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School of Medicine
Dr Valina L. Dawson
Director, Bioenergetics Core B
Valina L. Dawson, PhD, is a Professor of Neurology, Neuroscience, Physiology and the Graduate Program in Cellular & Molecular Medicine. She is co-director of the Neuroregeneration and Stem Cell Programs in the Institute for Cell Engineering. She has had a long-standing interest in mechanisms of neuronal cell death. She described for the first time that NO mediated glutamate neurotoxicity. In a series of studies she described the activation and regulation of nNOS in terms of neurotoxicity, and identified poly(ADP-ribose) polymerase (PARP-1) as a potential downstream target mediating neurotoxicity. Additionally, this team conducted experiments that showed that endogenously produced peroxynitrite is likely the nitrogen oxide moiety that mediates, in large part, NO neurotoxicity.
In 1994, Dr Valina L. Dawson joined the Department of Neurology at the Johns Hopkins University School of Medicine where she has continued to define the conditions under which NO is neurotoxic as well as define conditions in which NO is not neurotoxic and likely plays a role as a neuromodulator.
She has performed experiments describing the neurotoxic actions of iNOS and correlated this with the progression and severity of AIDS dementia. nNOS neurons, which produce neurotoxic quantities of NO, are themselves resistant to toxicity. She described increased expression of MnSOD as one factor contributing to nNOS neuronal resistance to NO neurotoxicity and excitotoxic mechanisms.
Recently her group has been instrumental in uncovering the role of AIF in mediating PARP-1 dependent neurotoxicity. Dr Dawson has contributed significantly to the field of neurotoxicity and has published over 260 full-length manuscripts and review articles, many with high citation impact. She showed that DJ-1 is an atypical peroxidoxine like peroxidase and showed that LRRK2 possesses kinase activity and disease causing mutations in LRRK2 lead to cell death that is kinase-dependent. Recently she identified drugs that block the neurotoxicity caused by LRRK2. These studies are providing major insights into understanding the pathogenesis of Parkinson’s disease and are providing novel opportunities for therapies aimed at preventing the degenerative process of Parkinson’s disease. She leads Project 3 investigating the role of LRRK2 in Parkinson’s disease.
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