Department of Neuropsychiatry & Research Institute of Medical Science, Konkuk University School of Medicine, Chungju, Republic of Korea.
Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea.
J Alzheimers Dis. 2023;93(1):87-95. doi: 10.3233/JAD-220911.
Ankle-brachial index (ABI), an indicator of atherosclerosis or arterial stiffness, has been associated with Alzheimer's disease (AD) dementia and related cognitive impairment. Nevertheless, only limited information is available regarding its contribution to brain alterations leading to cognitive decline in late-life.
We aimed to investigate the relationship of ABI with in vivo AD pathologies and cerebrovascular injury in cognitively impaired older adults.
Total 127 cognitively impaired (70 mild cognitive impairment and 57 AD dementia) individuals, who participated in an ongoing prospective cohort study, were included. All participants underwent comprehensive clinical and neuropsychological assessment, ABI measurement, apolipoprotein E (APOE) ɛ4 genotyping, and multi-modal brain imaging including [11C] Pittsburgh Compound B (PiB)-positron emission tomography (PET) and [18F] fludeoxyglucose (FDG)-PET, and MRI.
General linear model analysis showed significant relationship between ABI strata (low ABI: <1.00, normal ABI: 1.00-1.29, and high ABI: ≥1.30) and AD-signature region cerebral glucose metabolism (AD-CM), even after controlling age, sex, clinical dementia rating-sum of box, and APOE ɛ4 positivity (p = 0.029). Post hoc comparison revealed that low ABI had significantly lower AD-CM than middle and high ABI, while no difference of AD-CM was found between middle and high ABI. There was no significant difference of global Aβ deposition, AD-signature region cortical thickness, and white matter hyperintensity volume between the three ABI strata.
Our findings suggest that lower ABI, likely related to atherosclerosis, may contribute to the aggravation of AD-related regional neurodegeneration in cognitively impaired older adults.
踝臂指数（ABI）是动脉粥样硬化或动脉僵硬的指标，与阿尔茨海默病（AD）痴呆和相关认知障碍有关。然而，关于其对导致老年认知能力下降的脑改变的贡献，信息有限。
我们旨在研究 ABI 与认知障碍老年人体内 AD 病理学和脑血管损伤的关系。
共纳入 127 名认知障碍（70 名轻度认知障碍和 57 名 AD 痴呆）参与者，他们参加了一项正在进行的前瞻性队列研究。所有参与者均接受了全面的临床和神经心理学评估、ABI 测量、载脂蛋白 E（APOE）ɛ4 基因型检测以及多模态脑成像，包括[11C]匹兹堡化合物 B（PiB）-正电子发射断层扫描（PET）和[18F]氟脱氧葡萄糖（FDG）-PET 以及 MRI。
一般线性模型分析显示，ABI 分层（低 ABI：<1.00、正常 ABI：1.00-1.29 和高 ABI：≥1.30）与 AD 特征区域脑葡萄糖代谢（AD-CM）之间存在显著关系，即使在控制年龄、性别、临床痴呆评定总分和 APOE ɛ4 阳性后也是如此（p=0.029）。事后比较显示，低 ABI 的 AD-CM 明显低于中高 ABI，而中高 ABI 之间的 AD-CM 无差异。三个 ABI 分层之间的全球 Aβ 沉积、AD 特征区域皮质厚度和白质高信号体积无显著差异。
我们的研究结果表明，较低的 ABI 可能与动脉粥样硬化有关，可能导致认知障碍老年人 AD 相关区域神经退行性变的加重。
