New Genetic Risk Marker for Late-Life Depression
Discovered by new study in Biological Psychiatry
Discovered by new study in Biological Psychiatry
Philadelphia, PA, November 3, 2015
One of the most powerful predictors in neuropsychiatry is the epsilon 4 (ε4) allele of the apolipoprotein gene (APOE).
Individuals who carry this ε4 variant of APOE are at increased risk for developing Alzheimer’s disease, early age of Alzheimer’s disease onset, and more rapid progression of Alzheimer’s disease symptoms. APOE ε4 has also been associated with atherosclerosis as well as cardiovascular and cerebrovascular disease.
A new study published in the current issue of Biological Psychiatry suggests that even when controlling for the risk for Alzheimer’s disease, the APOE ε4 allele also conveys an increased risk for late-life depression.
In this study, researchers examined the relationship between APOE ε4 and depression in a large population-based sample of 839 older Swedish adults followed over 5 years.
“In our study, the presence of the APOE ε4 predicted future depression, even after excluding individuals who later developed dementia,” explained corresponding author Dr. Silke Kern at the University of Gothenburg. “It was also related to dementia. APOE ε4 might be a marker for identifying older persons at risk to develop depression or dementia, which could be important for prevention and early detection of these common disorders.”
“Late-life depression is an under-appreciated source of distress and disability in older people,” said Dr. John Krystal, Editor of Biological Psychiatry. “The current study suggests a new link to the biology of Alzheimer’s disease, even among people who do not show signs of memory impairment.”
The article is “A 9-Year Prospective Population-Based Study on the Association Between the APOE*E4 Allele and Late-Life Depression in Sweden” by Ingmar Skoog, Margda Waern, Paul Duberstein, Kaj Blennow, Henrik Zetterberg, Anne Börjesson-Hanson, Svante Östling, Xinxin Guo, Jürgen Kern, Deborah Gustafson, Pia Gudmundsson, Thomas Marlow, and Silke Kern (doi: 10.1016/j.biopsych.2015.01.006). The article appears in Biological Psychiatry, Volume 78, Issue 10 (November 15, 2015), published by Elsevier.
Notes for editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Dr. Silke Kern at + 0046 762365332 or email@example.com.
The authors’ affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine, Chief of Psychiatry at Yale-New Haven Hospital, and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
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