No Hyun-Jung, Yi Hyon-Ah, Won Kyoung Sook, Chang Hyuk Won, Kim Hae Won
Department of Nuclear Medicine, Keimyung University Dongsan Medical Center, Daegu, República de Corea.
Department of Neurology, Keimyung University Dongsan Medical Center, Daegu, República de Corea.
Rev Esp Med Nucl Imagen Mol (Engl Ed). 2019 May-Jun;38(3):160-166. doi: 10.1016/j.remn.2018.12.001. Epub 2019 Apr 30.
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.
Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and F-florbetaben positron emission tomography (PET) and F-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.
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.
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.
脑白质病变（WMLs）在T2加权磁共振成像（MRI）上表现为高信号，代表脑内小血管疾病，被认为是记忆和认知障碍的潜在危险因素。阿尔茨海默病患者的认知障碍是由WMLs以及β-淀粉样蛋白（Aβ）病理改变共同引起的，这一点尚未得到充分证实。本研究的目的是在调整脑Aβ负荷后，评估认知障碍患者中WMLs与脑葡萄糖代谢之间的关系。
本横断面研究纳入了83名认知表现从正常到痴呆的受试者，他们均接受了脑部MRI、F-氟比他班正电子发射断层扫描（PET）和F-氟脱氧葡萄糖PET检查。采用Fazekas量表对脑部T2加权MRI上的WMLs进行量化。使用感兴趣区分析定量估计脑Aβ负荷和脑葡萄糖代谢。比较低WML（Fazekas量表<2）组和高WML（Fazekas量表≥2）组之间局部脑葡萄糖代谢的差异。进行多因素线性回归分析，校正年龄、性别和脑Aβ负荷，以评估Fazekas量表评分与脑葡萄糖代谢之间的关系。
高WML组双侧额叶、颞叶、顶叶皮质以及边缘叶的局部脑葡萄糖代谢显著低于低WML组。Fazekas量表评分与双侧额叶、双侧颞叶、左侧顶叶皮质以及双侧边缘叶的局部脑葡萄糖代谢之间存在显著负相关。多因素线性回归分析显示，Fazekas量表评分是双侧额叶、颞叶皮质以及边缘叶葡萄糖代谢的独立决定因素。
WMLs与脑葡萄糖代谢降低有关。我们的研究结果表明，小血管疾病以及Aβ病理改变可能导致阿尔茨海默病患者的认知障碍。
