Sean P. Cregan
Why I Became a Scientist
As a scientist you have the opportunity to discover things that nobody else ever has and I have always found this to be exciting, motivating and challenging.
Cell death contributes to the loss of brain function in stroke and neurodegenerative diseases such as Parkinson’s, Alzheimer’s and Huntington’s disease. Dr. Cregan’s research program is focused on identifying the molecules that trigger cell death in the brain and determining how they are activated and function. These cell death regulating factors will be attractive targets for the development of drugs to promote cell survival and maintain brain function in individuals affected by these devastating neurodegenerative conditions.
What are the molecular pathways that regulate BAX activation in different neurodegenerative conditions?
What are the key p53-independent mediators of PUMA induction?
How does neuroinflammation affect neural precursor (stem) cell activity?
All three of these research questions could have major implications for stroke, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and ALS.
- PhD, Cell Biology, University of Ottawa
- BSc, Biochemistry, Cornell University
- Postdoctoral training, Ottawa Health Research Institute
- Canada Research Chair
- CIHR New Investigator
- Ontario Early Researcher Award
Steckley D, Karajgikar M, Dale LB, Fuerth B, Swan P, Drummond-Main C, Poulter MO, Ferguson SS, Strasser A, and Cregan SP (2007), PUMA is a dominant regulator of oxidative stress induced Bax activation and neuronal apoptosis. J. Neurosci. 27(47):12989-12999.
SP Cregan, N Arbour, JG MacLaurin, SM Callaghan, A Fortin, ECC Cheung, AE Mackenzie, DS Park, and RS Slack (2004), P53 activation domain 1 is essential for PUMA upregulation and p53-mediated neuronal cell death. J Neurosci. 24(44), 10003-10012.
Phone: 519-931-5777 ext. 24134