Affiliations: [a] Department of Psychiatry, New York University School of Medicine, New York, NY, USA | [b] Department of Clinical Neurophysiology, Nuclear Medicine Unit, University of Florence, Italy | [c] Nathan Kline Institute, Orangeburg, NY, USA | Center for Alzheimer's Research, Banner Sun Health Research Institute, Sun City, AZ, USA
Correspondence:
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Correspondence to: Lisa Mosconi, PhD, Department of Psychiatry, NYU School of Medicine 560 First Avenue, New York, NY 10016, USA. Tel.: +1 212 263 3255; Fax: +1 212 263 3279; E-mail: lisa.mosconi@nyumc.org.
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-β (Aβ) 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 Aβ PET imaging studies in AD and discuss the potential of combining symptoms-sensitive FDG-PET measures with pathology-specific Aβ-PET to improve the early detection of AD.
Keywords: Amyloid-β, cerebral metabolic rate of glucose (CMRglc), normal aging, positron emission tomography, preclinical detection
