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Neurology:临床前期阿尔茨海默病脑叶微出血发生率增加

2014-04-17 佚名 丁香园

脑微出血以及铁沉积通常可见于高血压性动脉硬化所致的微血管病或者脑淀粉样血管病(CAA)。既往也有研究报道AD患者存在脑微出血,出于安全性考虑,伴有多发性脑微出血的患者被排除在AD免疫治疗研究之外。尚没有研究显示临床前期阿尔茨海默病患者中脑微出血的发生率。因此,来自澳大利亚Paul A. Yates,等学者进行了一项研究,旨在采用11C匹斯堡复合物(PiB)PET成像在一项纵向的队列研究中明确临床前

脑微出血以及铁沉积通常可见于高血压性动脉硬化所致的微血管病或者脑淀粉样血管病(CAA)。既往也有研究报道AD患者存在脑微出血,出于安全性考虑,伴有多发性脑微出血的患者被排除在AD免疫治疗研究之外。尚没有研究显示临床前期阿尔茨海默病患者中脑微出血的发生率。

因此,来自澳大利亚Paul A. Yates,等学者进行了一项研究,旨在采用11C匹斯堡复合物(PiB)PET成像在一项纵向的队列研究中明确临床前期阿尔茨海默病患者(包括β淀粉样蛋白标志物阳性的正常人以及轻度认知功能障碍即MCI患者)脑叶微出血(LMBs)的发生率以及临床相关性。

研究者纳入了一项名为澳大利亚老年人影像、生物标志物以及生活方式的观察性研究中174例受试者,包括97 例认知功能正常 [NC], 37 例轻度认知功能障碍患者 [MCI], 40 例阿尔茨海默病型痴呆患者 [AD],通过3T磁敏感加权MRI成像以及11C-PiB PET成像在3年内3个时间点对受试者进行评估。计算年LMB发生率,采用logistic回归分析明确LMBs与PiB,APOE ε4阳性情况以及脑血管病之间的相关性。

研究发现,在正常组,MCI组以及AD组受试者中LMBs的发生率分别为18.6%,24.3%以及40%.正常组受试者中LMB发生率为0.2 ± 0.6/年,MCI组中为0.2 ± 0.5/年 , 痴呆组中为0.7 ± 1.4/年),且PiB+正常组与 PiB-正常组相比,其数值有6倍的增高。LMB发生率与年龄,APOE ε4+, PiB+, 以及基线LMB情况均相关。多发性LMB发生率也与腔隙性脑梗死以及白质高信号严重程度相关。

研究者总结道,临床前期阿尔茨海默病患者(PiB+阳性的正常人)脑叶微出血发生率增加。高龄,基线脑微出血情况,较高的β淀粉样蛋白负担以及合并存在脑血管病等均增加脑微出血的发生率。研究者建议在设计淀粉样蛋白修饰作用的临床研究中应该考虑到上述情况。

原始出处:


Yates PA1, Desmond PM, Phal PM, Steward C, Szoeke C, Salvado O, Ellis KA, Martins RN, Masters CL, Ames D, Villemagne VL, Rowe CC; AIBL Research Group.Incidence of cerebral microbleeds in preclinical Alzheimer disease.Neurology. 2014 Apr 8;82(14):1266-73. doi: 10.1212/WNL.0000000000000285. Epub 2014 Mar 12.

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    2014-08-08 yinhl1978
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表面铁沉积(SS)是中枢神经系统软脑膜下含铁血黄素沉积的影像学或病理学表现,可通过磁共振T2*或SWI序列检测。皮质SS被认为与脑淀粉样血管病(CAA)以及认知功能障碍相关,既往研究显示CAA患者中皮质SS的发生率为60.5%,无痴呆的老年人群中发生率为0.7%,然而其在阿尔茨海默病(AD)以及其他痴呆类型中的研究较少。【原文下载】 因此,来自荷兰的Frederik

神经心理测验和评价量表在阿尔茨海默病临床试验中的应用

    阿尔茨海默病为慢性进行性神经变性疾病,以认知功能损害、日常生活能力进行性下降及神经心理症状和精神行为异常为主要特征。阿尔茨海默病同很多其它精神类 疾病一样,没有非常特异的生物学标志,临床诊断主要依据病史、体检、实验室检查和辅助检查结果进行综合分析得出,确诊则有赖于脑神经病理检查。在临床诊断 标准中,需要心理测验和量表检查帮助诊断,病情严重程度的判断

Lancet:阿尔茨海默病患者生活质量亟待提高

今年3月19日,美国阿尔茨海默病协会发布了题为《2014年阿尔茨海默病事实与数据》的报告。据该报告称,该病目前已累及520万美国人,包括500万65岁及以上的老年人,预计至2050年这一数据将增加至1380万人。在美国65岁及以上老年人群中,由于阿尔茨海默病所致的死亡人数预计由2010年的60万增至2014年的70万。【原文下载】 世界范围内,2010年阿尔茨海默病以及其他类型痴呆的总患病人数为

PNAS:高糖基化终末产物饮食或可导致痴呆

           由Cai W教授等组成的一个国际科学家团队研究发现,西方饮食中富含晚期糖基化终末产物(AGEs)和糖毒性物质,这两者都可以通过抑制去乙酰化酶存活因子sirtuin 1(SIRT1),导致阿尔茨海默病和代谢综合征。该研究结果在线发表在2014年02月24日的Proceedings of

Nat Med:新型血液检测可提前三年预判阿尔茨海默病

英国新一期《自然—医学》杂志刊登报告说,一种新方法可通过检测血液中的特定脂类含量,来判断早老性痴呆症(又称阿尔茨海默氏症)的风险。新方法最多可提前三年预判这一风险,准确率约为90%。 早老性痴呆症会引发记忆力减退、认知能力下降等,但患者往往只能在这些症状出现后才能确诊,医学界一直在探索能够提前预判患病风险的方法。 美国罗切斯特大学医学院等机构研究人员报告说,他们

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