W Sue GriffinDepartment of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA F1000 Faculty Member (since 13 January 2011)
The Alexa and William T Dillard Professor and Vice Chair for Research of the Donald W Reynolds Department of Geriatrics and the Reynolds Institute on Aging at the University of Arkansas College of Medicine of the University of Arkansas for Medical Sciences and Director of Research at the Central Arkansas Veterans HealthCare System, Little Rock, Arkansas.
BS (with Honors) and MS in Nutrition, University of Tennessee, Knoxville, TN, and PhD in Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Editor-in-Chief, Journal of Neuroinflammation HTTP://jneuroinflammation.com
Society for Neuroscience
Founding Member, Medical and Scientific Advisory Council, National Alzheimers Association
Alzheimer Disease Research Center Advisory Board Member, University of Texas Southwestern Medical School
Board Member Arkansas Oklahoma Alzheimers Association Chapter
International Womens Forum
Advisory Council Member, Winrock International
Arkansas Women of Power
HONORS AND AWARDS:
Alpha Lambda Delta Fraternity Member
Predoctoral US Public Health Service Fellow
Postdoctoral Moss Fellow in Cardiology
United States Public Health Service National Institutes of Health Awards 1977 to 2014
Chairman National Institute on Aging Review Committee for Drug Discovery Groups for the Treatment of Cognitive Impairment
Member, National Institutes of Health Reviewers' Reserve
Favorite Faculty Woman Southwestern Medical School
Distinguished Faculty Scholar, University of Arkansas for Medical Sciences
Dr Griffin focuses on the mechanisms involved in driving forces underlying the progression of Alzheimer's Disease and other neurodegenerative disorders characterized by glial activation with elevated production and release of proinflammatory proteins, in particular the pluripotent immune response generating cytokine interleukin-1. Dr Griffin was first to demonstrate a link between excess expression of interleukin-1 and precocious of development of Alzheimer's disease in disorders such as head injury, epilepsy, AIDS, Downs syndrome, and Parkinsons disease. The findings of Dr Griffins team are seen as significant breakthroughs in the early detection and treatment of Alzheimer's, bringing nationwide acclaim for Dr Griffin and the Donald W Reynolds Department of Geriatrics and Institute on Aging. As part of these studies, the team has shown that interleukin-1 increases the expression of the precursors of each of the substrates necessary for formation of common features characteristic of the neuropathological changes in Alzheimer's disease. These interleukin-1-related activities include neuronal synthesis of betaAPP for Abeta plaque development: synthesis of the neuronal kinase MAPK-p38, which is required for tau hyperphosphorylation and for downregulation of synaptophysin; activation of astrocytes and their synthesis of S100B, the neurite growth promoting cytokine related to the presence of the neurites in Abeta plaques, which is the diagnostic feature of Alzheimer's disease. In addition, Dr Griffins team has shown that ApoE promotes synthesis of betaAPP, the neuronal acute phase protein, in a genotype specific manner with ApoE3 more effective that ApoE4. Moreover, the team demonstrated that such stress-induced betaAPP expression in neurons is compromised with aging and with regard to neuronal plaque proximity. Further research into specific mechanisms that may serve as drug targets are being pursued in Dr Griffins group.
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F1000 Medicine Reports 2011 3:(24) (01 Dec 2011)
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