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DEPRESSION GETS OLD FAST: DO STRESS AND DEPRESSION ACCELERATE CELL AGING?

期刊

DEPRESSION AND ANXIETY
卷 27, 期 4, 页码 327-338

出版社

WILEY
DOI: 10.1002/da.20686

关键词

depression; stress; aging; cortisol; BDNF; DHEA; telomeres; oxidation; inflammation; allopregnanolone

资金

  1. O'Shaughnessy Foundation
  2. University of California, San Francisco, Academic Senate
  3. Jazz Pharmaceuticals
  4. Merck Pharmaceuticals
  5. NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH083784] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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 cerebro vascular 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 mediatory explored in this theoretical review include the hypothalamic-pituitary-adrenal axis (e.g., hyperor 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 27:327-338, 2010. (C) 2010 Wiley-Liss, Inc.

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