2018 6th Annual Satellite Symposium

You Are Cordially Invited to our 6th Annual Symposium on Neuroinflammation and Neurodegeneration.

Brain-Immune System Interfaces in Health and Disease

                                    Sunday, November 4, 2018
                                    6:30 p.m. – 8:30 p.m.
                                    Manchester Grand Hyatt,
                                    Harbor Ballroom HI,
                                    San Diego, California USA

What occurs at brain-immune system interfaces in health and disease? Join us for great science, food, beer and wine at our Annual Satellite Symposium at Neuroscience 2018. Distinguished researchers on Neuroscience, Professors Doyle and Kipnis will discuss novel functions of the lymphatic vessels that drain the CNS, and present recent research concerning the role of myelin debris in driving prolonged inflammation following CNS injury.

There’s no place like this year’s symposium to get your synaptic juices flowing.  See you in San Diego.

While you're at the show, stop by Booth #2329 to get your complimentary "Pop Socket" and see our most recent innovations for Neuroscience Research!
 

Symposium Program:
6:15 PM Doors Open
6:30 PM Networking, Hors d’oeuvres, Beer and Wine
6:50 PM Welcome and Opening Remarks
7:00 PM Liquefaction of the brain following stroke shares a similar molecular and morphological profile with atherosclerosis (Read Abstract)
Professor Kristian Doyle,
Department of Immunobiology, Department of Neurology, and the Arizona Center on Aging, University of Arizona
About the Speaker: Dr. Doyle is an assistant professor in the Departments of Immunobiology and Neurology at the University of Arizona. He earned his Ph.D. from Oregon Health & Science University in 2007 developing novel therapeutics for stroke in the laboratory of Dr. Mary Stenzel-Poore. Dr. Doyle then trained as a postdoctoral scholar at Stanford University nder the mentorship of Dr. Marion Buckwalter researching the role of TGFbeta signaling after stroke and developing a model of post-stroke dementia. Dr. Doyle was awarded an American Federation of Aging Research Fellowship in 2009, an Anita Roberts Young Scientist Scholarship in 2010, and a K99/R00 faculty transition award from the National Institute of Nursing Research in 2012 to investigate links between the inflammation and the development of delayed cognitive dysfunction following stroke. His current research program is focused on determining precisely how long it takes for the inflammatory response to stroke to resolve and discovering why it resolves much more slowly in the brain than it does following ischemia in other tissues. His laboratory is also working on developing methods that accelerate the resolution of inflammation following stroke, and methods that mitigate the impact of chronic inflammation on the remainder of the surviving brain.
7:40 pm Meninges in the interface of neuroimmune interactions (Read Abstract)
Professor Jonathan Kipnis
, Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia
About the Speaker:
Dr. Jonathan (Jony) Kipnis’s research group focuses on the complex interactions between the immune system and the central nervous system (CNS). The goal is to elucidate the cellular and molecular mechanisms underlying the beneficial effects of immune system in brain function in neurodegenerative, neurodevelopmental, and mental disorders as well as in healthy aging. Dr. Kipnis’s research team showed that the brain function is dependent, in part, on the function and integrity of the immune system. The fascination with immunity and its role in healthy and diseased brain is what brought the team to a breakthrough discovery of lymphatic vessels that drain the CNS into the peripheral lymph nodes and thus serve as a physical connection between the brain and the immune system. The implications of this work are broad and range from Autism to Alzheimer’s disease through neuroinflammatory conditions, such as Multiple Sclerosis. Dr. Kipnis graduated from the Weizmann Institute of Science in Israel, where he was a Sir Charles Clore scholar and a recipient of distinguished prize for scientific achievements awarded by the Israeli Parliament, The Knesset. Jony joined UVA faculty in 2007. He is now a Harrison Distinguished Professor and Chair of the Neuroscience Since 2015 he is also a Gutenberg Research College Fellow at the Johannes Gutenberg University Mainz Medical Center, Germany.
8:20 pm Closing Remarks

 


Liquefaction of the brain following stroke shares a similar molecular and morphological profile with atherosclerosis

Abstract

The response to ischemic injury in the brain is different to the response to ischemic injury in other organs and tissues. Almost exclusive to the brain, and for unknown reasons, dead tissue liquefies in response to ischemia by the process of liquefactive necrosis. However, the data we present here indicate that at the macroscopic, microscopic, and molecular level, liquefactive necrosis strongly resembles atherosclerosis. We show that chronic stroke infarcts contain foamy macrophages, cholesterol crystals, high levels of osteopontin and matrix metalloproteinases, and a similar cytokine profile to atherosclerosis. Excessive cholesterol loading of macrophages is a principal driver of atherosclerosis. Therefore, because cholesterol is an important structural component of myelin, liquefactive necrosis in response to stroke may be caused by an inflammatory response to myelin debris that is prolonged by the formation of cholesterol crystals within macrophages. We propose that this results in the chronic production of high levels of proteases, which in a partially osteopontin dependent mechanism, causes secondary neurodegeneration and encephalomalacia of the surrounding tissue. In support of this, we show that genetically ablating osteopontin substantially reduces the production of degradative enzymes following stroke, reduces secondary neurodegeneration, and improves recovery. These findings suggest that treatments that target atherosclerosis, such as the inhibition of osteopontin, may also be useful for mitigating the harmful effects of liquefactive necrosis following stroke.

Meninges in the interface of neuroimmune interactions

Abstract

Immune cells and their derived molecules have major impact on brain function. Mice deficient in adaptive immunity have impaired cognitive and social function compared to that of wild-type mice. Importantly, replenishment of the T cell compartment in immune deficient mice restored proper brain function. Despite the robust influence on brain function, T cells are not found within the brain parenchyma, a fact that only adds more mystery into these enigmatic interactions between T cells and the brain. Our results suggest that meningeal space, surrounding the brain, is the site where CNS-associated immune activity takes place. We have recently discovered a presence of meningeal lymphatic vessels that drain CNS molecules and immune cells to the deep cervical lymph nodes. This communication between the CNS and the peripheral immunity is playing a key role in several neurological and psychiatric disorders and, therefore, may serve as a novel therapeutic target that is worth in-depth mechanistic exploration.