Mosconi, Lisa2; Rinne, Juha O2; Tsui, Wai H2; Murray, John2; Li, Yi2; Glodzik, Lidia2; McHugh, Pauline2; Williams, Schantel2; Cummings, Megan2; Pirraglia, Elizabeth2; Goldsmith, Stanley J2; Vallabhajosula, Shankar2; Scheinin, Noora2; Viljanen, Tapio2; Någren, Kjell3; de Leon, Mony J2
1 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU2 unknown3 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU
This study examines the relationship between fibrillar beta-amyloid (Aβ) deposition and reduced glucose metabolism, a proxy for neuronal dysfunction, in cognitively normal (NL) individuals with a parent affected by late-onset Alzheimer's disease (AD). Forty-seven 40-80-year-old NL received positron emission tomography (PET) with (11)C-Pittsburgh compound B (PiB) and 18F-fluoro-2-deoxy-d-glucose (FDG). These included 19 NL with a maternal history (MH), 12 NL with a paternal history (PH), and 16 NL with negative family history of AD (NH). Automated regions of interest, statistical parametric mapping, voxel-wise intermodality correlations, and logistic regressions were used to examine cerebral-to-cerebellar PiB and FDG standardized uptake value ratios across groups. The MH group showed higher PiB retention and lower metabolism in AD regions compared with NH and PH, which were negatively correlated in posterior cingulate, frontal, and parieto-temporal regions (Pearson r ≤ -0.57, p ≤ 0.05). No correlations were observed in NH and PH. The combination of Aβ deposition and metabolism yielded accuracy ≥ 69% for MH vs. NH and ≥ 71% for MH vs. PH, with relative risk = 1.9-5.1 (p values <0.005). NL individuals with AD-affected mothers show co-occurring Aβ increases and hypometabolism in AD-vulnerable regions, suggesting an increased risk for AD.
Neurobiology of Aging, 2013, Vol 34, Issue 1, p. 22-34