Karakis Ioannis, Pase Matthew P, Beiser Alexa, Booth Sarah L, Jacques Paul F, Rogers Gail, DeCarli Charles, Vasan Ramachandran S, Wang Thomas J, Himali Jayandra J, Annweiler Cedric, Seshadri Sudha
Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA.
Framingham Heart Study, Framingham, MA, USA.
J Alzheimers Dis. 2016;51(2):451-61. doi: 10.3233/JAD-150991.
Identifying nutrition- and lifestyle-based risk factors for cognitive impairment and dementia may aid future primary prevention efforts.
We aimed to examine the association of serum vitamin D levels with incident all-cause dementia, clinically characterized Alzheimer's disease (AD), MRI markers of brain aging, and neuropsychological function.
Framingham Heart Study participants had baseline serum 25-hydroxyvitamin D (25(OH)D) concentrations measured between 1986 and 2001. Vitamin D status was considered both as a continuous variable and dichotomized as deficient (<10 ng/mL), or at the cohort-specific 20th and 80th percentiles. Vitamin D was related to the 9-year risk of incident dementia (n = 1663), multiple neuropsychological tests (n = 1291) and MRI markers of brain volume, white matter hyperintensities and silent cerebral infarcts (n = 1139).
In adjusted models, participants with vitamin D deficiency (n = 104, 8% of the cognitive sample) displayed poorer performance on Trail Making B-A (β= -0.03 to -0.05±0.02) and the Hooper Visual Organization Test (β= -0.09 to -0.12±0.05), indicating poorer executive function, processing speed, and visuo-perceptual skills. These associations remained when vitamin D was examined as a continuous variable or dichotomized at the cohort specific 20th percentile. Vitamin D deficiency was also associated with lower hippocampal volumes (β= -0.01±0.01) but not total brain volume, white matter hyperintensities, or silent brain infarcts. No association was found between vitamin D deficiency and incident all-cause dementia or clinically characterized AD.
In this large community-based sample, low 25(OH)D concentrations were associated with smaller hippocampal volume and poorer neuropsychological function.
识别基于营养和生活方式的认知障碍及痴呆风险因素可能有助于未来的一级预防工作。
我们旨在研究血清维生素D水平与全因性痴呆、临床诊断为阿尔茨海默病(AD)、脑老化的MRI标志物以及神经心理功能之间的关联。
弗雷明汉心脏研究参与者在1986年至2001年间测量了基线血清25-羟基维生素D(25(OH)D)浓度。维生素D状态既作为连续变量进行考量,也被分为缺乏(<10 ng/mL),或处于队列特定的第20和第80百分位数。维生素D与9年痴呆发病风险(n = 1663)、多项神经心理测试(n = 1291)以及脑容量、白质高信号和无症状脑梗死的MRI标志物(n = 1139)相关。
在调整模型中,维生素D缺乏的参与者(n = 104,占认知样本的8%)在连线测验B-A(β = -0.03至-0.05±0.02)和胡珀视觉组织测试(β = -0.09至-0.12±0.05)中表现较差,表明执行功能、处理速度和视觉感知技能较差。当将维生素D作为连续变量进行检查或在队列特定的第20百分位数处进行二分法划分时,这些关联仍然存在。维生素D缺乏还与较小的海马体积相关(β = -0.01±0.01),但与全脑体积、白质高信号或无症状脑梗死无关。未发现维生素D缺乏与全因性痴呆发病或临床诊断的AD之间存在关联。
在这个基于社区的大样本中,低25(OH)D浓度与较小的海马体积和较差的神经心理功能相关。