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For over 35 years I have been engaged in the study of the molecular genetics, biochemistry and molecular biology of prion diseases, Alzheimer's disease and related dementias. My contributions are in three main areas: the genetics of human prion diseases; transgenic models of prion and Alzheimer's diseases; and the molecular basis of memory loss in Alzheimer's disease and related dementias. In the 1990s, my lab members and I created the Tg2576 transgenic mouse, which develops subtle memory problems as well as plaques composed of amyloid-beta protein. This mouse likely models the "pre-clinical" phase of Alzheimer's disease. During this phase, Alzheimer's disease processes are underway in the brain, but people do not yet notice symptoms. Today, this model is used around the world to study Alzheimer's disease. In the 2000s, we went on to create other mouse models of neurodegenerative disease, including the popular rTg4510 mouse, which develops neurodegeneration and another biological sign of Alzheimer's: neurofibrillary tangles made of tau protein. My current research focuses on:
Advancing our understanding of the molecular mechanisms of Alzheimer's disease to develop interventions that halt or reverse the progress of disease, focusing specifically on the amyloid-beta and tau proteins.
Developing a drug that will reverse memory loss and repair synapses by targeting caspase-2.
Finding biomarkers in blood that will enable us to detect the malfunctioning of synapses caused by the effects of caspase-2 in the brain.
My dream is to develop an effective, safe and affordable treatment for Alzheimer's disease.