Public Release: 

New Alzheimer's findings: High stress and genetic risk factor lead to increased memory decline

Elsevier

Philadelphia, PA, August 27, 2007 - High stress levels may contribute to memory loss among people at risk for developing Alzheimer's disease. The å4 variant of the apolipoprotein E (APOE) gene contributes to the risk for memory loss related to Alzheimer's disease. Similarly, high circulating levels of cortisol, associated with high stress levels, also impairs memory. However, the interactive effects of this risk genotype and chronic stress are not well understood, so a new study being published in the September 1st issue of Biological Psychiatry was designed to explore this relationship.

In their study, Peavy and colleagues performed genotyping and measured the chronic stress level in 91 older, healthy subjects (mean age was 78.8 years). Those low on stress or without the APOE-å4 risk factor performed better on memory measures than those with high stress or those positive for APOE-å4, respectively. Those individuals experiencing high stress and who were positive for APOE-å4 showed the greatest memory impairment.

One of the authors, Guerry M Peavy, Ph.D., comments, "Perhaps the most interesting result of the study was the interaction we found between genetic status and the experience of high stress events. That is, for some aspects of memory, highly stressful experiences had a detrimental effect only on those individuals who carried the APOE-å4 allele."

John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, adds:

This is a very exciting time in Alzheimer's disease (AD) research...The findings of Peavy et al. suggest that environmental factors, like chronic stress, may interact with an AD risk genotype, APOE-å4, to promote age-related memory impairment. These data raise the possibility that psycho-social interventions and psychotherapeutic medications might enhance the effectiveness of medication treatment strategies aimed at preserving memory function in older adults.

As noted in their article, because APOE-å4 status and high stress levels can be assessed at any time, these findings may represent an advantage with the earlier identification of elderly individuals who do not yet meet criteria for dementia, but who clearly are more cognitively vulnerable. Dr. Peavy explains, "The results of the study have implications for interventions that could prevent harmful responses to stressful experiences and, as a result, could prevent or slow the progression of cognitive changes in genetically vulnerable, older individuals." For now, longitudinal studies need to be undertaken to determine if these interactive effects of stress and APOE-å4 status become predictors of a clinical diagnosis of dementia.

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Notes to Editors:

The article is "The Effects of Prolonged Stress and APOE Genotype on Memory and Cortisol in Older Adults" by Guerry M. Peavy, Kelly L. Lange, David P. Salmon, Thomas L. Patterson, Sherry Goldman, Anthony C. Gamst, Paul J. Mills, Srikrishna Khandrika and Douglas Galasko. Drs. Peavy, Lange, Salmon, Gamst and Galasko are with the Department of Neurosciences at the University of California in San Diego, California. Dr. Gamst is also affiliated with the Department of Family and Preventive Medicine. Drs. Patterson, Goldman, and Mills are with the Department of Psychiatry, and Dr. Khandrika is with the Department of Medicine in the Clinical Research Center, also at the University of California in San Diego. Drs. Patterson, Goldman, and Galasko are also affiliated with the Veterans Administration Medical Center in San Diego. The article appears in Biological Psychiatry, Volume 62, Issue 5 (September 1, 2007), published by Elsevier.

Full text of the article mentioned above is available upon request. Contact Jayne M. Dawkins at (215) 239-3674 or ja.dawkins@elsevier.com to obtain a copy or to schedule an interview.

About Biological Psychiatry

This international rapid-publication journal, the Official Journal of the Society of Biological Psychiatry, covers the whole range of psychiatric neuroscience. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials, generally invited by the Editors, which focus on topics of current research and interest, are also published rapidly.

Biological Psychiatry (www.sobp.org/journal) is ranked 4th out of the 95 Psychiatry titles and 16th out of 199 Neurosciences titles on the 2007 Journal Citation Reports® published by Thomson Scientific.

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