Faculty of Medicine, University of New South Wales.
Departments of Neurology and HIV Medicine, St Vincent's Hospital, & Peter Duncan Neurosciences Unit, St Vincent's Centre for Applied Medical Research.
AIDS. 2022 May 1;36(6):785-794. doi: 10.1097/QAD.0000000000003165. Epub 2022 Jan 10.
We aimed to examine the relative contributions of HIV infection, age, and cardiovascular risk factors to subcortical brain atrophy in people with HIV (PWH).
Longitudinal observational study.
Virally suppressed PWH with low neuropsychological confounds (n = 75) and demographically matched HIV-negative controls (n = 31) completed baseline and 18-month follow-up MRI scans, neuropsychological evaluation, cardiovascular assessments, and HIV laboratory tests. PWH were evaluated for HIV-associated neurocognitive disorder (HAND). Subcortical volumes were extracted with Freesurfer after removal of white matter hyperintensities. Volumetric and shape analyses were conducted using linear mixed-effect models incorporating interactions between age, time, and each of HIV status, HAND status, HIV disease factors, and cardiovascular markers.
Across baseline and follow-up PWH had smaller volumes of most subcortical structures compared with HIV-negative participants. In addition, over time older PWH had a more rapid decline in caudate volumes (P = 0.041), predominantly in the more severe HAND subgroups (P = 0.042). Higher CD4+ cell counts had a protective effect over time on subcortical structures for older participants with HIV. Increased cardiovascular risk factors were associated with smaller volumes across baseline and follow-up for most structures, although a more rapid decline over time was observed for striatal volumes. There were no significant shape analyses findings.
The study demonstrates a three-hit model of general (as opposed to localized) subcortical injury in PWH: HIV infection associated with smaller volumes of most subcortical structures, HIV infection and aging synergy in the striatum, and cardiovascular-related injury linked to early and more rapid striatal atrophy.
我们旨在探讨 HIV 感染、年龄和心血管危险因素对 HIV 感染者（PWH）皮质下脑萎缩的相对贡献。
纵向观察性研究。
对合并有低神经心理学混杂因素的病毒抑制型 PWH（n = 75）和年龄匹配的 HIV 阴性对照者（n = 31）进行基线和 18 个月的 MRI 扫描、神经心理学评估、心血管评估和 HIV 实验室检查。评估 PWH 是否存在与 HIV 相关的神经认知障碍（HAND）。通过 Freesurfer 去除脑白质高信号后提取皮质下体积。采用线性混合效应模型进行体积和形状分析，该模型包含了年龄、时间与 HIV 状态、HAND 状态、HIV 疾病因素和心血管标志物之间的交互作用。
与 HIV 阴性参与者相比，在基线和随访期间，PWH 的大多数皮质下结构的体积均较小。此外，随着时间的推移，年龄较大的 PWH 的尾状核体积下降更快（P = 0.041），主要见于 HAND 更严重的亚组（P = 0.042）。较高的 CD4+细胞计数对 HIV 感染的老年参与者的皮质下结构具有保护作用。在基线和随访期间，较高的心血管危险因素与大多数结构的体积较小有关，尽管随着时间的推移，纹状体的体积下降更快。未发现明显的形状分析结果。
该研究表明 PWH 存在一种普遍（而非局部）皮质下损伤的三击模型：HIV 感染导致大多数皮质下结构的体积较小、HIV 感染和衰老在纹状体中协同作用以及与心血管相关的损伤与早期和更快的纹状体萎缩有关。
