Wei Li1, Shannon L Risacher2, Edgar Huang2, Andrew J Saykin2. 1. From Master of Physician Assistant Studies, School of Health and Rehabilitation Sciences (W.L.), and School of Informatics and Computing (E.H.), Indiana University Purdue University Indianapolis; and Center for Neuroimaging (S.L.R., A.J.S.), Department of Radiology and Imaging Sciences, and Indiana Alzheimer Disease Center, Indiana University School of Medicine, Indianapolis, IN. wl23@iu.edu. 2. From Master of Physician Assistant Studies, School of Health and Rehabilitation Sciences (W.L.), and School of Informatics and Computing (E.H.), Indiana University Purdue University Indianapolis; and Center for Neuroimaging (S.L.R., A.J.S.), Department of Radiology and Imaging Sciences, and Indiana Alzheimer Disease Center, Indiana University School of Medicine, Indianapolis, IN.
Abstract
OBJECTIVE: We investigated type 2 diabetes mellitus (T2DM) as a risk factor for brain atrophy and glucose hypometabolism in older adults with or at risk of cognitive impairment. METHODS: Participants with the T2DM were identified from the Alzheimer's Disease Neuroimaging Initiative (ADNI-1/GO/2 cohorts). Analysis of covariance models were used to compare participants with and without T2DM, controlling for potential confounding factors. RESULTS: Whole brain volume and whole brain [(18)F]-fluorodeoxyglucose (FDG) uptake were significantly different as a function of T2DM status, independent of baseline clinical diagnosis. On post hoc analysis, a lower whole brain volume was seen in participants with both mild cognitive impairment (MCI) and T2DM (n = 76) compared with participants who had MCI but not T2DM (n = 747; p = 0.009). Similarly, mean FDG uptake in gray matter and white matter was lower in participants with both MCI and T2DM (n = 72) than in participants with MCI without T2DM (n = 719; p = 0.04). Subsequent regional analysis revealed that the decreased FDG uptake in participants with both MCI and T2DM was mainly manifested in 3 brain regions: frontal lobe, sensory motor cortex, and striatum. CONCLUSIONS: T2DM may accelerate cognition deterioration in patients with MCI by affecting glucose metabolism and brain volume.
OBJECTIVE: We investigated type 2 diabetes mellitus (T2DM) as a risk factor for brain atrophy and glucose hypometabolism in older adults with or at risk of cognitive impairment. METHODS: Participants with the T2DM were identified from the Alzheimer's Disease Neuroimaging Initiative (ADNI-1/GO/2 cohorts). Analysis of covariance models were used to compare participants with and without T2DM, controlling for potential confounding factors. RESULTS: Whole brain volume and whole brain [(18)F]-fluorodeoxyglucose (FDG) uptake were significantly different as a function of T2DM status, independent of baseline clinical diagnosis. On post hoc analysis, a lower whole brain volume was seen in participants with both mild cognitive impairment (MCI) and T2DM (n = 76) compared with participants who had MCI but not T2DM (n = 747; p = 0.009). Similarly, mean FDG uptake in gray matter and white matter was lower in participants with both MCI and T2DM (n = 72) than in participants with MCI without T2DM (n = 719; p = 0.04). Subsequent regional analysis revealed that the decreased FDG uptake in participants with both MCI and T2DM was mainly manifested in 3 brain regions: frontal lobe, sensory motor cortex, and striatum. CONCLUSIONS: T2DM may accelerate cognition deterioration in patients with MCI by affecting glucose metabolism and brain volume.
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