Department Neurology Hospital Title Senior Associate in Neurology Academic Title Associate Professor of Neurology Phone 617-919-2634 Fax 617-919-2380 Email Paul Rosenberg Location 300 Longwood Avenue CLS 13073 Boston MA 02115 Research Overview Paul Rosenberg's current research focuses on two areas--disorders of the brain and sleep disturbances. In the first line of research, he seeks to understand the mechanisms of brain injury in order to provide a rational basis for preventing and treating important neurological disorders and diseases. In pursuit of this goal, he is working to characterize pathways of cell death in neurons and oligodendrocytes. He is currently investigating how expression and function of the glutamate transporter GLT1 is regulated at normal synapses and how GLT1 function is compromised in neurodegenerative diseases. In the second, he is investigating the biochemical and molecular basis of behavioral state regulation to provide the foundation for developing better pharmacological treatments for sleep disorders. To this end, he is currently investigating the role of nitric oxide and adenosine in regulating behavioral states. About Paul Rosenberg Paul Rosenberg received his MD and PhD degrees from Albert Einstein College of Medicine. He completed an internship at University Hospital, Boston, a neurology residency through the Harvard-Longwood Neurological Training Program, and a fellowship at Children's Hospital Boston. Key Publications Chen, W. Mahadomrongkul, V., Berger, U.V., Bassan, M., DeSilva, T., Tanaka, K., Irwin, N., Aoki, C., Rosenberg, P.A. 2004. The glutamate transporter GLT1a is expressed in excitatory axon terminals of mature hippocampal neurons. Journal of Neuroscience. 24: 1136-1148. Baud, O., Greene, A.E., Li, J., Wang, H., Volpe, J.J., and Rosenberg, P.A. 2004. Glutathione peroxidase-catalase cooperativity is required for resistance to hydrogen peroxide by mature rat oligodendrocytes. Journal of Neuroscience. 24: 1531-1540 Rosenberg PA, Le M, Li Y. 2000. Nitric oxide stimulated increase in extracellular adenosine accumulation in rat forebrain neurons in culture is associated with ATP hydrolysis and inhibition of adenosine kinase activity. Journal of Neuroscience. 20: 6294-6301
Mental retardation can occur as a result of perinatal brain injury in both the term and preterm neonate. The overall goal of this research program is to elucidate age-specific mechanisms of hypoxic/ischemic perinatal brain injury and to devise age-specific therapeutic strategies for this injury. The specific focus of the laboratory is on two common sequelae of hypoxia/ischemia in the newborn, neonatal seizures and periventricular leukomalacia (PVL). The highest incidence of seizures during life occurs in the neonatal period, and one of the most common causes of seizures in this period is hypoxic/ischemic encephalopathy. Seizures associated with hypoxia are often refractory to therapy and can be associated with long term epilepsy. A research goal is to determine the age-specific mechanisms of such seizures that might contribute to their relative resistance to conventional antiepileptic drugs that are effective at older ages and also to determine the effect of these seizures on subsequent brain development and epileptogenesis later in life. The second major focus of the laboratory is on age-specific mechanisms of white matter injury in the developing brain. PVL occurs in preterm infants, is thought to be a result of cerebral hypoxia/ischemia, and is the most common pathology associated with the subsequent diagnosis of cerebral palsy in premature infants. Research goals associated with this project evaluate age-specific mechanisms of OL injury in vitro and in vivo and extend these studies to pharmacologic protective trials in vivo.
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