Accelerated aging of selective brain structures in human immunodeficiency virus infection: a controlled, longitudinal magnetic resonance imaging study.

Accelerated aging of selective brain structures in human immunodeficiency virus infection: a controlled, longitudinal magnetic resonance imaging study.
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DOI:
10.1016/j.neurobiolaging.2014.01.008
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发表时间:
2014-07
影响因子:
4.2
通讯作者:
Sullivan EV
Sullivan EV
中科院分区:
医学2区
文献类型:
--
作者:
Pfefferbaum A;Rogosa DA;Rosenbloom MJ;Chu W;Sassoon SA;Kemper CA;Deresinski S;Rohlfing T;Zahr NM;Sullivan EV

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治疗方面的进展已使艾滋病毒感染从势不可挡地发展到严重发病和过早死亡,转变为可控制的慢性病,通常以健康状况良好为标志。因此,受感染的个体活得足够长,以至于有可能与包括大脑在内的各种器官系统的正常衰老效应相互作用。为了研究这种相互作用,研究人员使用351个MRI和一系列神经心理学测试对51名HIV感染者和65名未感染对照者的大脑进行了研究,这些测试在6个月至8年的随访期间收集了两次或两次以上。感兴趣的脑组织区域显示出预期的年龄相关体积减少;两组的CSF填充空间显示出体积增加。虽然HIV感染者总体健康状况良好,没有临床可检测到的痴呆症,但支持高阶认知和功能整合的几个大脑区域显示出正常衰老轨迹的加速,包括从额叶和颞极延伸到顶叶的新皮层和丘脑。除了预期的侧脑室和侧裂体积增加和组织体积减少(特别是额叶和感觉运动新皮质、丘脑和海马),疾病持续时间更长,大多数区域也显示出疾病进展加速。这种皮质组织的加速损失可能代表过早认知和运动损害的风险因素,如果不是痴呆的话。在一个更有希望的注意,艾滋病毒感染的患者增加CD 4细胞计数表现出缓慢的扩大侧裂体积和缓慢下降的额叶和颞顶皮质,海马和海马组织体积。因此,这些脑区的萎缩减弱,可能与适当的药物治疗和进一步感染的控制,有可能减轻相关的下降,高阶功能,特别是外显记忆,执行功能,自我调节,和视觉空间能力。
Advances in treatment have transformed HIV infection from an inexorable march to severe morbidity and premature death to a manageable chronic condition, often marked by good health. Thus, infected individuals are living long enough that there is a potential for interaction with normal senescence effects on various organ systems including the brain. To examine this interaction, the brains of 51 individuals with HIV infection and 65 uninfected controls were studied using 351 MRIs and a battery of neuropsychological tests collected two or more times over follow-up periods ranging from 6 months to 8 years. Brain tissue regions of interest showed expected age-related decrease in volume; CSF-filled spaces showed increase in volume for both groups. Although HIV infected individuals were in good general health, and free of clinically-detectable dementia, several brain regions supporting higher-order cognition and integration of functions showed acceleration of the normal aging trajectory, including neocortex, which extended from the frontal and temporal poles to the parietal lobe, and the thalamus. Beyond an anticipated increase in lateral ventricle and Sylvian fissure volumes and decrease in tissue volumes (specifically, the frontal and sensorimotor neocortices, thalamus, and hippocampus) with longer duration of illness, most regions also showed accelerated disease progression. This accelerated loss of cortical tissue may represent a risk factor for premature cognitive and motor compromise if not dementia. On a more promising note, HIV-infected patients with increasing CD4 counts exhibited slower expansion of Sylvian fissure volume and slower declines of frontal and temporoparietal cortices, insula, and hippocampus tissue volumes. Thus, attenuated shrinkage of these brain regions, likely with adequate pharmacological treatment and control of further infection, has the potential of abating decline in associated, higher-order functions, notably, explicit memory, executive functions, self-regulation, and visuospatial abilities.
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