FMRI INDICES & CSF VIRAL LOAD IN HIV-INFECTION
FMRI INDICES & CSF VIRAL LOAD IN HIV-INFECTION
批准号:
8171021
负责人:
TERRY L. JERNIGAN
金额:
$0.32万
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-08-01 至 2011-07-31
关键词:
AffectAgeAttentionAttentional deficitBiological MarkersBrainComputer Retrieval of Information on Scientific Projects DatabaseCorpus striatum structureEducationFundingGrantHIVImpairmentInfectionInstitutionLinkMatched GroupMeasuresMethodsMotorMultimodal ImagingNeurocognitiveNeurocognitive DeficitParietal LobePatternPerfusionPlayProcessResearchResearch PersonnelResourcesRiskRisk FactorsRoleSourceSpin LabelsStructureTestingUnited States National Institutes of HealthViralViral Load resultcaudate nucleuscognitive changeindexingneurobehavioralneuromechanismneurotoxicrelating to nervous systemresponse
中文摘要
这个子项目是许多研究子项目中利用
资源由NIH/NCRR资助的中心拨款提供。子项目和
调查员(PI)可能从NIH的另一个来源获得了主要资金,
并因此可以在其他清晰的条目中表示。列出的机构是
该中心不一定是调查人员的机构。
这是Jernigan修改后的项目申请。在之前的资助期间,我们定义并对比了与艾滋病毒和冰毒相关的大脑结构变化的模式。纹状体和顶叶皮质体积在冰毒中增加(可能与强烈的小胶质细胞和星形胶质细胞激活有关),而在艾滋病毒中存在广泛的体积损失(可能反映与神经毒性病毒产品相关的更大的神经损伤)。重要的是,尾状核中的特异性损伤与艾滋病毒有关,而顶叶皮质中与冰毒相关的不成比例的影响。在这里,我们关注这些变化对认知运动处理的影响,并假设与冰毒相关的顶叶变化(以前未被探索)与纹状体变化相互作用,并产生不成比例的注意力缺陷。该项目的主要目的是建立结构变化与艾滋病毒和冰毒中存在的神经运动和神经认知缺陷之间的联系。这些研究是由特定的假设驱动的,这些假设是关于艾滋病毒和冰毒的不同神经变化在产生神经运动和神经认知缺陷方面所起的作用。将多模式成像与复杂的神经行为和生物标记物指数相结合,我们将研究以下年龄和教育匹配的组:HIV-/meth-、HIV-/meth+、HIV+/meth-和HIV+/meth+。由于我们观察到了与每个危险因素相关的结构变化,我们将确定在受艾滋病毒和/或冰毒影响的结构中是否存在基线血流灌注异常。动脉自旋标记(ASL)方法将被用来测量基线血流灌注。为了测试HIV相关和冰毒相关的神经认知和神经运动障碍的假说,将使用两种激活范式来获得大胆的效果,这两种激活范式预计会在两个风险组中引起不同的(受损的)反应:反应性运动转换(RMS)和全局/局部分离注意(Glo/Loc)。这些研究的结果将促进对与艾滋病毒和冰毒相关的神经异常的表现和机制的理解。
英文摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
This is a revised application for Project by Jernigan. During the previous funding period, we defined and contrasted the patterns of HIV- and METH-related brain structural alterations. Striatal and parietal cortex volumes are increased in METH (possibly related to strong microglial and astrocytic activation), while there are widespread volume losses in HIV (probably reflecting greater neural damage associated with neurotoxic viral products). Importantly, specific damage in caudate nucleus is associated with HIV, and disproportionate effects in parietal cortex associated with METH. We focus here on the implications of these changes for cognitive-motor processing, and hypothesize that the METH-related parietal lobe alterations (previously unexplored) interact with striatal changes and produce disproportionate attentional deficits. The major aim of the project is to establish links between the structural alterations and the neuromotor and neurocognitive deficits present in HIV and METH. The studies are driven by specific hypotheses about the roles that the distinct neural alterations of HIV and METH play in producing neuromotor and neurocognitive deficits. Combining multimodal imaging with sophisticated neurobehavioral and biomarker indices, we will study the following age- and education-matched groups: HIV-/METH-, HIV-/METH+, HIV+/METH-, and HIV+/METH+. Because we have observed structural alterations associated with each risk factor, we will determine whether baseline perfusion abnormalities exist in the structures affected by HIV and/or METH. Arterial spin labeling (ASL) methods will be used to measure baseline perfusion. To test hypotheses about HIV-related and METH-related neurocognitive and nueromotor impairment, BOLD effects will be obtained using 2 activation paradigms expected to elicit different (impaired) responses in the two risk groups: responsive motor switching (RMS) and global/local divided attention (Glo/Loc). The findings of these studies will advance the understanding of manifestations and mechanisms of neural abnormalities associated with HIV and METH.
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