Finding May Aid in the Treatment of Dementia
Newswise, October 6, 2015 — Brooklyn, NY – Researchers led by Deborah Gustafson, PhD, MS, professor of neurology at SUNY Downstate Medical Center, have shown that women with a gene variant (APOEe4 allele) associated with Alzheimer’s disease experience a steeper decline in body mass index (BMI) after age 70 than those women without the version of the gene, whether they go on to develop dementia or not.
The finding adds to a body of evidence suggesting that body weight change may aid in the diagnosis and management of Alzheimer's disease.
The results of the study are published online in the Journal of Alzheimer's Disease 48(4). The article is entitled, “37 Years of Body Mass Index and Dementia: Effect Modification by the APOE Genotype: Observations from the Prospective Population Study of Women in Gothenburg, Sweden.” Dr. Gustafson is also docent and affiliate researcher, University of Gothenburg, Sahlgrenska Academy, Neuropsychiatric Epidemiology Research Unit, in Sweden.
Dr. Gustafson notes that women tend to evidence a U-shaped relationship between age and body weight or body mass index (BMI), a common marker of overweight and obesity. From middle age to approximately 70 years of age, adults gain weight on average.
After age 70, weight tends to decrease on average. This weight change over the life course may be due to aging, changes in body composition, energy metabolism, sensory changes, and changes in the brain related to regulation of basic body processes.
Among adults who develop dementia, however, the life course of BMI differs. Studies have shown that being more overweight or obese in mid-life may increase risk for dementia.
Studies have also shown that after age 70 years, adults who develop dementia may lose weight more rapidly compared to those who do not develop dementia and that if one is a bit more overweight in later life, it is protective for both dementia and death.
Dr. Gustafson explains, “In this study, we followed Swedish women for almost 40 years from mid-life ages of 38-60 years. We tracked their BMI in relation to dementia onset, and considered the potential role of the APOEe4 allele, a known risk factor for late-onset dementia.”
She adds, “In a previous publication, we showed that development of dementia is associated with specific pattern of BMI change over the life course. Women who developed dementia after age 65 tended to gain BMI at a slower rate during middle age.”
Dr. Gustafson concludes, “Now, we show that those with the APOEe4 allele experience greater or steeper decline in BMI after age 70 years, whether they develop dementia or not. Body weight change and BMI are easily measured, noninvasive potential prognostic indicators for dementia. Better understanding of a relatively common risk allele such as APOEe4 and how it modifies risk may aid in our understanding of how we can better intervene among those at highest risk for dementia.”
An abstract of the article,
An abstract of the article,
Bäckman, EJ, Waern, M, Östling, S, Guo,X, Blennow, K, Skoog, I, Gustafson, DR, 37 Years of Body Mass Index and Dementia: Effect Modification by the APOE Genotype: Observations from the Prospective Population Study of Women in Gothenburg, Sweden, Journal of Alzheimer’s Disease (2015), doi: 10.3233/JAD-150326., is available here: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad150326 .
More information about the APOE gene is available from Genetics Home Reference, a service of the U.S. National Library of Medicine, here: http://ghr.nlm.nih.gov/gene/APOE .
The research leading to the results published in the Journal of Alzheimer's Disease has received funding from the EU 7th framework LipiDiDiet project (FP7/2007-2015) under grant agreement no211696; Swedish Research Council for Health, Working Life and Welfare (AGECAP 2013-2300; 2013-2496); National Institutes of Health (NIH)/National Institute of Allergy and Infectious Diseases(NIAID) U01 318345; Swedish Research Council (523-2005-8460; 2013-8717; 11267; 825-2012-5041) and the State University of New York Research Foundation.
Other funders include the National Institutes of Health/National Institutes on Aging; Swedish Council for Working Life and Social Research, The Alzheimer's Association Stephanie B. Overstreet Scholars (IIRG-00-2159), Sahlgrenska University Hospital (ALF),Swedish Alzheimer Association, Stiftelsen Söderström-Königska Sjukhemmet, Stiftelsen för Gamla Tjänarinnor, Hjalmar Svenssons Foundation, The Swedish Society of Medicine, The Gothenburg Medical Society, the Lions Foundation, the Dr. Felix Neubergh Foundation, the Wilhelm and Martina Lundgren Foundation, the Elsa and Eivind Kison Sylvan Foundation, the Alzheimer’s Association Zenith Award, and State University of New York Research Foundation. All researchers are independent of funders.
The content of the published article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, NIAID, or other funders.