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Web Desc
Clinical and Molecular Biology of Acute and Chronic Traumatic Encephalopathies
joint with ApoE, Alzheimer's and Lipoprotein Biology
Organizer(s): Sam Gandy, Steven T. DeKosky and Ann C. McKee
Date: February 26 - March 02, 2012
Location: Keystone Resort, Keystone, CO, USA
Supported by the Directors' Fund
Summary of Meeting:
Acute traumatic brain injury (TBI) and its long-term neurodegenerative complications (known collectively as chronic traumatic encephalopathy, or CTE) are increasingly recognized as major public health issues, especially in the context of sports-related head injury and battlefield blast (military) exposure. Awareness of these issues has risen as neurological, psychiatric and neurodegenerative phenomena are associated with professional athletes and with veterans returning from Iraqi and Afghan theaters. The physics of head injury, as well as the epidemiological and neuropsychiatric aspects of sports-related and blast-related syndromes, will be reviewed in the initial sessions of this three-day meeting. Advances in functional neuroimaging and in the rapid and convenient determination of peptides and proteins in the cerebrospinal fluid and plasma will be reviewed in terms of their possible pathobiological significance as well as their identities as possible biomarkers. Later sessions will focus on the overlap between CTE and major neurodegenerative diseases, such as Alzheimer’s Disease (AD), frontotemporal dementia and amyotrophic lateral sclerosis. CTE is associated with accumulation of aggregated proteins or protein fragments, including tau, TDP-43, the Alzheimer’s amyloid precursor protein (APP) and the APP metabolite, amyloid-b. New experimental therapeutics research targets the roles these abnormal protein structures play in injury severity and subsequent outcome. Ab-lowering medications, currently in clinical trials for AD, improve outcome following acute brain trauma in rodent models, suggesting a pathway toward potential therapeutic interventions. Because apolipoprotein E (ApoE) isotype is an important determinant of outcome from acute severe as well as mild repetitive TBI, this meeting coincides in time and venue with the Keystone Symposia meeting on ApoE, Alzheimer’s and Lipoprotein Biology. Opening plenary sessions and an optional fourth day of sessions are available for those interested in learning more about basic biology and/or clinical interventions related to APOE.
Scholarship Deadline: October 26 2011
Discounted Abstract Deadline: October 26 2011
Abstract Deadline: December 2 2011
Discounted Registration Deadline: January 4 2012
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Avid Radiopharmaceuticals, Inc.

Eli Lilly and Company

Merck & Co., Inc.
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Neurological Disorders and Stroke (NINDS)
Grant No. 1R13NS077709-01
The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

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Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

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