The authors disclose the following financial relationships within the past 3 years.
Depression gets old fast: do stress and depression accelerate cell aging?†
Article first published online: 1 APR 2010
© 2010 Wiley-Liss, Inc.
Depression and Anxiety
Volume 27, Issue 4, pages 327–338, April 2010
How to Cite
Wolkowitz, O. M., Epel, E. S., Reus, V. I. and Mellon, S. H. (2010), Depression gets old fast: do stress and depression accelerate cell aging?. Depress. Anxiety, 27: 327–338. doi: 10.1002/da.20686
- Issue published online: 1 APR 2010
- Article first published online: 1 APR 2010
- Manuscript Accepted: 13 FEB 2010
- Manuscript Revised: 12 FEB 2010
- Manuscript Received: 9 NOV 2009
- O'Shaughnessy Foundation
- University of California
Vol. 27, Issue 7, 693, Article first published online: 28 APR 2010
Depression has been likened to a state of “accelerated aging,” and depressed individuals have a higher incidence of various diseases of aging, such as cardiovascular and cerebrovascular diseases, metabolic syndrome, and dementia. Chronic exposure to certain interlinked biochemical pathways that mediate stress-related depression may contribute to “accelerated aging,” cell damage, and certain comorbid medical illnesses. Biochemical mediators explored in this theoretical review include the hypothalamic–pituitary–adrenal axis (e.g., hyper- or hypoactivation of glucocorticoid receptors), neurosteroids, such as dehydroepiandrosterone and allopregnanolone, brain-derived neurotrophic factor, excitotoxicity, oxidative and inflammatory stress, and disturbances of the telomere/telomerase maintenance system. A better appreciation of the role of these mediators in depressive illness could lead to refined models of depression, to a re-conceptualization of depression as a whole body disease rather than just a “mental illness,” and to the rational development of new classes of medications to treat depression and its related medical comorbidities. Depression and Anxiety, 2010. © 2010 Wiley-Liss, Inc.