women at greater risk for Alzheimer’s disease than men. New research unveils a possible cause.

Research News
Eye-Brain Research Uncovers Potential New Way to Treat Glaucoma
New research by Alzheimer’s Disease Research grantee, Oleg Butovsky, PhD, has uncovered a potential new way to treat glaucoma based on a common gene variant that increases the risk of Alzheimer's disease.