Research:

Keywords:

Neuroimmunology, Neuroinflammation, Innate immunity, Metabolism, Immunometabolism

Research Activities

Our laboratory conducts basic and translational research in autoimmunity and neuroimmunology. Our aim is to develop therapies and identify novel therapeutic targets for multiple sclerosis (MS) and other autoimmune and neurodegenerative diseases, while uncovering fundamental insights into the biology of the immune and nervous systems. Specific areas of research include:

Metabolism as a modulator of immune, neuronal, and glial function: Previously considered part of homeostatic housekeeping, basic metabolic pathways are increasingly recognized to determine downstream cellular function, regulating phenotypic decisions and providing metabolites that serve as signaling molecules. Our lab is studying how metabolic pathways regulate differentiation and function of peripheral immune cells, oligodendrocyte precursor cells (OPCs), microglia, and astrocytes. We hope to exploit these pathways with drugs and diet to prevent injury and promote repair in MS and other autoimmune conditions.

Modulating the innate immune system in MS and other neurodegenerative diseases: Innate immune cells in the CNS – microglia and macrophages (and now astrocytes!) – appear to modulate the course of neurologic diseases, both inflammatory diseases like MS but also classic neurodegenerative diseases like Alzheimer’s and Parkinson’s. These cells take on distinct phenotypes and can be either helpful or harmful, contributing to injury or setting the stage for repair. We are studying the mechanisms that modulate microglia and astrocyte phenotype in the brain and how to manipulate them pharmacologically to prevent neurodegeneration and promote repair

Identifying pathways by which nitric oxide (NO) and other free radicals cause neuronal and axonal damage: Although myelin is thought to be the primary target of attack in MS, neurodegeneration is nearly universal, particularly in progressive MS, and appears to be the underlying cause of permanent disability. NO and other free radicals are toxic products resulting from inflammation and chronic demyelination that contribute to neurodegeneration, but the exact mechanisms by which they cause injury are unclear. Our lab is identifying specific signaling pathways initiated by NO and other free radicals that can be targeted by drugs to produce neuroprotection. We are particularly interested in identifying druggable pathways by which NO produces mitochondrial injury.

Publications and Interests: https://jhu.pure.elsevier.com/en/persons/michael-kornberg