脑淀粉样血管病中脑微出血负荷与认知障碍的关系：白质异常的作用。
Role of White Matter Abnormalities in the Relationship Between Microbleed Burden and Cognitive Impairment in Cerebral Amyloid Angiopathy.
机构信息
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Department of Medical Science and Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
出版信息
J Alzheimers Dis. 2022;86(2):667-678. doi: 10.3233/JAD-215094.
BACKGROUND
Cerebral amyloid angiopathy (CAA) often presents as cognitive impairment, but the mechanism of cognitive decline is unclear. Recent studies showed that number of microbleeds were associated with cognitive decline.
OBJECTIVE
We aimed to investigate how microbleeds contribute to cognitive impairment in association with white matter tract abnormalities or cortical thickness in CAA.
METHODS
This retrospective comparative study involved patients with probable CAA according to the Boston criteria (Aβ+ CAA) and patients with Alzheimer's disease (Aβ+ AD), all of whom showed severe amyloid deposition on amyloid PET. Using mediation analysis, we investigated how FA or cortical thickness mediates the correlation between the number of lobar microbleeds and cognition.
RESULTS
We analyzed 30 patients with Aβ+ CAA (age 72.2±7.6, female 53.3%) and 30 patients with Aβ+ AD (age 71.5±7.6, female 53.3%). The two groups showed similar degrees of cortical amyloid deposition in AD-related regions. The Aβ+ CAA group had significantly lower FA values in the clusters of the posterior area than did the Aβ+ AD group(family-wise error-corrected p < 0.05). The correlation between the number of lobar microbleeds and visuospatial function was indirectly mediated by white matter tract abnormality of right posterior thalamic radiation (PTR) and tapetum, while lobar microbleeds and language function was indirectly mediated by the abnormality of left PTR and sagittal stratum. Cortical thickness did not mediate the association between lobar microbleeds and cognition.
CONCLUSION
This result supports the hypothesis that microbleeds burden leads to white matter tract damage and subsequent cognitive decline in CAA.
背景
脑淀粉样血管病（CAA）常表现为认知障碍，但认知下降的机制尚不清楚。最近的研究表明，微出血数量与认知下降有关。
目的
我们旨在研究微出血如何通过与 CAA 中的白质束异常或皮质厚度相关，导致认知障碍。
方法
本回顾性对照研究纳入了根据波士顿标准（Aβ+CAA）诊断的可能 CAA 患者（Aβ+CAA）和阿尔茨海默病患者（Aβ+AD），所有患者的淀粉样蛋白 PET 均显示严重的淀粉样蛋白沉积。我们通过中介分析，研究了 FA 值或皮质厚度如何介导脑叶微出血数量与认知之间的相关性。
结果
我们分析了 30 例 Aβ+CAA 患者（年龄 72.2±7.6，女性 53.3%）和 30 例 Aβ+AD 患者（年龄 71.5±7.6，女性 53.3%）。两组在 AD 相关区域的皮质淀粉样蛋白沉积程度相似。Aβ+CAA 组后区簇的 FA 值明显低于 Aβ+AD 组（经家族-wise 错误校正 p<0.05）。脑叶微出血数量与视空间功能的相关性通过右侧丘脑后辐射（PTR）和脉络膜的白质束异常间接介导，而脑叶微出血数量与语言功能的相关性通过左侧 PTR 和矢状层的异常间接介导。皮质厚度不能介导脑叶微出血与认知之间的关联。
结论
该结果支持微出血负荷导致 CAA 中白质束损伤和随后认知下降的假说。
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