David Chaim Rubinsztein (born 1963)
FRS[3]FMedSci[5] is the Deputy Director of the Cambridge Institute of Medical Research (CIMR),[6] Professor of Molecular Neurogenetics at the
University of Cambridge[7] and a UK Dementia Research Institute Professor.
Education
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.[8]
Career
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 400 scientific papers,[4][9] and was ranked as the 4th most cited European author from 2007 to 2013 in
cell biology.[10] Rubinsztein has been invited to give talks at major international conferences, including
Gordon Research Conferences and
Keystone Symposia.[11][12][13]
Research
Rubinsztein has made major contributions to the field of
neurodegeneration[4] 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.[14][15][16][17][18] His lab has found that
autophagy may be inhibited in various neurodegenerative diseases[19] and has elucidated the pathological consequences of
autophagy compromise.[20] In addition his research has advanced the basic understanding of autophagy, identifying the
plasma membrane as a source of autophagosome membrane[21] and characterising early events in autophagosome biogenesis,.[22][23][24] Furthermore, he studied how lysosomal positioning regulates
autophagy.[25] 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[6][26]
^Davies, J. E.; Rubinsztein, D. C. (2005). "Doxycycline attenuates and delays toxicity of the oculopharyngeal muscular dystrophy mutation in transgenic mice". Nature Medicine. 11 (6): 672–677.
doi:
10.1038/nm1242.
PMID15864313.
S2CID13190118.