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American physician (born 1943) From Wikipedia, the free encyclopedia
Dennis J. Selkoe (born 25 September 1943) is an American physician (neurologist) known for his research into the molecular basis of Alzheimer's disease.[1] In 1985 he became Co-Director of the Center for Neurological Diseases and from 1990, Vincent and Stella Coates Professor of Neurological Diseases at Harvard Medical School.[2] He is also a Fellow of the AAAS and a member of the National Academy of Medicine.[3]
Dennis J. Selkoe | |
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Born | |
Alma mater |
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Known for |
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Spouse | Polly Selkoe |
Children | 2 including Greg Selkoe |
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Scientific career | |
Fields | Medicine, Neurology |
Selkoe studied at Columbia University (Bachelor's degree 1965) and the University of Virginia School of Medicine (M. D. 1969).[4] He took up a residency at the University of Pennsylvania Hospital (1969). From 1970 to 1972, he performed research at the National Institutes of Health and continued his residency as a neurologist at the Peter Bent Brigham Children's Hospital and Beth Israel Hospital in Boston.
In 1975, he held the position of instructor at the Brigham and Women's Hospital in Boston, before moving up to assistant professor in 1978.[5]
In 1978, he established a laboratory at Brigham and Women's to apply biochemical and cell biological methods to the study of degenerative neural diseases such as Alzheimer's and Parkinson's disease.[6]
In 1982, he and collaborators isolated the clusters of neurofibrils typical of Alzheimer's disease and described their chemical properties. With other laboratories, he showed that the tau protein of the microfibrils is their main component. With his laboratory, he also conducted extensive research on the second pathogenic component, senile plaques of beta-amyloid (Aβ).[7] They discovered in 1992 that Aβ is also formed in normal cells from its precursor amyloid precursor protein. The study of these processes led to the identification of inhibitors for the formation of Aβ. Selkoe was also able to show with his laboratory that innate mutations in the APP genes and the presenilin genes cause Alzheimer's disease (increased Aβ production). In 1999, he and co-workers identified presenilin as a component of the long-sought-after gamma-secretase, one of the enzymes involved in the pathogenic conversion of APP to Aβ in Alzheimer's disease. In his laboratory, it could also be shown that small, soluble oligomers from Aβ can damage the synapses and have an influence on memory performance.
He was the principal founding scientist of the pharmaceutical company Athena Neurosciences (later Elan Corporation).[8] In 2001 he was one of the founders of the Harvard Medical Center for Neurodegeneration and Repair.[9] He has been on the board of Prothena Corporation since 2013.[10]
He has an h-index of 183 according to Semantic Scholar.[11]
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