Mosconi, L., Tsui, W.H., Herholz, K., Pupi, A., Drzezga, A., Lucignani, G., Reiman, E.M., Holthoff, V., Kalbe, E., Sorbi, S., Diehl-Schmid, J., Perneczky, R., Clerici, F., Caselli, R., Beuthien-Baumann, B., Kurz, A., Minoshima, S. and de Leon, M.J. (2008) Multicenter Standardized 18F-FDG PET Diagnosis of Mild Cognitive Impairment, Alzheimer’s Disease, and Other Dementias. Journal of Nuclear Medicine, 49, 390-398.
http://dx.doi.org/10.2967/jnumed.107.045385

has been cited by the following article:

• TITLE: FDG and Amyloid PET in Cognitively Normal Individuals at Risk for Late-Onset Alzheimer’s Disease

  AUTHORS: John Murray, Wai H. Tsui, Yi Li, Pauline McHugh, Schantel Williams, Megan Cummings, Elizabeth Pirraglia, Lilja Solnes, Ricardo Osorio, Lidia Glodzik, Shankar Vallabhajosula, Alexander Drzezga, Satoshi Minoshima, Mony J. de Leon, Lisa Mosconi

  KEYWORDS: Alzheimer’s Disease, Early Detection, Positron Emission Tomography, Amyloid Imaging, Glucose Metabolism, Normal Aging

  JOURNAL NAME: Advances in Molecular Imaging, Vol.4 No.2, April 16, 2014

  ABSTRACT: Having a parent affected by late-onset Alzheimer’s disease (AD) is a major risk factor for cognitively normal (NL) individuals. This study explores the potential of PET with 18F-FDG and the amyloid-β (Aβ) tracer 11C-Pittsburgh Compound B (PiB) for detection of individual risk in NL adults with AD-parents. Methods: FDG- and PiB-PET was performed in 119 young to late-middle aged NL individuals including 80 NL with positive family history of AD (FH+) and 39 NL with negative family history of any dementia (FH-). The FH+ group included 50 subjects with maternal (FHm) and 30 with paternal family history (FHp). Individual FDG and PiB scans were Z scored on a voxel-wise basis relative to modality-specific reference databases using automated procedures and rated as positive or negative (+/-) for AD-typical abnormalities using predefined criteria. To determine the effect of age, the cohort was separated into younger (49 ± 9 y) and older (68 ± 5 y) groups relative to the median age (60 y). Results: Among individuals of age >60 y, as compared to controls, NL FH+ showed a higher frequency of FDG+ scans vs. FH- (53% vs. 6% p β pathology in the younger cohort, suggesting that neuronal dysfunction may precede major aggregated Aβ burden in young NL FH+. Longitudinal follow-up is required to determine if the observed abnormalities predict future AD.