Conrad Alano, PhD
|School||UCSF School of Medicine|
|Address||4150 Clement St|
San Francisco CA 94121
Conrad C. Alano, Ph.D. is a graduate of UC Berkeley (B.A.) and University of Rochester School of Medicine (Ph.D.). He further received training as a REAP fellow in the Neurology Department with Raymond A. Swanson, M.D. at the San Francisco VA Medical Center. Dr. Alano's research has advanced our understanding of the role of mitochondria in various CNS and cardiovascular injury models. Dr. Alano is an active member of the Society for Neuroscience, American Heart Association, American Stroke Association, Mitochondrial Research Society, and the United Mitochondrial Disease Foundation. He has served as an ad hoc reviewer for various journals including Journal of Neuroscience, Journal of Neurochemistry, Journal of Cell Biology, Journal of Neuroscience Research, and the Journal of Cardiovascular Pharmacology. Dr. Alano has received numerous awards and honors for his work, including the Kelsey Wright Award for Scientific Excellence in 2003, the Laverna Titus Award in 2004, and a VA Merit Award in 2007.
Various acute and chronic injuries lead to cell death and brain injury. In neurodegenrative diseases, cells die as a result of a complex cascade of events, such as an increase in free radical generation or activation of cell death pathways. In stroke, cells die because they are deprived of oxygen and nutrients. Mitochondria in cells use oxygen and glucose products to produce energy for the cell, which is why they are nicknamed the “powerhouse” of cells. In addition, mitochondria play a central role in numerous fundamental cellular processes ranging from ATP generation and calcium (Ca2+) homeostasis. However, mitochondria also serve as a signal for cells to die. When mitochondria are failing, they send out molecules that signal the initiation of cell death cascades. For example, dysfunction of the mitochondrial Ca2+ homeostasis and an increase in free radical production has been implicated in the development of neurodegenerative diseases, aging, and cardiac injury. These studies should allow us to identify potential therapeutic intervention targeted towards the treatment of brain injury after an acute stroke episode.
To better understand the mechanism of stroke leading to brain injury, the goals of our group are the following:
- Identifying the role of mitochondria in the life and death of brain cells.
- Determining the signals to mitochondrial that switches its role from life to death.
- Characterizing the effects of mitochondrial failure leading to cell death.
- Translating the findings from cell culture models to animal models of stroke, with the overall goal of identifying potential therapeutic intervention for stroke.
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