Neurology:A-beta和血管危险因素,如何影响大脑萎缩?

2022-08-09 Freeman MedSci原创

血管风险升高和较高的Aβ负担与纵向脑萎缩之间的相互作用

越来越多的数据表明,血管危险因素,如肥胖、高血压、高胆固醇糖尿病,不仅是心血管疾病的危险因素,也是阿尔茨海默病(AD)痴呆的危险因素。我们小组的最新数据支持这样的观点,即血管危险因素可能独立地和通过典型的AD途径来促进AD痴呆的进展。 具体来说,先前的工作表明,在临床上无障碍的成年人中,系统性血管风险升高和β-淀粉样蛋白(Aβ)负担较高与皮质tau沉积较多和认知能力下降较快有关。tau沉积升高和认知障碍与神经变性密切相关,因此神经变性可能是血管风险和AD病理学导致痴呆的最后一条共同途径。

图1: 论文封面图

研究将血管风险和Aβ沉积作为脑萎缩的独立预测因素,表明这两个过程与磁共振成像(MRI)量化的脑萎缩的重叠和不同模式有关。

血管风险因素主要与额叶和颞叶区域的萎缩有关,而Aβ沉积最常与内侧顶叶和颞叶区域的优先皮质变薄有关。 很少有研究考察血管风险和Aβ负担对脑萎缩的综合影响,以及这反过来如何影响认知能力的下降。

此外,目前仍不清楚血管风险因素是否通过白质变化加剧了脑萎缩,或者这是否通过独立的途径发生。需要进行纵向研究以促进我们对血管风险和Aβ负担对脑萎缩模式的相互作用的理解。

藉此,哈佛大学的Jennifer S. Rabin等人,调查了哈佛大学老龄化大脑研究(HABS)中临床上无障碍者的系统性血管风险和Aβ负担对纵向脑萎缩模式的互动与独立关联。 其次,研究了系统性血管风险是否与脑萎缩有关,独立于白质损伤的成像标志物,包括扩散衍生的微结构异常和白质高密集度(WMH)。最后,基于先前的工作表明,血管风险升高与Ab负担相互作用,加速认知衰退,他们研究了这种关联是否由脑萎缩介导。


参与者是哈佛大学脑部老化研究的196名成年人(年龄=73.8±6.1岁)。基线Aβ负担用匹兹堡复合B型PET进行量化。基线血管风险用Framingham心脏研究心血管疾病风险评分来测量。

大脑萎缩用结构磁共振成像进行纵向量化,时间中位数为4.50(±1.26)年。认知能力每年用临床前阿尔茨海默症认知综合指数进行评估,中位数为6.25(±1.40)年。线性混合效应模型研究了血管风险和Aβ负担作为灰质萎缩的互动和独立预测因素,调整了年龄、性别、受教育年限、APOE ε4状态、颅内体积(如适用),以及它们与时间的交互作用。

图2:论文结果图

在随后的模型中,他们调整了白质损伤的标志物,以确定血管风险是否独立于基于扩散和FLAIR的标志物而加速脑萎缩。中介分析考察了脑萎缩是否介导了血管风险和Aβ负担对认知衰退的互动关系。

该研究的重要意义在于发现了:较高的血管风险和升高的Aβ负担相互作用,预测额叶和颞叶、丘脑和纹状体会出现更严重的萎缩。

较高的Aβ负担,但不是血管风险,与顶叶和枕叶以及海马体更严重的萎缩有关。

调整基于扩散和FLAIR的白质损伤标志物对上述关联没有什么影响。灰质萎缩在较高的Aβ负担水平上介导了血管风险和认知能力下降之间的关联。

该研究的重要意义在于发现了:血管风险升高和较高的Aβ负担与纵向脑萎缩之间的相互作用,这反过来影响了认知能力的下降。这些结果支持将血管危险因素管理作为一种潜在的干预措施,以减缓临床前阿尔茨海默病的神经变性和认知能力下降。

 

原文出处:

Rabin JS, Pruzin J, Scott M, et al. Association of β-Amyloid and Vascular Risk on Longitudinal Patterns of Brain Atrophy. _Neurology_. 2022;99(3):e270-e280. doi:[10.1212/WNL.0000000000200551](https://doi.org/10.1212/WNL.0000000000200551)

 

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    2023-04-30 docwu2019
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    2023-04-27 chendoc252
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    2022-08-26 yinhl1978
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