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April 23, 2019 | 12:00 p.m. - 1:00 p.m.
Category: Seminar
Location: Mazurek Medical Education Commons Margherio | Map
320 E. Canfield
Detroit, MI 48201
Cost: Free
Audience: Academic Staff, Alumni, Community, Current Graduate Students, Current Undergraduate Students, Faculty, Staff

The Campus Community is invited to a research seminar 

Subtle myelinopathy triggers inflammatory demyelination and progressive atrophy

hosted by

the Department of Neurology

 and the Office of the Vice President for Research

with guest speaker, Andrew V. Caprariello, Ph.D.,

Postdoctoral Research Fellow, Department of Pharmacy Practice

Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University

April 23, 2019

12 noon to 1 p.m.

Margherio Family Conference Center

Mazurek Medical Education Commons

320 E. Canfield

The Wayne State University community is invited to attend a research seminar with guest speaker, Andrew V. Caprariello, Ph.D., postdoctoral research fellow, Department of Pharmacy Practice, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University. 

The presentation will be held on April 23, 2019 at 12 noon at the Margherio Family Conference Center located in the Mazurek Medical Education Commons. The seminar is free and open to the entire university community. 

Dr. Caprariello will present, "Subtle myelinopathy triggers inflammatory demyelination and progressive atrophy."

Dr. Caprariello earned his B.A. degree in Neuroscience and Biology at Oberlin College and a Ph.D. in Physiology and Biophysics at Case Western Research University School of Medicine. 

Abstract:

The etiology of inflammatory demyelination in multiple sclerosis (MS) remains unresolved. MS lesions are generally assumed to begin with unchecked immune attacks on healthy CNS myelin, a concept that is recapitulated in experimental autoimmune encephalitis (EAE). Whether the converse may also be true—that destabilized CNS myelin elicits secondary autoimmunity—remains unproven and has important therapeutic implications. In a proof-of-concept study, mice fed cuprizone briefly enough to destabilize but not destroy myelin prior to peripheral immune adjuvant developed widespread inflammatory demyelination two weeks later. Associated with periventricular gadolinium enhancement, myelin-reactive T cells and peripheral macrophages/monocytes infiltrated in proportion to the extent of primary myelinopathy. Small molecule inhibitors of myelin-modifying enzymes implicated in MS, called peptidyl arginine deiminase (PAD), virtually eliminated Gd enhancement and subsequent inflammatory demyelination. Left untreated, acute lesions atrophied months later, with residual, as-yet undetermined, hypercellularity. The modified-EAE, or CAE, model therefore provides the means to ascribe molecular mechanisms to “inside-out” inflammation in both its acute and chronic stages for clues as to the biological basis of multiple sclerosis and related neuroinflammatory disorders.

We hope you can join us for this interesting seminar!  

For more information about this event, please contact Julie O'Connor at 3135775600 or julie.oconnor@wayne.edu.