David C. Rubinsztein
| David Rubinsztein | |
|---|---|
David Rubinsztein in 2014 at the University of Cambridge
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| Born |
David Chaim Rubinsztein 1963 (age 53–54) |
| Alma mater | University of Cape Town (MBChB, PhD) |
| Known for | autophagy and polyglutamine expansions |
| Awards |
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| Website | |
| Scientific career | |
| Fields |
Autophagy Neurodegenerative diseases |
| Institutions |
University of Cambridge Cambridge Institute for Medical Research Cambridge Drug Discovery Institute |
| Thesis | Monogenic hypercholesterolemia in South Africans: familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100 (1993) |
| Doctoral advisor | Prof. D.R. van der Westhuyzen |
David Chaim Rubinsztein (born 1963) FRSFMedSci is the Deputy Director of the Cambridge Institute of Medical Research (CIMR), the Academic Lead of the Alzheimer's Research UK (ARUK) Cambridge Drug Discovery Institute, and Professor of Molecular Neurogenetics at the University of Cambridge.
Rubinsztein completed his Bachelor of Medicine, Bachelor of Surgery (MB ChB) in 1986 and PhD in 1993 in the Medical Research Council/University of Cape Town Unit for the Cell Biology of Atherosclerosis. In 1993 he went to Cambridge as a senior registrar in Genetic Pathology.
In 1997, Rubinsztein acquired his Certificate of Completion of Specialist Training at the University of Cambridge. He was appointed to a Personal Readership at the University of Cambridge in 2003. In 2005, he was promoted to Professor of Molecular Neurogenetics at the University of Cambridge (personal chair). He has been an author on more than 300 scientific papers, and was ranked as the 4th most cited European author from 2007 to 2013 in cell biology. Rubinsztein has been invited to give talks at major international conferences, including Gordon Research Conferences and Keystone Symposia.
Rubinsztein has made major contributions to the field of neurodegeneration with his laboratory's discovery that autophagy regulates the levels of intracytoplasmic aggregate-prone proteins that cause many neurodegenerative diseases, including Huntington's, Parkinson's and Alzheimer's disease. His lab has found that autophagy may be inhibited in various neurodegenerative diseases and has elucidated the pathological consequences of autophagy compromise. In addition his research has advanced the basic understanding of autophagy, identifying the plasma membrane as a source of autophagosome membrane and characterising early events in autophagosome biogenesis,. Furthermore, he studied how lysosomal positioning regulates autophagy. His goal is to understand the links between these diseases and autophagy. He is currently focused on understanding how to induce autophagy in vivo to remove toxic proteins and avoid the development of neurodegenerative disease
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