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的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
这是一个由Jernigan项目修改后的应用程序。在上一个资助期间,我们定义并对比了HIV和MET相关的大脑结构改变的模式。METH中纹状体和顶叶皮质体积增加(可能与强烈的小胶质细胞和星形胶质细胞激活有关),而HIV中存在广泛的体积损失(可能反映了与神经毒性病毒产物相关的更大神经损伤)。重要的是,尾状核的特定损伤与HIV相关,顶叶皮质的不成比例效应与METH相关。在这里,我们专注于这些变化对认知运动处理的影响,并假设METH相关的顶叶改变(以前未探索)与纹状体的变化相互作用,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改变与HIV和METH中存在的神经运动和神经认知缺陷之间的联系。这些研究是由关于HIV和METH的不同神经改变在产生神经运动和神经认知缺陷中所起作用的特定假设驱动的。将多模式成像与复杂的神经行为和生物标志物指数相结合,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+。因为我们已经观察到与每个危险因素相关的结构改变,我们将确定是否存在基线灌注异常的结构受HIV和/或METH。将使用动脉自旋标记(ASL)方法测量基线灌注。为了检验关于HIV相关和METH相关神经认知和神经功能损害的假设,将使用预期在两个风险组中引起不同(受损)反应的2种激活范例获得BOLD效应:反应性运动转换(RMS)和全局/局部分散注意力(Glo/Loc)。这些研究的结果将促进与HIV和METH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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