Mechanisms of Beta Amyloid Peptide ToxicityMechanisms of Beta Amyloid Peptide Toxicityhttp://www.haverford.edu/calendar/details/249391KINSC Sharpless Auditorium2014-04-07T14:30:002014-04-07T16:30:00
April 7, 2:30PM–4:30PM
KINSC Sharpless Auditorium
Distinguished Visitor Chris Link, Department of Integrative Physiology, University of Colorado, Boulder
There is compelling data indicating that accumulation of the beta amyloid peptide (Abeta) is central to Alzheimer's disease, but the actual mechanism by which Abeta leads to neuronal dysfunction and death is still unresolved. Accumulation of Abeta is toxic in many contexts, including in transgenic C. elegans worms genetically engineered to express human Abeta. We have used these transgenic worms to investigate both the toxic form of Abeta and the mechanisms of toxicity. Our studies support a model in which soluble, oligomeric Abeta is neurotoxic by damaging cell membranes. We speculate that another pathological component of Alzheimer's disease, accumulation of hyperphosphorylated tau protein, is a downstream consequence of membrane damage caused by toxic Abeta oligomers. These studies suggest potential interventions in Alzheimer's disease and may give insights into other neurodegenerative conditions such as chronic traumatic encephaly.
Tea at 2:15PM
Sponsored by the Department of Biology in conjunction with the Distinguished Visitors Program
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