SODIUM MRI OF THE BRAIN OF PATIENTS WITH ALZHEIMER?S DISEASE
SODIUM MRI OF THE BRAIN OF PATIENTS WITH ALZHEIMER?S DISEASE
批准号:
7600825
负责人:
Eric Albert Mellon
金额:
$1.65万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-06-01 至 2008-05-31
关键词:
AffectAlzheimer&aposs DiseaseAmericanBrainComputer Retrieval of Information on Scientific Projects DatabaseDevelopmentDiagnosisDiagnostic ImagingDiseaseElderlyFacultyFundingGoalsGrantHealth Care CostsIndividualInstitutionLeadMagnetic Resonance ImagingMemory LossMonitorNeuronsParietal LobePatientsPsyche structureResearchResearch PersonnelResourcesSenile PlaquesSignal TransductionSodiumSourceTherapeuticUnited States National Institutes of Healthimprovedinterestoutcome forecastresponse
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,
因此可以在其他CRISP条目中表示。列出的机构是
研究中心,而研究中心不一定是研究者所在的机构。
本研究涉及钠MR成像的开发,用于检测β淀粉样斑块中钠的变化。 阿尔茨海默老年痴呆症(AD)是一种破坏性的和相对常见的疾病,导致受影响的老年人丧失记忆和智力。超过200万的美国老年人患有AD,这导致每年超过500亿美元的总医疗保健费用。有显着的兴趣,在AD的诊断成像的目标,改善诊断,预后,并监测治疗反应的治疗。在病理学上,AD的部分特征是神经细胞的损失和淀粉样β斑块的形成,主要在额叶和顶叶中。我们假设这些变化将通过两种机制导致钠信号的增加。
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 research involves development of Sodium MR Imaging for detecting changes in sodium in the Beta-Amyloid Plaques. Alzheimers Disease (AD) is a devastating and relatively common disease resulting in loss of memory and mental faculties in the affected elderly individual. Upwards of 2 million elderly Americans have AD and this results in a total health care cost of >$50 billion dollars annually. There is significant interest in the diagnostic imaging of AD for the goal of improved diagnosis, prognosis, and monitoring of therapeutic responses to treatment. Pathologically, AD is marked in part by a loss of neural cells and formation of amyloid-beta plaques, primarily in the frontal and parietal lobes. We hypothesize that these changes would lead to an increase in sodium signal by two mechanisms.
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