Differential effects of blood insulin and HbA1c on cerebral amyloid burden and neurodegeneration in nondiabetic cognitively normal older adults

Publication date: November 2017
Source:Neurobiology of Aging, Volume 59
Author(s): Min Soo Byun, Hyun Jung Kim, Dahyun Yi, Hyo Jung Choi, Hyewon Baek, Jun Ho Lee, Young Min Choe, Bo Kyung Sohn, Jun-Young Lee, Younghwa Lee, Hyunwoong Ko, Yu Kyeong Kim, Yun-Sang Lee, Chul-Ho Sohn, Jong Inn Woo, Dong Young Lee
We tested the hypothesis that lower insulin or higher glycated hemoglobin (HbA1c) levels in blood are associated with increased cerebral beta amyloid (Aβ) deposition and neurodegeneration in nondiabetic cognitively normal (CN) older adults. A total of 205 nondiabetic CN older adults underwent comprehensive clinical assessment, [¹¹C]Pittsburgh compound B (PiB)-positron emission tomography (PET), [¹⁸F]fluorodeoxyglucose-PET, magnetic resonance imaging, and blood sampling for fasting insulin and HbA1c measurement. Lower blood insulin was significantly associated with increased Aβ positivity rates and decreased cerebral glucose metabolism in the AD-signature region. In contrast, higher HbA1c levels were not associated with Aβ positivity rates but were significantly associated with higher rates of having neurodegeneration in the AD-signature regions. Our results suggest different roles of insulin and HbA1c in AD pathogenesis, in that decreased blood insulin below optimal levels may contribute to increasing cerebral Aβ deposition and neurodegeneration whereas impaired glycemic control may aggravate neurodegeneration through a nonamyloid mechanism in nondiabetic CN older adults.



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