Large Perivascular Spaces Visible on Magnetic Resonance Imaging, Cerebral Small Vessel Disease Progression, and Risk of Dementia: The Age, Gene/Environment Susceptibility-Reykjavik Study.

Large Perivascular Spaces Visible on Magnetic Resonance Imaging, Cerebral Small Vessel Disease Progression, and Risk of Dementia: The Age, Gene/Environment Susceptibility-Reykjavik Study.
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DOI:
10.1001/jamaneurol.2017.1397
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发表时间:
2017-09-01
期刊:
影响因子:
29
通讯作者:
Launer LJ
Launer LJ
中科院分区:
医学1区
文献类型:
--
作者:
Ding J;Sigurðsson S;Jónsson PV;Eiriksdottir G;Charidimou A;Lopez OL;van Buchem MA;Guðnason V;Launer LJ

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随着年龄的增长,磁共振成像(MRI)上血管周围间隙的可见性增加被假设为代表脑组织间液引流受损,并可能反映潜在的脑小血管疾病(SVD)。然而,大的MRI可见的血管周围间隙(直径>3 mm; L-PVS)是否与老年人的SVD和认知功能减退有关尚不清楚。确定L-PVS,更具体地说,其计数和位置是否与已确定的SVD MRI标志物的进展、认知能力下降和痴呆风险增加相关。前瞻性基于人群的年龄、基因/环境易感性-雷克雅未克研究在基线(2002年9月1日至2006年2月28日)对2612名年龄在65-97岁(59.0%女性)的参与者进行了脑部MRI研究,评估了L-PVS。参与者从2007年4月1日至2011年9月30日返回进行第二次MRI扫描,并在两个时间点进行神经心理学测试,平均(SD)为5.2(0.2)年。L-PVS的存在、数量和位置。在MRI上检测到的偶发性皮质下梗死、脑微出血和白色高信号进展;认知下降定义为记忆、信息处理速度和执行功能领域的基线和随访之间的复合评分变化;根据国际指南诊断的裁定的偶发性痴呆病例。L-PVS患病率为16.2%(中位数:1 [范围,1-17])。校正年龄、性别和基线与随访扫描之间的时间间隔后,L-PVS的存在与皮质下梗死(校正风险比2.54; 95%置信区间1.76-3.68)和微出血(1.43; 95%CI 1.18-1.72)的风险增加显著相关,并且白色高信号体积的5年进展更大。L-PVS的存在也与信息处理速度的急剧下降有关,并使血管性痴呆的风险增加了四倍多。当进一步调整遗传和脑血管危险因素时,所有相关性仍然存在。与认知结果的关联独立于教育、抑郁和其他SVD MRI标志物。L-PVS是SVD的MRI标志物,与老年人血管相关认知功能障碍的发病机制相关。
With advancing age, an increased visibility of perivascular spaces on magnetic resonance imaging (MRI) is hypothesized to represent impaired drainage of intersitital fluid from the brain and may reflect underlying cerebral small vessel disease (SVD). However, whether large MRI-visible perivascular spaces (>3 mm in diameter; L-PVS) are associated with SVD and cognitive deterioration in older people are unknown. To determine whether L-PVS, and more specifically their count and location, are associated with the progression of established MRI markers of SVD, cognitive decline and an increased risk of dementia. The prospective population-based Age, Gene/Environment Susceptibility–Reykjavik Study, assessed L-PVS at baseline (September 1, 2002, through February 28, 2006) on MRI studies of the brain in 2612 participants aged 65–97 years (59.0% women). Participants returned for a second MRI scan from April 1, 2007, through September 30, 2011 and underwent neuropsychological testing at the two time points a mean (SD) of 5.2 (0.2) years apart. L-PVS presence, number and location. Incident subcortical infarcts, cerebral microbleeds and progression of white matter hyperintensities detected on MRIs; cognitive decline defined as composite score changes between baseline and follow-up in the domains of memory, information processing speed and executive function; adjudicated incident dementia cases diagnosed according to international guidelines. L-PVS prevalence was 16.2% (median number: 1 [range, 1–17]). After adjusting for age, sex and time interval between baseline and follow-up scanning, the presence of L-PVS was significantly associated with an increased risk of incident subcortical infarcts (adjusted risk ratio 2.54; 95% confidence interval 1.76–3.68) and microbleeds (1.43; 95%CI 1.18–1.72), and a greater 5-year progression of white matter hyperintensities volume. The presence of L-PVS was also associated with a steeper decline in information processing speed and more than quadrupled the risk of vascular dementia. All associations persisted when further adjusted for genetic and cerebrovascular risk factors. The associations with cognitive outcomes were independent of education, depression and other SVD MRI markers. L-PVS are an MRI marker of SVD and associated with the pathogenesis of vascular-related cognitive impairment in older people.
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