Daniel M. Michaelson
Daniel M. Michaelson,PhD
Daniel M. Michaelson,PhD,is Professor of Neurobiology at the Department of Neurobiology at Tel Aviv University. He received his Ph.D. in Biophysics at the University of California, Berkeley. His post doctoral training was in neurochemistry at the laboratory of Professor M.A. Raftery at the California Institute of Technology where he studied the nictonic acetylcholine receptors and it's functional reconstitution Professor Michaelson returned to Israel in 1975 to become a lecturer in iochemistry at Tel Aviv University.
He became a full Professor of Neurobiology in 1988, and has spent time as a Visiting Professor at both Stanford and Yale Universities. The research in the Michaelson laboratory is directed at unraveling the basic cellular and molecular mechanisms underlying neurodegenration in Alzheimer's disease and at the development of novel therapeutic approaches to counteract them. The research focuses on apolipoprotein E4 (apoE4) , the most prevalent genetic risk factor of the disease and on the development of therapeutic approaches for counteracting its brain pathological effects.
These range from biochemical approaches directed at repairing structural impairments in apoE4 to immunotherapy which is directed at the removal of apoE4 from the brain.
Daniel M. Michaelson,PhD,is Professor of Neurobiology at the Department of Neurobiology at Tel Aviv University. He received his Ph.D. in Biophysics at the University of California, Berkeley. His post doctoral training was in neurochemistry at the laboratory of Professor M.A. Raftery at the California Institute of Technology where he studied the nictonic acetylcholine receptors and it's functional reconstitution Professor Michaelson returned to Israel in 1975 to become a lecturer in iochemistry at Tel Aviv University.
He became a full Professor of Neurobiology in 1988, and has spent time as a Visiting Professor at both Stanford and Yale Universities. The research in the Michaelson laboratory is directed at unraveling the basic cellular and molecular mechanisms underlying neurodegenration in Alzheimer's disease and at the development of novel therapeutic approaches to counteract them. The research focuses on apolipoprotein E4 (apoE4) , the most prevalent genetic risk factor of the disease and on the development of therapeutic approaches for counteracting its brain pathological effects.
These range from biochemical approaches directed at repairing structural impairments in apoE4 to immunotherapy which is directed at the removal of apoE4 from the brain.
