[BIC-announce] FW: Killam Lecture - Tomorrow - Generic and Metabolic Regulation of Autoimmune Demyelinating Disease by Mgat5 N-Glycosylation

[Jennifer Chew, Ms.]

PLEASE DISCARD IF THIS IS A DUPLICATE.  JENNIFER 
 

Jennifer Chew

McConnell Brain Imaging Centre

Montreal Neurological Institute

Room WB317

3801 University Street

Montreal, Quebec, Canada

H3A 2B4

Tel:  (514) 398-8554

Fax:  (514) 398-2975

 

 

________________________________

From: MNISTAFF - Montreal Neurological Institute Staff
[mailto:MNISTAFF at LISTS.MCGILL.CA] On Behalf Of Enza Ferracane, Ms.
Sent: Monday, January 16, 2006 3:05 PM
To: MNISTAFF at LISTS.MCGILL.CA
Subject: Killam Lecture - Tomorrow


*****KILLAM*****
 
Speaker:  Michael Demetriou, M.D., Ph.D.
Director MS Program,  University of California
 
Title:  Genetic and Metabolic Regulation of Autoimmune Demyelinating
Disease by Mgat5 N-Glycosylation
 
Place:  de Grandpre Communication Centre
 
Time:  4:00 pm
 
Date:  Tuesday, January 17, 2006
----------------------------------------------------------
 
The Killam series speaker for Tuesday, January 17, is Dr. Michael
Demetriou, Assistant Professor at UC Irvine.
 
Michael will leave sunny California to share insights from his emerging
work, in a Killam lecture titled "Genetic and Metabolic Regulation of
Autoimmune Demyelinating Disease by Mgat5 N-Glycosylation". 
 
This work investigates the role of protein glycosylation in altering
immune function leading to spontaneous CNS demyelinating disease in mice
and humans. Michael's lab has a manuscript currently under review at
Science demonstrating that MS patients and inbred mouse models may have
inherent genetic defects in the protein glycosylation pathway that
promotes CNS autoimmunity. These genetic defects can be rescued by
metabolic supplementation of the hexosamine pathway to enhance protein
glycosylation, implicating both environmental and genetic factors in the
disease, and the potential for simple oral therapeutic treatment that
might target a genetic defect promoting disease.Their mice also display
a neurodegenerative component and defects in protein glycosylation
induce neuronal apoptosis in vivo, suggesting a role that may extend
beyond inflammatory aspects of MS and possibly of relevance in other CNS
pathologies. 
 
In an earlier Nature article, Michael's lab studied Mgat5-deficient
mice. These mice displayed an enhanced susceptibility to experimental
autoimmune encephalomyelitis (EAE) the commonly used animal model of MS.
He used elegant techniques of visualizing cell:cell interactions, and
captured molecular mechanisms involved in formation of the 'immune
synapse' between T cells and antigen presenting cells of the immune
system. There are intriguing parallels between 'immune' and 'neural'
synapses, establishing Michael's work as very relevant to studies of
neural and neuro-immune cellular interactions. 
 
We look forward to seeing you at what promises to be a very interesting
Killam lecture.
 
Thanks and best, 
 
Amit Bar-Or 
 
 
 
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