White matter hyperintensity microstructure in amyloid dysmetabolism
White matter hyperintensity microstructure in amyloid dysmetabolism
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DOI：
10.1177/0271678x15627465
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发表时间：
2017-01-01
影响因子：
6.3
通讯作者：
Selnes, Per
中科院分区：
文献类型：
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作者：
Kalheim, Lisa F.;Bjornerud, Atle;Selnes, Per
越来越多的证据表明脑血管疾病(CVD)和阿尔茨海默病(AD)之间存在联系。在轻度认知障碍(MCI)和AD患者中，推测血管起源的白质高信号(WMHs)增加，但确切的病理机制联系尚不清楚。本研究根据脑脊液中淀粉样蛋白-b肽(Aβ，42)的病理水平或正常水平，研究了淀粉样蛋白代谢异常对MCI或主观认知功能减退(N=51)受试者WMHs微观结构的影响。应用磁共振扩散张量成像(DTI)对31例脑脊液Aβ低(42例)(Aβ+)和20例脑脊液Aβ(42例)正常(Aβ-)患者进行检测，测定各向异性分数(FA)、径向扩散系数(DR)、轴向扩散系数(DA)和平均扩散系数(MD)。两组间WMH体积或分布无显著差异，年龄和WMH体积对DTI指数均无显著影响。然而，Aβ+的WMH的DA、DR和MD显著高于Aβ-，而FA则没有发现差异。目前的结果表明，淀粉样蛋白的积聚与WMH的结构完整性受损(例如，与更广泛的脱髓鞘和轴突丢失有关)可能增加了缺血的影响。
Accumulating evidence suggests associations between cerebrovascular disease (CVD) and Alzheimer's disease (AD). White matter hyperintensities of presumed vascular origin (WMHs) are increased in subjects with mild cognitive impairment (MCI) and AD, but the exact pathomechanistic link is unknown. The current study investigated effects of amyloid dysmetabolism on the microstructure of WMHs in subjects with MCI or subjective cognitive decline (N = 51), dichotomized according to pathological or normal levels of amyloid-b peptide (A beta(42)) in cerebrospinal fluid (CSF). Thirty-one subjects with low CSF A beta(42) (A beta+) and 20 subjects with normal CSF A beta(42) (A beta-) were assessed with magnetic resonance diffusion tensor imaging (DTI), and fractional anisotropy (FA), radial diffusivity (DR), axial diffusivity (DA), and mean diffusivity (MD) were determined. There were no significant differences in WMH volume or distribution between the groups, and neither age nor WMH volume had significant impact on the DTI indices. Nevertheless, there were significantly higher DA, DR, and MD in WMHs in A beta+ relative to A beta-; however, no differences in FA were found. The present results suggest that amyloid accumulation is associated with impaired structural integrity (e.g. relating to more extensive demyelination and loss of axons) in WMHs putatively adding to effects of ischemia.