Haakon Nygaard, MD

Postdoctoral Fellow
Neurology

Thesis Advisor

Stephen M. Strittmatter

Thesis Project

The role of cellular prion protein in Alzheimer’s disease

For many years, the leading hypothesis for the pathogenesis of Alzheimer’s disease (AD) involved the toxic effects of a gradual buildup of insoluble amyloid-(Ain the brain. More recently, however, several independent groups have established that soluble A-oligomers may be the most toxic species in AD. These interesting findings have suggested a putative cell surface receptor for A, and the Strittmatter laboratory recently identified cellular prion protein (PrPc) as a high affinity binding site for A-oligomers. They also found that PrPc mediates the toxic effects of A oligomers on synaptic plasticity. The focus of Dr. Nygaard’s project will be to characterize the mechanism by which the A-oligomer-PrPc interaction regulates synaptic plasticity and function in Alzheimer’s disease.