Peter Davies (scientist)
| Peter Davies | |
|---|---|
| Born |
Peter Davies 1948 Wales |
| Nationality | Welsh |
| Education | University of Leeds |
| Occupation | Scientist |
| Employer | The Feinstein Institute for Medical Research |
| Known for | Medical Research |
| Website | |
Peter Davies, a scientist and active researcher, was born in Wales in 1948. He is the head and director of the Litwin-Zucker Research Center for The Study of Alzheimer’s Disease and Memory Disorders [1] associated with The Feinstein Institute for Medical Research in Manhasset, NY.
Education
Peter Davies received his B.Sc. (Hons., 1st class) and Ph.D. 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.
Academic appointments
In 1977, Davies moved to Albert Einstein College of Medicine in the Bronx, where he was an assistant professor from 1977 to 1981, an associate professor from 1981 to 1986, and a professor from 1986 to date.[2] 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.
Principal scientific contributions
For more than 35 years, Davies’ research has been focused on the biochemistry of Alzheimer's disease. His early work was instrumental in the development of the currently approved drugs for Alzheimer’s disease: Aricept, Exelon, and Razodyne. Davies is interested in the pathway of Alzheimer’s disease and has said that the disease may be a process of cell cycle division gone wild. He has 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.[3] They put a viral oncogene into differentiated neurons and watched as pathological events unfolded. Davies and his collaborators have already identified a marker in cerebrospinal fluid (CSF) that can distinguish Alzheimer’s disease from normal aging, as well as discriminate between Alzheimer’s and other forms of dementia.[4] The overall goal of Davies’ research is to develop treatments to slow or halt the progression of Alzheimer’s disease. Davies is internationally known for his work in unravelling the mystery of Alzheimer’s disease.
Awards and honors
- Sex Education Award
- International Congress on Alzheimer’s Disease (ICAD) Lifetime Achievement Award
- Metropolitan Life Foundation Prize
- National Institute of Health (NIH) MERIT award NIMH, 1989–1999
- National Institute of Health (NIH) MERIT award NIA, 2003–2013
- Author of over 250 published research papers
- The Bahbhani award for scientific achievement
- The 2012 Long Island Alzheimer's Foundation (LIAF) award
• The 2015 Potamkin Award for research in Pick's, Alzheimer's, and related diseases
Multimedia
Selected publications
- Hampel H, Buerger K, Zinkowski R, Goernitz A, Teipel SJ, Andreasen N, Sjogren M, DeBernardis J, Kerkman D, Ishiguro K, Ohno H, Vanmechelen E, Vanderstichele H, McCulloch C, Möller HJ, Davies P, Blennow K. Measurement of phosphorylated tau epitopes in the differential diagnosis of Alzheinmer's disease - a comparative CSF study, Archives of General Psychiatry, 61; 95-102, 2004
- Conrad C. Vianna C. Schultz C. Thal DR. Ghebremedhin E. Lenz J. Braak H. Davies P. Molecular Evolution and Genetics of the Saitohin Gene and tau haplotype in Alzheimer’s Disease and Argyrophilic Grain Disease. J Neurochem, 89, 179-188, 2004.
- Bargorn S. Davies P. Mandelkow E. Tau paired helical filaments from Alzheimer’s disease brain and assembled in vitro are based on beta-structure in the core domain" Biochemistry 43, 1694–1703, 2004.
- Andorfer CA. Acker CM. Kress Y. Hof PR. Duff K. Davies P. Cell Cycle Re-entry and Cell Death In Transgenic Mice Expressing Non-Mutant Human Tau Isoforms" J Neurosci 25; 5446-5454, 2005.
- Marambaud P. Zhao H. Davies P. Resveratrol promotes clearance of Alzheimer’s disease amyloid-beta peptides" J Biol Chem 280, 37377-37382, 2005.
- de Leon MJ. DeSanti S. Zinkowski R. Mehta PD. Pratico D. Segala S. Rusinek H. Lia J. Tsui W. Saint Louis LA. Clark CM. Tarshish C. Lia Y. Lair L. Javier E. Rich K. Lesbre P. Mosconi L. Reisberg B. Sadowski M. DeBernadis JF. Kerkman DJ. Hampel H. Wahlund L-O. Davies P. Longitudinal CSF and MRI biomarkers improve the diagnosis of mild cognitive impairment. Neurobiology of Aging 27, 394-401, 2006.
- d’Abramo C. Ricciarelli R. Pronzato MA. Davies P. Troglitazone, a Peroxisome Proliferator-activated Receptor-gamma agonist, decreases tau phosphorylation in CHOtau4R cells" J. Neurochem 98, 1068–1077, 2006.
- Park KHJ. Hallows JL Chakrabarty P Davies P Vincent I. Conditional neuronal SV40 T Antigen expression induces Alzheimer-like tau and amyloid pathology in mice" J Neurosci 27, 2969–2978, 2007.
- Espinoza M. de Silva R. Dickson DW. Davies P. Differential Incorporation of Tau Isoforms in Alzheimer’s Disease. Journal of Alzheimer’s Disease, 14, 1-16, 2008.
References
- ↑ http://www.feinsteininstitute.org/research-topics/neuroscience/alzheimers/
- ↑ "Faculty Profile: Peter Davies". Albert Einstein College of Medicine Directory. Retrieved 1 August 2011.
- ↑ "Cell Cycle Re-entry and Cell Death In Transgenic Mice Expressing Non-Mutant Human Tau Isoforms". J Neurosci. 25: 5446–5454. 2005. doi:10.1523/jneurosci.4637-04.2005.
- ↑ "Measurement of phosphorylated tau epitopes in the differential diagnosis of Alzheinmer's disease - a comparative CSF study". Archives of General Psychiatry. 61 (1): 95–102. 2004. doi:10.1001/archpsyc.61.1.95. PMID 14706948.