期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 20, 期 3, 页码 843-854出版社
IOS PRESS
DOI: 10.3233/JAD-2010-091504
关键词
Amyloid-beta; cerebral metabolic rate of glucose (CMRglc); normal aging; positron emission tomography; preclinical detection
资金
- NIH/NIA [AG032554, AG13616]
- NIH/NCRR [M01-RR0096]
- Alzheimer's Association
- Anonymous foundation
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000096] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG013616, R01AG035137, P30AG008051, R21AG032554] Funding Source: NIH RePORTER
The development of prevention therapies for Alzheimer's disease (AD) would greatly benefit from biomarkers that are sensitive to subtle brain changes occurring in the preclinical stage of the disease. Early diagnostics is necessary to identify and treat at risk individuals before irreversible neuronal loss occurs. In vivo imaging has long been used to evaluate brain structural and functional abnormalities as predictors of future AD in non-demented persons. Prior to development of amyloid-beta (A beta) tracers for positron emission tomography (PET), the most widely utilized PET tracer in AD was 2-[18F]fluoro-2-Deoxy-D-glucose (FDG) PET. For over 20 years, FDG-PET has been used to measure cerebral metabolic rates of glucose (CMRglc), a proxy for neuronal activity, in AD. Many studies have shown that CMRglc reductions occur early in AD, correlate with disease progression, and predict histopathological diagnosis. This paper reviews reports of clinical and preclinical CMRglc reductions observed in association with genetic and non-genetic risk factors for AD. We then briefly review brain A beta PET imaging studies in AD and discuss the potential of combining symptoms-sensitive FDG-PET measures with pathology-specific A beta-PET to improve the early detection of AD.
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