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Amyloid b-peptides in Alzheimer’s Disease: Pathways, Polymorphism, Interfaces and Inhibition

Start Date: 09/15/2010
End Date: 09/15/2010
Time: 12:00 -1:00 pm
Location: Room 1302 of the Biomedical Sciences Building
Area: Central Campus
City: Tallahassee
State: Florida
URL: More event information
Event Type: Seminar
Event Sponsor: Department of Biomedical Sciences

AD is a progressive neurodegenerative disorder that results in memory loss and dementia in the elderly. AD is one of many diseases in which poly-peptides form amyloid aggregates. The hallmark of AD is the deposition of 40- and 42-residue Ab peptides (Ab40 and Ab42 respectively) in cerebral vessel walls as well as in brain parenchyma. Monomeric Ab self-associates to large fibrillar aggregates that eventually deposit as amyloid plaques. A growing number of evidence suggests soluble aggregates of low-molecular weight, commonly referred as ‘soluble oligomers’, are highly toxic to the neuronal cells. Interfaces have indicated to have pronounced effect on Ab aggregation and have become a major focus of our investigations. We have explored a variety of interfaces that seem have distinct effects on aggregation pathways. Besides this, we are also interested in developing inhibitors of Ab aggregation by designing conformation-specific compounds. Results from these experiments will be presented.

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