Department of Radiology, University of Maryland Baltimore School of Medicine, 419 W. Redwood Street, Suite 225, Baltimore, MD, 21201, USA.
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
J Neuroimmune Pharmacol. 2018 Dec;13(4):509-522. doi: 10.1007/s11481-018-9810-9. Epub 2018 Sep 17.
HIV-infected individuals (HIV+) have 2-3 times higher prevalence of tobacco smoking than the general U.S. population. This study aims to evaluate the independent and combined effects of tobacco-smoking and HIV-infection on brain microstructure and cognition using a 2 × 2 design. 21 HIV + Smokers, 25 HIV + Nonsmokers, 25 Seronegative (SN)-Smokers and 23 SN-Nonsmokers were evaluated using diffusion tensor imaging. Fractional anisotropy (FA), mean (MD), radial (RD) and axial (AD) diffusivity were assessed in 8 major cerebral fiber tracts and 5 subcortical regions. Cognitive performance in 7 neurocognitive domains was also assessed. Compared to SN, HIV+ had higher AD in genu of corpus callosum (GCC, p = 0.002). Smokers also had higher diffusivities in GCC, splenium of corpus callosum (SCC), anterior corona radiata (ACR), sagittal stratum (SS) and superior fronto-occipital fasciculus (SFO), than Nonsmokers (p-values<0.001-0.003). Tobacco-Smoking and HIV-infection showed synergistic effects on AD_SS (p = 0.002) and RD_SFO (p = 0.02), but opposite effects in FA_putamen (p = 0.024). Additive effects from HIV+ and Tobacco-Smoking were observed in 9 other white matter tracts, with highest diffusivities and lowest FA in HIV + Smokers. Higher diffusivities in the GCC, SCC, ACR and SS predicted poorer cognitive performance across all participants (p ≤ 0.001). Higher AD_GCC also predicted slower Speed of information processing and poorer Fluency and Attention only in HIV + Smokers (p = 0.001-0.003). Chronic tobacco smoking and HIV-infection appear to have additive and synergistic adverse effects on brain diffusivities, suggesting greater neuroinflammation, which may contribute to poorer cognition. Therefore, chronic tobacco-smoking may be a risk factor for HIV-associated neurocognitive disorders. Graphical Abstract ᅟ.
HIV 感染者（HIV+）的吸烟率比美国普通人群高 2-3 倍。本研究旨在采用 2×2 设计，评估吸烟和 HIV 感染对大脑微观结构和认知的独立和联合影响。对 21 名 HIV+吸烟者、25 名 HIV+非吸烟者、25 名血清阴性（SN）吸烟者和 23 名 SN 非吸烟者进行了弥散张量成像评估。在 8 条主要脑纤维束和 5 个皮质下区域评估了各向异性分数（FA）、平均弥散度（MD）、径向弥散度（RD）和轴向弥散度（AD）。还评估了 7 个神经认知领域的认知表现。与 SN 相比，HIV+患者胼胝体膝部（GCC）的 AD 更高（p=0.002）。与非吸烟者相比，吸烟者在胼胝体压部（SCC）、前放射冠（ACR）、矢状层（SS）和额枕上束（SFO）的 ADC 也更高（p 值<0.001-0.003）。吸烟和 HIV 感染对 AD_SS（p=0.002）和 RD_SFO（p=0.02）有协同作用，但对 FA_putamen 有相反的作用（p=0.024）。在其他 9 条白质束中观察到 HIV+和吸烟的附加效应，HIV+吸烟者的 ADC 最高，FA 最低。GCC、SCC、ACR 和 SS 的弥散度升高预示着所有参与者的认知表现较差（p≤0.001）。GCC 的 AD 升高也预示着 HIV+吸烟者的信息处理速度较慢，流畅性和注意力较差（p=0.001-0.003）。慢性吸烟和 HIV 感染似乎对脑弥散度有累加和协同的不良影响，提示有更强的神经炎症，这可能导致认知能力下降。因此，慢性吸烟可能是 HIV 相关神经认知障碍的一个危险因素。
