Tracy L Bale
Department of Animal Biology, University of Pennsylvania, Philadelphia, PA, USA F1000 Section Head (since 24 September 2010)BIOGRAPHY
ACADEMIC POSITION:Associate Professor of Neuroscience, Department of Animal Biology and Psychiatry, Director Neuroscience Center, Vice Chair Neuroscience Graduate Group, University of Pennsylvania.
EDUCATION:
Dr Bale earned her PhD in neurobiology and pharmacology from the University of Washington, Seattle in 1997. Dr Bale completed her postdoctoral training in stress neuroendocrinology at the Salk Institute in La Jolla, CA with Dr Wylie Vale. She joined the faculty at the University of Pennsylvania in 2003 as an Assistant Professor of Neuroscience.
MEMBERSHIPS (including editorial):
• 1995-present Member, Society for Neuroscience
• 1998-present Member, Endocrine Society
• 2008-present Member, Organization for the Study of Sex Differences
• 2007-2011 Editorial Board, Endocrinology
• 2008-2011 Editorial Board, Journal of Neuroscience
• 2007-2010 Editorial Board, Frontiers in Behavioral Neuroscience
• 2010-2013 Editorial Board, Biology of Sex Differences
• 2008-2011 Annual Meeting Steering Committee, Endocrine Society
• 2009-2012 Council, Organization for the Study of Sex Differences
• 2009-2010 International Advisory Board, The Parental Brain Conference
• 2009 Organizer, Early Life Programming of Neurodevelopmental Disorders Conference
HONORS AND AWARDS:
• 1997 National Science Foundation Young Investigator Award
• 2001 American Neuroendocrine Society Fellowship Award
• 2002 American College of Neuropsychopharmacology (ACNP) Award
• 2003 Frank Beach Award, Outstanding Young Investigator in Behavioral Neuroscience, Society for Behavioral Neuroendocrinology
• 2008 Ziskind-Somerfeld Award, most influential paper of the year, Society for Biological Psychiatry
• 2008 Career Development Award, for early career achievement and promise, Society for Neuroscience
• 2011 Richard E Weitzman Memorial Award, exceptionally promising young investigator, Endocrine Society
RESEARCH INTERESTS:
Our research focuses on developing mouse models of increased stress sensitivity related to sex-biased neurodevelopmental and neuropsychiatric diseases. We have initiated multiple lines of investigation that will provide insight into the timing and sex specificity of early life events promoting disease susceptibility, the maturation of central stress pathways during key periods of development, and the epigenetic mechanisms involved in long-term effects following stress exposure. We have focused on utilizing approaches that range from fetal antecedents in programming of long-term disease risk to genetic targeting of cell type specific knockout mice. As women present with affective disorders at more than 2-fold the rate of men, our research aims at defining sex differences in stress pathway development and maturation, and the epigenetic programming events that intersect with these events that may underlie disease etiology.
HOME PAGE
http://www.med.upenn.edu/apps/faculty/index.php/g293/p4061130
VIDEO
At the Society for Neuroscience (SfN) meeting last week, Tracy Bale, F1000 Section Head in Neural homeostasis, talked to us about her research on how stress dysregulation underlies neuropsychiatric disease.
It seems that there is truth behind the age-old belief that stress in pregnancy can harm the child. Tracy explains that stress experienced by the mother in early pregnancy can determine sex differences in how the offspring deal with stress. Early prenatal stress changes the microRNA environment in the brain of the offspring, affecting the male prenatal testosterone surge, which is thought to be the key factor behind gender identity development.
Tracy believes that these pathways could account for the sex biases in neurodevelopmental diseases such as autism, where boys are 4 times more likely than girls to be affected. And the next step in this research? Tracing what genes these micro RNAs target, so that in the future we may be able to intervene to alter the affects of prenatal stress. [Video recorded 19 April 2012]
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