Pre-clinical detection of Alzheimer's disease using FDG-PET, with or without amyloid imaging.

Publication Type	Review
Authors	Mosconi L, Berti V, Glodzik L, Pupi A, De Santi S, de Leon M
Journal	J Alzheimers Dis
Volume	20
Issue	3
Pagination	843-54
Date Published	01/01/2010
ISSN	1875-8908
Keywords	Alzheimer Disease, Amyloid beta-Peptides, Fluorodeoxyglucose F18, Positron-Emission Tomography
Abstract	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 (Abeta) 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 Abeta PET imaging studies in AD and discuss the potential of combining symptoms-sensitive FDG-PET measures with pathology-specific Abeta-PET to improve the early detection of AD.
DOI	10.3233/JAD-2010-091504
PubMed ID	20182025
PubMed Central ID	PMC3038340