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Welsh scientist and active researcher (1948–2020) From Wikipedia, the free encyclopedia
Peter Davies (1948 - 2020[1]) was a Welsh scientist and active researcher. He was the head and director of the Litwin-Zucker Research Center for The Study of Alzheimer's disease and memory disorders,[2] associated with the Feinstein Institute for Medical Research in Manhasset, New York, US.
The topic of this article may not meet Wikipedia's notability guideline for academics. (August 2011) |
Peter Davies | |
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Born | Peter Davies 18 July 1948 Tredegar, Wales |
Died | 26 August 2020 72)[1] | (aged
Nationality | Welsh |
Education | University of Leeds |
Occupation | Scientist |
Employer | The Feinstein Institute for Medical Research |
Known for | Medical Research |
Website | feinstein |
Davies received his BSc (Hons., 1st class) and PhD, both in biochemistry, from the University of Leeds in 1971 and 1974, respectively. He was a post-doctoral fellow in the Department of Pharmacology at the University of Edinburgh, Scotland, before joining the staff of the Medical Research Council Brain Metabolism Unit in Edinburgh in 1974, where he began his research on Alzheimer's disease.[1]
In 1977, Davies moved to Albert Einstein College of Medicine in the Bronx, New York City, where he was an assistant professor from 1977 to 1981, an associate professor from 1981 to 1986, and a professor from 1986 to date.[3] He became the scientific director of the Litwin-Zucker Center for Research on Alzheimer's disease at the Feinstein Institute for Medical Research, North Shore-LIJ Health System, in 2006.
Davies' research was focused on the biochemistry of Alzheimer's disease. His early work was in the development of the currently approved drugs for Alzheimer's disease: Aricept, Exelon and Razodyne. He was interested in the pathway of Alzheimer's disease, and said that the disease may be a process of uncontrolled cell cycle division. He had evidence that the switch that drives the cell cycle of neurons, which is a one-time event when the neuron is born, is somehow tripped and reactivated late in life. He and his team designed an experiment to turn on the cell cycle in laboratory models.[4] They put a viral oncogene into differentiated neurons and watched as pathological events progressed. In 2004 Davies and his collaborators identified a marker in cerebrospinal fluid (CSF) that can distinguish Alzheimer's disease from normal ageing, as well as discriminate between Alzheimer's and other forms of dementia.[5] The overall goal of Davies' research was to develop treatments to slow or halt the progression of Alzheimer's disease.
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