Department of Pharmacology & Chemical Biology at the University of Pittsburgh
Jane Cavanaugh, PhD
Adjunct Research Assistant Professor
Mellon Hall, Room 455
600 Forbes Avenue, Pittsburgh, PA 15282

Email:
cavanaughj@duq.edu
Phone: 412-396-6358

Fax: 412-396-4660


Education
BA, Franklin and Marshall.
PhD, Pennsylvania State College of Medicine.
Photo of Jane Cavanaugh, PhD

Neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's Diseases, are progressively debilitating disorders that alter mood, higher mental and motor functions and ultimately result in death. Caloric restriction (CR) has been shown to increase lifespan and decrease susceptibility to neurodegenerative disorders. However, limited studies have examined the physiological and molecular mechanisms by which CR protects neurons. My current research involves examination of the regulation of the mitogen activated protein kinase (MAPK) signal transduction pathways and apoptosis in the aging hippocampus of ad libitum and CR animals. I am currently examining the activity of two MAP kinases shown to play a role in neuronal survival and cell death, ERK1/2 and p38, respectively.


Accumulation of ß-amyloid (Aß) peptides is a common feature of Alzheimer's disease (AD). Reports suggest that fibrillar Aß induces apoptosis in neurons and that this cell death is partially responsible for the cognitive decline experienced by AD patients. Neurotransmitter loss has also been implicated in the etiology of AD, with a degeneration of serotonin (5-hydroxytryptamine; 5HT)-containing neurons in the brains of AD patients. Interestingly, 5HT activates the MAPK pathways that are involved in neuroprotection. However, a protective role for 5HT- mediated activation of MAPKs in mediation of Aß- induced neuronal apoptosis remains to be explored. Therefore, a second area of current research involves examination of the roles of ERK1/2, PI3K and ERK5 activation in 5HT- mediated neuroprotection from A? - induced apoptosis. Knowledge of these signaling mechanisms is essential to the development of new therapeutic approaches for the treatment of Alzheimer's and other neurodegenerative diseases.





Important Publications
Cavanaugh JE. Role of extracellular signal regulated kinase 5 in neuronal survival. Eur J Biochem 271(11):2056-2059, 2004.
Liu L=, JE Cavanaugh=, Y Wang, H Sakagami, Z Moa and Z Xia. ERK activation of MEF2-mediated gene expression plays a critical role in BDNF-mediated survival of developing but not mature cortical neurons. Proc Nat Acad Sci 100(14):8532-8537 =these authors contributed equally, 2003.
Cavanaugh JE, J Ham, M Hetman, S Poser, C Yan and Z Xia. Differential regulation of mitogen activated protein kinases ERK1/2 and ERK5 by neurotrophins, neuronal activity and cAMP in neurons. J Neurosci 21(2):434-443, 2001.
Hetman M, JE Cavanaugh, D Kimelman and Z Xia. Role of glycogen synthase kinase-3ƒÒ in neuronal apoptosis induced by trophic withdrawal. J Neurosci 20(7): 2567-2574, 2000.
Hetman M, K Kanning, JE Cavanaugh and Z Xia. Neuroprotection by brain-derived neurotrophic factor is mediated by extracellular signal-related kinase and phosphatidylinositol-3-kinase. J Biol Chem 274:22569-22580, 1999.




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