Obese mice with a particular version of a gene strongly associated with Alzheimer's disease (AD) in humans show increased Alzheimer's pathology, according to new research published in eNeuro. The study suggests lifestyle changes could reduce the likelihood of developing AD in individuals with this genetic predisposition.
Individuals who inherit the gene APOE4 -- approximately 12 percent of the U.S. population -- have an increased risk of late-onset AD, but not all carriers develop the disease. Although the role of APOE4 in AD is not known, environmental factors that also increase risk of dementia, such as obesity, may contribute to development of AD.
Christian Pike and Alexandra Moser investigated the interaction between APOE4 and obesity in a mouse model of AD, in which some male mice carry the human version of APOE4 and others carry the more common human version APOE3. The authors found that APOE4-carrying mice fed a Western-like diet high in saturated fat and sugars for 12 weeks had increased deposits of β-amyloid protein as well a greater number of glial cells, characteristic of AD. These changes were not observed in mice carrying APOE3, which could mean that carriers of APOE4 are more susceptible to the effects of obesity on AD.
Article: Obesity accelerates Alzheimer-related pathology in APOE4 but not APOE3 mice
Corresponding author: Christian Pike (Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, USA), email@example.com
eNeuro is an online, open-access journal published by the Society for Neuroscience. Established in 2014, eNeuro publishes a wide variety of content, including research articles, short reports, reviews, commentaries and opinions.
The Society for Neuroscience is the world's largest organization of scientists and physicians devoted to understanding the brain and nervous system. The no