Faculty Research
Raymond Scott Turner, MD, PhD ( raymondt@umich.edu )
Associate Professor
Chief, Neurology Service, VA Ann Arbor Healthcare System
Research Scientist, VA Geriatric Research Education and Clinical Center
Site Principal Investigator, Alzheimer's Disease Cooperative Study ( www.adcs.ucsd.edu )
Dr.Turner's research interests include both basic and clinical research in neurodegenerative diseases causing dementia, particularly Alzheimer's disease. His basic research interest is in the regulation of amyloid precursor protein (APP) processing in brain. The major components of amyloid plaques in Alzheimer's disease (AD) brain are Abeta peptides which are derived from the normal metabolism of APP in neurons. The progressive accumulation and deposition of Abeta/amyloid in the brain is thought to cause AD. Thus, strategies being investigated to prevent or treat AD include drug-discovery to inhibit Abeta generation from APP and vaccine-based strategies to promote Abeta clearance from brain. Current therapies available for patients with AD include cholinesterase inhibitors and memantine. However, these medications are palliative and provide only modest and temporary clinical benefits. Research studies in progress are searching for disease-modifying therapies for AD. Transgenic mice expressing human APP are now being utilized to probe disease mechanisms and to test novel treatment strategies that may then go on to clinical trials of patients with AD. We discovered that the interaction of APP with X11/mint inhibits Abeta generation in cells in culture. We are now probing effects of this protein interaction in neurons and in transgenic mice expressing human APP and human X11/mint. These studies may lead to novel gene-therapy based or perhaps pharmacologic treatment strategies of transgenic mouse models of AD. Other research includes the generation of transgenic rat models of AD to enable PET neuroimaging of amyloid burden in brain. These transgenic rats may then be used for longitudinal studies of putative therapies for AD.
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