Hyun-Jung No1, Hyon-Ah Yi2, Kyoung Sook Won1, Hyuk Won Chang3, Hae Won Kim4. 1. Department of Nuclear Medicine, Keimyung University Dongsan Medical Center, Daegu, República de Corea. 2. Department of Neurology, Keimyung University Dongsan Medical Center, Daegu, República de Corea. 3. Department of Radiology, Semyung Radiology Clinic, Gumi, República de Corea. 4. Department of Nuclear Medicine, Keimyung University Dongsan Medical Center, Daegu, República de Corea. Electronic address: hwkim.nm@gmail.com.
Abstract
AIM: White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment. It has not been sufficiently evident that cognitive impairment in patients with Alzheimer's disease is caused by WMLs as well as β-amyloid (Aβ) pathology. The aim of this study was to evaluate relationship between WMLs and cerebral glucose metabolism in patients with cognitive impairment after adjustment of cerebral Aβ burden. MATERIALS AND METHODS: Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and 18F-florbetaben positron emission tomography (PET) and 18F-fluorodeoxyglucose PET, were included in this cross-sectional study. The Fazekas scale was used to quantify WMLs on brain T2-weighted MRI. The cerebral Aβ burden and cerebral glucose metabolism were quantitatively estimated using volume-of-interest analysis. Differences in the regional cerebral glucose metabolism were evaluated between low-WML (Fazekas scale<2) and high-WML (Fazekas scale≥2) groups. Multiple linear regression analysis adjusted for age, sex and cerebral Aβ burden was performed to evaluate the relationship between the Fazekas scale score and cerebral glucose metabolism. RESULTS: The regional cerebral glucose metabolism for the bilateral frontal, temporal, and parietal cortices, and limbic lobes in the high-WML group were significantly lower than those in the low-WML group. There were significant negative correlations between the Fazekas scale score and regional cerebral glucose metabolism in the bilateral frontal, bilateral temporal and left parietal cortices, and bilateral limbic lobes. Multiple linear regression analysis revealed that the Fazekas scale score was an independent determinant of the glucose metabolism in the bilateral frontal and temporal cortices and limbic lobes. CONCLUSIONS: WMLs are associated with decreased cerebral glucose metabolism. Our findings suggest that small vessel disease, as well as Aβ pathology, may contribute to cognitive impairment in patients with Alzheimer's disease.
AIM: White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment. It has not been sufficiently evident that cognitive impairment in patients with Alzheimer's disease is caused by WMLs as well as β-amyloid (Aβ) pathology. The aim of this study was to evaluate relationship between WMLs and cerebral glucose metabolism in patients with cognitive impairment after adjustment of cerebral Aβ burden. MATERIALS AND METHODS: Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and 18F-florbetaben positron emission tomography (PET) and 18F-fluorodeoxyglucose PET, were included in this cross-sectional study. The Fazekas scale was used to quantify WMLs on brain T2-weighted MRI. The cerebral Aβ burden and cerebral glucose metabolism were quantitatively estimated using volume-of-interest analysis. Differences in the regional cerebral glucose metabolism were evaluated between low-WML (Fazekas scale<2) and high-WML (Fazekas scale≥2) groups. Multiple linear regression analysis adjusted for age, sex and cerebral Aβ burden was performed to evaluate the relationship between the Fazekas scale score and cerebral glucose metabolism. RESULTS: The regional cerebral glucose metabolism for the bilateral frontal, temporal, and parietal cortices, and limbic lobes in the high-WML group were significantly lower than those in the low-WML group. There were significant negative correlations between the Fazekas scale score and regional cerebral glucose metabolism in the bilateral frontal, bilateral temporal and left parietal cortices, and bilateral limbic lobes. Multiple linear regression analysis revealed that the Fazekas scale score was an independent determinant of the glucose metabolism in the bilateral frontal and temporal cortices and limbic lobes. CONCLUSIONS: WMLs are associated with decreased cerebral glucose metabolism. Our findings suggest that small vessel disease, as well as Aβ pathology, may contribute to cognitive impairment in patients with Alzheimer's disease.
Keywords:
(18)F-FDG PET; Alzheimer's disease; Daños en la sustancia blanca; Enfermedad de Alzheimer; Enfermedad de pequeños vasos; PET con (18)F-FDG; Small vessel disease; White matter lesion; β-Amiloide; β-Amyloid