English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Life stress, glucocorticoid signaling, and the aging epigenome: Implications for aging-related diseases

MPS-Authors
/persons/resource/persons80333

Gassen,  Nils C.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

/persons/resource/persons80272

Binder,  Elisabeth B.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

/persons/resource/persons160236

Zannas,  Anthony S.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Gassen, N. C., Chrousos, G. P., Binder, E. B., & Zannas, A. S. (2017). Life stress, glucocorticoid signaling, and the aging epigenome: Implications for aging-related diseases. NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 74(Part B SI), 356-365. doi:10.1016/j.neubiorev.2016.06.003.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002D-A78C-0
Abstract
Life stress has been associated with accelerated cellular aging and increased risk for developing aging related diseases; however, the underlying molecular mechanisms remain elusive. A highly relevant process that may underlie this association is epigenetic regulation. In this review, we build upon existing evidence to propose a model whereby exposure to life stress, in part via its effects on the hypothalamic pituitary axis and the glucocorticoid signaling system, may alter the epigenetic landscape across the lifespan and, consequently, influence genomic regulation and function in ways that are conducive to the development of aging-related diseases. This model is supported by recent studies showing that life stressors and stress-related phenotypes can accelerate epigenetic aging, a measure that is based on DNA methylation prediction of chronological age and has been associated with several aging-related disease phenotypes. We discuss the implications of this model for the prevention and treatment of aging-related diseases, as well as the challenges and limitations of this line of research. (C) 2016 Elsevier Ltd. All rights reserved.