Association Between Midlife Vascular Risk Factors and Estimated Brain Amyloid Deposition. JAMA. 2017 Apr 11;317(14):1443-1450. Abstract Importance: Midlife vascular risk factors have been associated with late-life dementia . Whether these risk factors directly contribute to brain amyloid deposition is less well understood. Objective: To determine if midlife vascular risk factors are associated with late-life brain amyloid deposition, measured using florbetapir positron emission tomography (PET). Design, Setting, and Participants: The Atherosclerosis Risk in Communities (ARIC)-PET Amyloid Imaging Study, a prospective cohort study among 346 participants without dementia in 3 US communities (Washington County, Maryland; Forsyth County, North Carolina; and Jackson, Mississippi) who have been evaluated for vascular risk factors and markers since 1987-1989 with florbetapir PET scans in 2011-2013. Positron emission tomography image analysis was completed in 2015. Exposures: Vascular risk factors at ARIC baseline (age 45-64 years; risk factors included body mass index ≥30, current smoking, hypertension, diabetes, and total cholesterol ≥200 mg/dL ) were evaluated in multivariable models including age, sex, race, APOE genotype, and educational level. Main Outcomes and Measures: Standardized uptake value ratios (SUVRs) were calculated from PET scans and a mean global cortical SUVR was calculated. Elevated florbetapir (defined as a SUVR 1.2 ) was the dependent variable. Results: Among 322 participants without dementia and with nonmissing midlife vascular risk factors at baseline (mean age, 52 years; 58% female; 43% black), the SUVR (elevated in 164 participants) was measured more than 20 years later (median follow-up, 23.5 years; interquartile range, 23.0-24.3 years) when participants were between 67 and 88 (mean, 76) years old. Elevated body mass index in midlife was associated with elevated SUVR (odds ratio , 2.06 ; 95% CI, 1.16-3.65). At baseline, 65 participants had no vascular risk factors, 123 had 1, and 134 had 2 or more; a higher number of midlife risk factors was associated with elevated amyloid SUVR at follow-up (30.8% , 50.4% , and 61.2% , respectively). In adjusted models, compared with 0 midlife vascular risk factors, the OR for elevated SUVR associated with 1 vascular risk factor was 1.88 (95% CI, 0.95-3.72) and for 2 or more vascular risk factors was 2.88 (95% CI, 1.46-5.69). No significant race × risk factor interactions were found. Late-life vascular risk factors were not associated with late-life brain amyloid deposition (for ≥2 late-life vascular risk factors vs 0: OR, 1.66; 95% CI, 0.75-3.69). Conclusions and Relevance: An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR ; this association was not significant for late-life risk factors. These findings are consistent with a role of vascular disease in the development of Alzheimer disease . 经典文章回顾 帕金森病患者的康复治疗 帕金森病患者的疾病预防和保健常识 10条老年性痴呆患者的护理常识 四条建议教老年人预防老年性痴呆 老年性痴呆患者的饮食禁忌和饮食调理 2016年阿尔茨海默病10大研究进展 2016年帕金森病10大研究进展 你对老年性痴呆症到底懂多少？ 地中海饮食最健康的神经科学分析 八种食物提高记忆力，增强脑活力！ 预防老年性痴呆症，先从这些小事做起！ 睡眠不足增加肥胖风险的神经科学解释 运动是大脑的最佳保健品 预防痴呆和脑中风，减少PM2.5是我们可以做的 益生菌也能够治疗痴呆、抑郁症和精神分离症？ 喜欢我，关注我 拉到最上方标题下，点击上方蓝字关注 搜索公众号名称：神经科学临床和基础 也请你推荐给你身边的医学朋友，感谢你~
在 前文 我提到一个加拿大小组做的小鼠脑血管结构的基础工作。这篇文章聊聊另一篇一个德国小组做的一组精巧的小鼠脑血管阻断与血管增生实验。 小鼠头脑供血如人一样，由两根颈动脉（IA)与两根椎动脉(VA)供血。德国普朗克学院的Busch等人做了这样一个实验，他们阻断两根VA及一根IA，再观察剩下一根的IA的生理变化（最右边示意图）。 他们发现，实验小鼠大都活下来。那么剩下的唯一一根IA必然负担整个脑部的供血，由Willis环传递。相应的，那根IA因为要负担比常量多得多的流量，所以管径变粗，管壁变薄： 看右边的IA明显变粗： 三根脑血管阻断后，脑供血整体减少。同时刺激毛细血管增生，减少脑缺血风险。下图为histological分析，及biomarker Ki-67与ED-1在血管壁内层及外层的增加，为明显血管增生证据。 是一篇由实验到内容都漂亮的好文。 参考文献： H. Busch, I. R. Buschmann, G. Mies, C. Bode, and K. Hossmann, Arteriogenesis in Hypoperfused Rat Brain, J Cereb Blood Flow Metab , vol. 23, no. 5, pp. 621-628, May. 2003.
标签: 脑血管
