CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE
CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE
批准号:
7718404
负责人:
MONY J. de LEON
金额:
$0.22万
依托单位国家:
美国
项目类别:
财政年份:
2008
资助国家:
美国
项目状态:
已结题
起止时间:
2008-04-01 至 2009-03-31
关键词:
Age-YearsAlzheimer&aposs DiseaseAlzheimer&aposs disease riskBrainClinicalCognitive deficitsComputer Retrieval of Information on Scientific Projects DatabaseDetectionDeteriorationElderlyFundingGrantHippocampus (Brain)HyperglycemiaImpaired cognitionInstitutionMagnetic Resonance ImagingMemoryPathologyPerformancePopulationPositron-Emission TomographyResearchResearch PersonnelResourcesSourceTestingUnited States National Institutes of Healthbaseentorhinal cortexglucose metabolismglucose transporthealthy volunteerneuropsychologicalpre-clinicalresearch clinical testing
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。
这项研究将尝试使用FDG-PET确定临床前阿尔茨海默病(AD)记忆和大脑恶化的最早预测因素。假说是,内嗅皮层葡萄糖代谢的纵向减少预示着轻微认知损伤的发生。两组身体健康的老年人将被研究:一组将有记忆力衰退的证据。第三组为20-30岁的正常健康志愿者。对于第1组和第2组,将在基线和36个月时评估临床评估、神经心理学组合和阿尔茨海默氏症相关的认知缺陷。PET和MRI将在基线和36个月时进行,以评估海马区的病理(MRI也在18个月时进行)。
利用这一人群,将检验以下假设:1)肠嗅皮层葡萄糖代谢是否预示着神经心理功能的下降?2)在观察到高血糖导致正常而不是AD患者的葡萄糖代谢和记忆增加的基础上,海马区葡萄糖运输减少(在稳态高血糖和正常血糖下评估)是否预示着进行性脑退化?这项研究可能有助于检测AD的高危人群。
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 study will attempt to identify the earliest predictors of memory and brain deterioration in preclinical Alzheimer's disease (AD) using FDG-PET. The hypothesis is that longitudinal reductions in glucose metabolism in the entorhinal cortex predict the onset of minimal cognitive impairment. Two groups of medically healthy elderly will be studied: one group will have evidence of memory decline. A third group will be normal healthy volunteers 20-30 years of age. For groups 1&2, clinical evaluations, a neuropsychological battery and Alzheimer's-associated cognitive deficits will be evaluated at baseline and at 36 months. PET and MRI will be performed at baseline and at 36 months to evaluate hippocampal pathology (MRI also at 18 months).
Using this population, the following hypotheses will be tested: 1) Does enterorhinal cortex glucose metabolism predict decline in neuropsychological performance? 2) On the basis of observation of hyperglycemia-induced increase in glucose metabolism and memory in normal but not in AD, does decreased hippocampus glucose transport (evaluated under steady-state hyperglycemia and euglycemia) predict progressive brain deterioration? This study may help in the detection of subjects at risk for AD.
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