Association of midlife blood pressure to late-life cognitive decline and brain morphology

Association of midlife blood pressure to late-life cognitive decline and brain morphology
复制标题

DOI:
10.1212/wnl.51.4.986
复制
发表时间:
1998-10-01
期刊:
影响因子:
9.9
通讯作者:
Carmelli, D
Carmelli, D
中科院分区:
医学1区
文献类型:
--
作者:
Swan, GE;DeCarli, C;Carmelli, D

文献摘要

被引文献

相似文献

目的:在68 - 79岁的社区居住老年男性样本中调查中年收缩压(SBP)与晚年认知能力下降和脑形态学之间的关系。研究方法:受试者是来自前瞻性国家心脏,肺和血液研究所双胞胎研究(摄入量,1969年至1972年)的幸存成员,在1995年至1997年进行第四次检查时,接受了脑MRI和神经行为功能的重复评估。对392名受试者进行定量MR图像,确定脑体积和白色高信号(WMHI)的总体积。在1970年,1980年和1985年测量的中年SEP水平被用来将受试者分为低,中,高中年SEP类别。还计算了这些受试者在简易精神状态检查、数字符号替代测验、本顿视觉保持测验和言语流畅性测验上的10年变化。对于所有报告的分析,患者均被视为遗传无关个体。结果如下:高中年SEP的受试者经历了更大的认知能力下降,并有更大的WMHI体积在随访中的晚年比那些低中年SEP。减少脑实质和增加WMHI体积与神经行为功能下降,在晚年独立的年龄,教育和认知的基线水平进行测量。结论:中年SEP是老年认知功能下降和脑萎缩MR体积测量的重要预测因子。由于神经行为功能的下降与脑体积的减少和WMHI体积的增加有关,因此我们得出结论,SEP升高对晚年神经行为功能下降的长期影响可能是通过其对大脑结构特征的慢性负面影响来介导的。
Objective: To investigate the association between midlife systolic blood pressure (SBP) and late-life cognitive decline and brain morphology in a sample of community-dwelling elderly men 68 to 79 years of age. Methods: Subjects are surviving members from the prospective National Heart, Lung, and Blood Institute Twin Study (intake, 1969 to 1972) who, when examined for a fourth time in 1995 through 1997, underwent brain MRI and repeated assessment of neurobehavioral functioning. Quantification of the MR images determined cerebral volume and total volume of white matter hyperintensities (WMHIs) for 392 subjects. Midlife SEP levels measured in 1970, 1980, and 1985 were used to classify subjects into low, medium, and high midlife SEP categories. A 10-year change in performance on the Mini-Mental State Examination, Digit Symbol Substitution Test, Benton Visual Retention Test, and Verbal Fluency Test was also calculated for these subjects. For all reported analyses, patients were treated as genetically unrelated individuals. Results: Subjects with high midlife SEP experienced a greater decline in cognitive performance and had larger WMHI volumes at follow-up in late life than did those with low midlife SEP. Decreased brain parenchyma and increased WMHI volumes were associated with decline in neurobehavioral functioning as measured in late life independent of age, education, and baseline levels of cognition. Conclusions: Midlife SEP is a significant predictor of both decline in cognitive function and MR volumetric measures of brain atrophy in late life. Because decline in neurobehavioral functioning was associated with decreased brain volume and increased WMHI volume, we conclude that the long-term impact of elevated SEP on decline in late-life neurobehavioral functioning is Likely to be mediated through its chronic, negative effect on structural characteristics of the brain.