8th Annual Symposium on Glial-Neuronal Interactions
9 Jan 2015
University of California, Riverside, HUB
Abstract Submission Deadline:
Friday, December 19, 2014
Description:
Brian A. MacVicar, professor and director of the Djavad Mowafaghian Centre for Brain Health at the University of British Columbia, will present the keynote Glenn Hatton Lecture titled “Synaptic sensing and modulation by microglia: a role for neurodegeneration?” Dr. G. Richard Olds, vice chancellor for Health Affairs and dean of the UCR School of Medicine, will give a brief welcome address.
The annual symposium is intended to bring together a diverse group of researchers who study neuronal-glial interactions in brain and spinal cord functions. It is presented by the Center for Glial-Neuronal Interactions (CGNI) in the UCR School of Medicine. The center involves faculty campuswide with research interests related to optimal brain and spinal cord function, as well as prevention and therapeutic intervention of neurodevelopmental, neurologic and neurodegenerative diseases.
The symposium is scheduled for 9 a.m. to 6 p.m. in HUB 302 on the UCR campus. Registration is free, but required, for attendees from nonprofit organizations. For those attending from for-profit organizations, the registration fee is $175. Poster abstract submissions will be accepted through Friday, Dec. 19.
Additional symposium speakers include:
- Michelle Monje Deisseroth, M.D., Ph.D., Stanford Institute for Stem Cell Biology and Regenerative Medicine, “Myelin plasticity in health and disease.”
- Joshua Weiner, Ph.D., University of Iowa, “Roles for astrocytic gamma-Protocadherin adhesion molecules in neural circuit formation.”
- Rona Giffard, Ph.D., M.D., Stanford University, “Glia, microRNAs and models of cerebral ischemia, a new hope for therapy?”
- Anandora Bruce-Keller, Ph.D., Pennington Biomedical Research Center, Louisiana State University, “CNS Inflammation: Other Voices, Other Rooms.”
- Lloyd Kasper, M.D., Dartmouth School of Medicine, “Harvesting from the gut microbiome: the role of commensal bacteria in CNS demyeliniation.”