Abstract
Because the reported heightened female predisposition in these diseases seems to present after puberty, determination of stress pathway maturation may shed light on whether differences in disease presentation, treatment, and risk are a function of gonadal hormone profiles and/or more inherent to genetic sex (Fig. 2). Unarguably, our work in understanding sex differences in these diseases has just scratched the surface. We have only begun exploring the possible involvement of exciting areas such as intrauterine environment, epigenetics, and proteomics in longterm disease risk. An even greater scarcity exists for information on how these regulatory mechanisms could be built into sex-specific outcomes. It is clear, to answer the question of whether "being female is a predisposing factor," we are in desperate need of novel animal models and paradigms (Kalueff et al., 2007), in which such comparisons can be carefully studied. Copyright © 2007 Society for Neuroscience.
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Becker, J. B., Monteggia, L. M., Perrot-Sinal, T. S., Romeo, R. D., Taylor, J. R., Yehuda, R., & Bale, T. L. (2007). Stress and disease: Is being female a predisposing factor? In Journal of Neuroscience (Vol. 27, pp. 11851–11855). https://doi.org/10.1523/JNEUROSCI.3565-07.2007
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