Lower Risk For Alzheimer’s Associated With High Blood Pressure

People with a genetic predisposition to high blood pressure may be at lower risk of developing Alzheimer’s disease, reports a new study. Researchers caution this link is likely due to antihypertensive medications and the conditions.

The sixth-leading cause of death in the US, Alzheimer’s is expected to claim the lives of around 700,000 people aged 65 and older this year. It is the sole cause of death in the top 10 that cannot be prevented, cured or slowed.

Study co-author John Kauwe, associate professor of biology at Brigham Young University, along with his colleagues, write that researchers are now working to find risk factors for Alzheimer’s:

“If such risk factors exist,” they say, “it might be possible to limit the predicted increase in future Alzheimer’s disease cases.”

The study looked at genetic data of 17,008 individuals with Alzheimer’s and 37,154 people without the disease. The team researched for associations between Alzheimer’s disease and numerous of health conditions such as obesity, diabetes, and high cholesterol.

The only significant association found was higher systolic blood pressure and reduced Alzheimer’s risk.

Co-author Paul Crane, associate professor of internal medicine at University of Washington, said:

“Our results are the opposite of what people might think. It may be that high blood pressure is protective or it may be that something that people with high blood pressure are exposed to more often, such as antihypertensive medication, is protecting them from Alzheimer’s disease.”

Associations between Potentially Modifiable Risk Factors and Alzheimer Disease: A Mendelian Randomization Study
Søren D. Østergaard, Shubhabrata Mukherjee, Stephen J. Sharp, Petroula Proitsi, Luca A. Lotta, Felix Day, John R. B. Perry, Kevin L. Boehme, Stefan Walter, John S. Kauwe, Laura E. Gibbons, Alzheimer’s Disease Genetics Consortium , The GERAD1 Consortium , EPIC-InterAct Consortium , Eric B. Larson, John F. Powell, Claudia Langenberg, Paul K. Crane, Nicholas J. Wareham, Robert A. Scott
PLOS Medicine 10.1371/journal.pmed.1001841

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