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。
这项研究涉及到钠核磁共振成像的开发,用于检测β淀粉样斑块中钠的变化。阿尔茨海默病(AD)是一种破坏性的、相对常见的疾病,会导致受影响的老年人的记忆和智力丧失。超过200万的美国老年人患有阿尔茨海默病,这导致每年的医疗保健总成本高达500亿美元。为了改善诊断、预后和监测治疗反应,人们对AD的诊断成像有很大的兴趣。病理上,阿尔茨海默病的部分特征是神经细胞的丧失和淀粉样β斑块的形成,主要是在额叶和顶叶。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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