CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE
CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE
批准号:
7607903
负责人:
MONY J. de LEON
金额:
$0.02万
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:
2007-03-23 至 2007-11-30
关键词:
AllelesAlzheimer&aposs DiseaseAmyloidAtrophicBrainClinicalComputer Retrieval of Information on Scientific Projects DatabaseDefectFundingGlucose Transport InhibitionGlucose TransporterGlutamatesGrantInstitutionNeuronsNumbersPeripheralResearchResearch PersonnelResourcesRestSignal TransductionSourceTestingUnited States National Institutes of Healthapolipoprotein E-4glucose metabolismglucose transport
中文摘要
这个子项目是众多研究子项目之一
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.
Several observations have contributed to speculation that brain glucose metabolism is altered in Alzheimer's disease (AD), these include: reduced numbers and function of glucose transporters [1;2], amyloid ? inhibition of glucose transport [3;4], defective neuronal glutamate signaling of astrocytic glucose metabolism [5], glycolytic enzymatic defects [6], and altered peripheral glucoregulatory function [7-9]. Further contributing to such speculation have been observations that resting brain glucose metabolism is reduced among unimpaired carriers of the ApoE ? 4 allele, in the absence of structural atrophic changes. The proposed study will directly test the hypothesis that brain glucose transport is altered in AD.
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