CHICAGO -- Moderately elevated levels of insulin increase the levels ofinflammatory markers and beta-amyloid in plasma and in cerebrospinalfluid, and these markers may contribute to Alzheimer's disease,according to a new study posted online today from Archives ofNeurology, one of the JAMA/Archives journals. The study will bepublished in the October print edition of the journal.
According to background information in the article, "conditions ofinsulin resistance and hyperinsulinemia are associated with elevatedlevels of inflammatory markers and increase the risk for Alzheimerdisease (AD). Inflammation has been proposed as a key pathogenic factorfor AD."
Mark A. Fishel, M.D., from the University of Washington,Seattle, and colleagues, raised blood insulin levels (while maintainingnormal blood sugar levels) in 16 healthy older adults ranging in agefrom 55 to 81 years, and then measured the changes in levels ofinflammatory markers, modulators, and beta-amyloid (a proteinassociated with AD) in plasma and cerebrospinal fluid.
"Moderate peripheral hyperinsulinemia (increased levels ofinsulin) provoked striking increases in CNS (central nervous system)inflammatory markers," the authors report. "Our findings suggest thatinsulin-resistant conditions such as diabetes mellitus and hypertensionmay increase the risk for AD, in part through insulin-inducedinflammation."
"Although this model has obvious relevance for diabetesmellitus, hyperinsulinemia and insulin resistance are widespreadconditions that affect many nondiabetic adults with obesity, impairedglucose tolerance, cardiovascular disease, and hypertension. Ourresults provide a cautionary note for the current epidemic of suchconditions, which, in the context of an aging population, may provoke adramatic increase in the prevalence of AD. More encouragingly, greaterunderstanding of insulin's role in AD pathogenesis may lead to noveland more effective strategies for treating, delaying, or evenpreventing this challenging disease," the authors conclude.
(Arch Neurol. 2005; 62: 1-6. Available pre-embargo for the media at www.jamamedia.org)Editor's Note: This work was supported by the Department of VeteransAffairs, Washington, D.C., by grants from the National Institute onAging, Bethesda, Md., and by the Alvord Endowment, University ofWashington, Seattle.
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