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| Francesca Bosetti, Ph.D., Investigator |
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Dr. Bosetti received her Pharm.D. from the University of Pisa, Italy in 1996 and her Ph.D. in Molecular and Experimental Medicine in 2000 from "Sant' Anna School of Advanced Studies", Italy. She did her postdoctoral training with Stanley Rapoport at the National institute on Aging, where she identified the arachidonic acid cascade as a common therapeutic target of mood stabilizers.
She joined the National institute on Aging as an investigator in the Brain Physiology and Metabolism Section in 2004, where she is currently investigating the mechanisms underlying inflammatory and excitotoxic brain damage.
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Staff:
- Saba Aid, Ph.D., Postdoctoral Fellow, (301) 496-6636 aidsab@mail.nih.gov
- Robert Bonow, Post baccalaureate Fellow, (301) 402-7672 bonowrh@mail.nih.gov
- Sang-Ho Choi, Ph.D., Postdoctoral Fellow, (301) 594-5079 choisa@mail.nih.gov
- Sara Palumbo, Predoctoral Fellow, (301) 496-8970 palumbos@mail.nih.gov
- Christopher D. Toscano, Ph.D., Postdoctoral Fellow, (301) 594-3890 toscanoc@mail.nih.gov
Research Interests:
Glutamate neurotransmission, inflammatory mediators, and oxidative stress are increased in acute and chronic neurological and neurodegenerative diseases, as well as aging. While the exact sequence of events that culminate in neuronal death are unknown, an understanding of the genetic characteristics and molecular mechanisms that trigger excitotoxic and inflammatory cell death may offer therapeutic strategies for such disorders. The research goal of our group is to elucidate the role of the arachidonic acid cascade in the mechanism of neuroinflammation and neurodegeneration using knockout and transgenic mice models.
Since excitotoxicity is thought to play a role in neurodegenerative diseases, we are using cyclooxygenase (COX)-1 and COX-2 deficient mice to examine the role of these enzymes in mediating excitotoxic neuronal damage. Our data indicate that COX-2 deficient mice are more vulnerable to kainate and NMDA-induced seizures and neuronal damage and that their increased susceptibility may involve changes in GABAergic neurotransmission. We have also demonstrated specific and distinct roles of COX-1 and COX-2 in mediating the neuroinflammatory response to intracerebroventricularly (icv) injected lipopolysaccharide (LPS), a model of directly activated innate immunity in brain. Our goals are to elucidate the role of COX-1 and COX-2 and their downstream signaling pathways in neuroinflammation in order to develop better therapeutic approaches for those neurodegenerative diseases with a marked inflammatory component.
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Selected Recent Publications:
Toscano CD , Ueda Y , Tomita YA , Vicini S , Bosetti F . (2008) Altered GABAergic neurotransmission is associated with increased kainate-induced seizure in prostaglandin-endoperoxide synthase-2 deficient mice., Brain Res Bull 75, 598-609.
Choi SH , Langenbach R , Bosetti F . (2008) Genetic deletion or pharmacological inhibition of cyclooxygenase-1 attenuate lipopolysaccharide-induced inflammatory response and brain injury., FASEB J 22, 1491-501.
Aid S, Langenbach R, Bosetti F. (2008) Neuroinflammatory response to lipopolysaccharide is exacerbated in mice genetically deficient in cyclooxygenase-2., J Neuroinflammation 5, 17.
Bosetti F . (2007) Arachidonic acid metabolism in brain physiology and pathology: lessons from genetically altered mouse models., J. Neurochem 102, 577-86.
Toscano CD , Prabhu VV , Langenbach R , Becker KG , Bosetti F . (2007) Differential gene expression patterns in cyclooxygenase-1 and cyclooxygenase-2 deficient mouse brain., Genome Biol 8(1), R14.
Choi SH, Langenbach R, Bosetti F. (2006) Cyclooxygenase-1 deficient mice show compensatory upregulation of cyclooxygenase-2 and changes in upstream and downstream enzymes in brain arachidonic acid cascade., J Neurochem 98, 801-811.
All Selected Publications
Contact Information:
Dr. Francesca Bosetti
Bldg. 9, Rm. 1S126
Bethesda, MD 20892-
Telephone: (301) 594-5077 (office),
(301) 402-0074 (fax)
Email: frances@mail.nih.gov
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