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Vascular risk factors are associated with faster decline of Alzheimer disease: a longitudinal SPECT study

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Abstract

We investigated the effects of cardiovascular risk factors, such as hypertension, diabetes mellitus, and hypercholesterolemia, on longitudinal regional cerebral blood flow (rCBF) changes in Alzheimer’s disease (AD). We followed 68 outpatients with probable AD for an average of 40 months. They were divided into three groups based on no (n = 24), single (n = 27), and multiple (n = 17) vascular risk factors. We assessed longitudinal changes on the Mini-Mental State Examination, Functional Assessment Staging scores, and in rCBF deficits using repeated single photon emission computed tomography (SPECT) using N-isopropyl-p-[123I] iodoamphetamine. During follow-up, the multiple vascular risk factor group showed faster cognitive and functional decline than the no and single vascular risk factor groups. When compared with the initial SPECT, the follow-up SPECT showed a significant rCBF reduction in widespread regions, including the parietotemporal, frontal, and limbic lobes, in the multiple and single vascular risk factor groups, while there was rCBF reduction in small scattered regions of the temporoparietal lobe in the no vascular risk factor group. Multiple vascular risk factors are associated with a greater rate of decline in cognition, function, and rCBF in patients with AD. Our results highlight the contribution of vascular risk factors on the progression of AD.

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Acknowledgments

We thank Professor K. Koizumi of the Department of Nuclear Medicine, Tokyo Medical University, for his support and technical assistance. We are also grateful to Assistant Professor Edward F. Barroga and Professor J. Patrick Barron of the Department of International Medical Communications of Tokyo Medical University for their review of the manuscript.

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Correspondence to Haruo Hanyu.

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Kume, K., Hanyu, H., Sato, T. et al. Vascular risk factors are associated with faster decline of Alzheimer disease: a longitudinal SPECT study. J Neurol 258, 1295–1303 (2011). https://doi.org/10.1007/s00415-011-5927-y

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  • DOI: https://doi.org/10.1007/s00415-011-5927-y

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