Department of Neuroscience
Professor and Chair, Department of Neurosciences
Lerner Research Institute, Cleveland Clinic
Professor, Department of Molecular Medicine
Cleveland Clinic Lerner College of Medicine of CWRU
- Multiple sclerosis
Cellular and Molecular Biology of Myelination
The aim of Dr. Trapp's lab is to obtain a better understanding of cellular/molecular events that regulate production and differentiation of oligodendrocytes and central nervous system (CNS) myelination. Using transgenic mice, they study the role of myelin and myelin proteins in maintaining axonal function and survival. They also investigate the role of CNS progenitor cells as a source of new oligodendrocytes in the adult brain.
A common theme of these research programs is that novel information about the normal function of myelin-forming cells and myelin-axon interactions will help them understand the mechanisms involved in human diseases that destroy myelin or myelin-forming cells.
Pathogenesis of Neurological Deficits in Multiple Sclerosis
In these studies, the lab seeks to determine the causes of MS, an inflammatory demyelinating disease of the CNS, and to therapeutically prevent irreversible neurological disability in patients with MS. Historically, it has been assumed that axons were spared most of the pathological consequences of inflammatory demyelination. They have described axonal degeneration during demyelination and as a result of chronic demyelination. They also focus on neuronal degeneration and axonal pathology in the cerebral cortex and hippocampus of MS patients. Recent studies also focus on the therapeutic potential of progenitor cells to repair demyelinated or dysmyelinated brain.
- How does myelin provide trophic support to axons?
- How do demyelination and dysmyelination affect neurons and their synaptic connections?
- How does subpial cortical demyelination occur?
- What are the characteristics of astrocyte diversity and mitochondrial biology in subpopulations of gray matter astrocytes in mouse models of autism spectrum disorders (ASDs)?
His laboratory has played a significant role in identifying axonal and neuronal degeneration in brains from individuals with (MS). They leveraged these data to develop animal models that recapitulate mechanistic aspects of myelin-induced axonal and neuronal degeneration. The biggest challenge now facing the myelin research community is the development of neuroprotective therapies. Their efforts are dedicated to identifying new therapeutic targets that cause axonal and neuronal degeneration in myelin diseases. This is essential for the development of neuroprotective therapies that delay and possibly reverse permanent neurological disability in individuals with myelin disease.
Furthermore, while astrocyte diversity has been recognized for over a century, the molecular and cellular mechanisms underlying this diversity in vivo and the consequences for psychiatric disorders remain poorly understood. They are therefore characterizing astrocyte diversity and mitochondrial biology in subpopulations of gray matter astrocytes in animal models of autism spectrum disorders.
Education: Loyola University
Postdoctoral Fellow: NIH/NINCDS