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David R Borchelt


Neuroscience
University of Florida
Portugal

Biography

David R Borchelt has been with the University of Florida since April of 2005 after 13 years on the faculty of Johns Hopkins University School of Medicine. He has authored, or co-authored, more than 100 research papers focusing on human neurodegenerative disorders. He gained his PhD from the University of Kentucky in 1986, where he studied the viruses that are similar to the virus that causes AIDS. After receiving his doctorate, he worked as a post-doctoral fellow with Dr. Stanley Prusiner at the University of California in San Francisco. In 1999, he won the Nobel Prize in Medicine for his work on infectious proteins that cause Mad Cow disease, Cruetzfeldt-Jakob disease, and other neurodegenerative diseases of animals and humans. During his time with Dr. Prusiner, he produced some of the seminal work on prion protein that supported this hypothesis. From this work, he began to realize that most human neurodegenerative diseases, including amyotrophic lateral sclerosis, Huntington’s disease, and Alzheimer’s disease, share similarities with prion disease in that the symptoms and pathology are caused by the accumulation of proteins in altered conformations. David R Borchelt has been with the University of Florida since April of 2005 after 13 years on the faculty of Johns Hopkins University School of Medicine. He has authored, or co-authored, more than 100 research papers focusing on human neurodegenerative disorders. He gained his PhD from the University of Kentucky in 1986, where he studied the viruses that are similar to the virus that causes AIDS. After receiving his doctorate, he worked as a post-doctoral fellow with Dr. Stanley Prusiner at the University of California in San Francisco. In 1999, he won the Nobel Prize in Medicine for his work on infectious proteins that cause Mad Cow disease, Cruetzfeldt-Jakob disease, and other neurodegenerative diseases of animals and humans. During his time with Dr. Prusiner, he produced some of the seminal work on prion protein that supported this hypothesis. From this work, he began to realize that most human neurodegenerative diseases, including amyotrophic lateral sclerosis, Huntington’s disease, and Alzheimer’s disease, share similarities with prion disease in that the symptoms and pathology are caused by the accumulation of proteins in altered conformations.

Research Interest

Alzheimer’s disease

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