We are especially interested in the mechanisms of synaptic dysfunction in prion diseases such as Creutzfeldt-Jakob disease. Additionally, we investigate the role the prion protein plays in dementias.
Generation and accumulation of abnormally processed proteins such as a misfolded form of the prion protein for Creutzfeldt-Jakob disease and beta-amyloid for Alzheimers disease lead to synaptic failure leading to irreversible nerve cell loss and progressive dementia. How the generation of pathological prions and deposition of these in the brain lead to neurodegeneration is not fully understood. Likewise, the role of the prion protein in Alzheimers disease or other dementias is not well defined.