Please use this identifier to cite or link to this item: https://observatorio.fm.usp.br/handle/OPI/2160
Title: Cardiovascular risk in cognitively preserved elderlies is associated with glucose hypometabolism in the posterior cingulate cortex and precuneus regardless of brain atrophy and apolipoprotein gene variations
Authors: TAMASHIRO-DURAN, Jaqueline HatsukoSQUARZONI, PaulaDURAN, Fabio Luis de SouzaCURIATI, Pedro KallasVALLADA, Homero PintoBUCHPIGUEL, Carlos AlbertoLOTUFO, Paulo AndradeWAJNGARTEN, MauricioMENEZES, Paulo RossiSCAZUFCA, MarciaALVES, Tania Correa de Toledo FerrazBUSATTO, Geraldo Filho
Citation: AGE, v.35, n.3, p.777-792, 2013
Abstract: Cardiovascular risk factors (CVRF) possibly contribute to the emergence of Alzheimer's disease (AD). Fluorodeoxyglucose-positron emission tomography (FDG-PET) has been widely used to demonstrate specific patterns of reduced cerebral metabolic rates of glucose (CMRgl) in subjects with AD and in non-demented carriers of the apolipoprotein epsilon 4 (APOE epsilon 4) allele, the major genetic risk factor for AD. However, functional neuroimaging studies investigating the impact of CVRF on cerebral metabolism have been scarce to date. The present FDG-PET study investigated 59 cognitively preserved elderlies divided into three groups according to their cardiovascular risk based on the Framingham 10-year risk Coronary Heart Disease Risk Profile (low-, medium-, and high-risk) to examine whether different levels of CVRF would be associated with reduced CMRgl, involving the same brain regions affected in early stages of AD. Functional imaging data were corrected for partial volume effects to avoid confounding effects due to regional brain atrophy, and all analyses included the presence of the APOE epsilon 4 allele as a confounding covariate. Significant cerebral metabolism reductions were detected in the high-risk group when compared to the low-risk group in the left precuneus and posterior cingulate gyrus. This suggests that findings of brain hypometabolism similar to those seen in subjects with AD can be detected in association with the severity of cardiovascular risk in cognitively preserved individuals. Thus, a greater knowledge about how such factors influence brain functioning in healthy subjects over time may provide important insigths for the future development of strategies aimed at delaying or preventing the vascular-related triggering of pathologic brain changes in the AD.
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