Insulin resistance, glucose uptake in the brain in adults at risk for Alzheimer's

July 27, 2015

An imaging study suggests insulin resistance, a prevalent and increasingly common condition, was associated with lower brain glucose metabolism in a group of late middle-age adults at risk for Alzheimer disease, according to an article published online by JAMA Neurology.

Insulin resistance is broadly defined as reduced tissue responsiveness to the action of insulin. According to the American Diabetes Association, 29.1 million individuals in the United States have diabetes and more than half of adults older than 64 have prediabetes. Type 2 diabetes is associated with an increased risk for Alzheimer disease (AD). Insulin has been increasingly recognized as playing an important role in the brain, according to the study background.

Barbara B. Bendlin, Ph.D., of the University of Wisconsin School of Medicine and Public Health, Madison, and coauthors studied 150 cognitively normal, late middle-age adults (average age nearly 61), who underwent cognitive testing, a fasting blood draw and fludeoxyglucose F 18-labeled positron emission tomography of the brain.

Of the 150 participants, 108 (72 percent) were women, 103 (68.7 percent) had a parental history of AD, 61 (40.7%) had an APOE ε4 allele and seven (4.7 percent) had type 2 diabetes.

The authors found insulin resistance was associated with lower global glucose metabolism and lower regional glucose metabolism across large portions of the brain in the frontal, lateral, parietal, lateral temporal and medial temporal lobes. Lower glucose metabolism in the left medial temporal lobe was related to worse performance in immediate memory.

"The prevalence of AD continues to grow, and midlife may be a critical period for initiating treatments aimed at preventing or delaying the onset of AD. Accumulating evidence suggests that treatments targeting mechanisms involved in insulin signaling may affect central glucose metabolism and should be investigated in the context of presymptomatic AD," the study concludes.

(JAMA Neurol. Published online July 27, 2015. doi:10.1001/jamaneurol.2015.0613. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor's Note: This study was supported by a variety of sources. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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Media Advisory: To contact corresponding author Barbara B. Bendlin, Ph.D., call Susan Lampert Smith at 608-890-5643 or email SSmith5@uwhealth.org.

To place an electronic embedded link in your story: Links will be live at the embargo time: http://archneur.jamanetwork.com/article.aspx?doi=10.1001/jamaneurol.2015.0613

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