Dr. Kambiz Alavian is a Lecturer in the Division of Brain Sciences, Department of Medicine, Imperial College London. He is also an Adjunct Assistant Professor of Medicine at Yale University School of Medicine. He received his PhD in Neuroscience from the University of Heidelberg and completed postdoctoral trainings at Harvard and Yale. He currently investigates mitochondrial bioenergetics and cell death and their implications in neurological disorders and cancer.
Mitochondria perform several critical functions including cellular energy production and initiation of cellular apoptosis. Resistance to mitochondrial cell death is one of the main features of cancer cells and mitochondrial dysfunction, including changes in the structural integrity of mitochondria, disruption of energy metabolism and abnormal calcium (Ca2+) buffering, has been implicated in neurodegenerative disorders. The current scientific interests of Dr. Alavian’s group include the study of basic molecular mechanisms leading to such dysfunctions and translation of these findings to novel therapeutic approaches for neurodegenerative conditions and cancer.
et al., 2015, Decreased SGK1 Expression and Function Contributes to Behavioral Deficits Induced by Traumatic Stress, PLOS Biology, Vol:13, ISSN:1545-7885
et al., 2014, An uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition pore, Proceedings of the National Academy of Sciences of the United States of America, Vol:111, ISSN:0027-8424, Pages:10580-10585
et al., 2013, A Bcl-x(L)-Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis, Nature Cell Biology, Vol:15, ISSN:1465-7392, Pages:773-+
et al., 2011, Bcl-x(L) regulates metabolic efficiency of neurons through interaction with the mitochondrial F1F0 ATP synthase, Nature Cell Biology, Vol:13, ISSN:1465-7392, Pages:1224-U130
et al., 2012, N-terminally cleaved Bcl-x(L) mediates ischemia-induced neuronal death, Nature Neuroscience, Vol:15, ISSN:1097-6256, Pages:574-580