Vlassenko A, Blazey T, Su Y, Xiong C, Goate A, Benzinger T, Mintun M, Morris J.
Conversion to Preclinical Alzheimer’s Disease in Cognitively Normal Adults: The Characteristics from Longitudinal [11C] PIB PET Study.
Human Amyloid Imaging Abstract. 2012 Jan 1;
The concept of preclinical Alzheimer’s disease (AD) implies that beta-amyloid (Aβ) deposits may accumulate in the brain years prior to the clinical manifestations. Cognitively normal individuals with preclinical AD as detected by increased uptake of [11C] PIB have a greater risk of progression to symptomatic AD. However the conversion to preclinical AD in cognitively normal individuals has not been characterized yet. In this study, we evaluated Aβ accumulation in46 cognitively normal older adults who underwent two [11C] PIB PET scans about.6 years apart. Global Aβ deposition was estimated using mean cortical binding potential (MCBP) from gyrus rectus, prefrontal cortex, precuneus and lateral temporal cortex, and MCBP > 0.18 was considered abnormal representing PIB-positive state or preclinical AD. Of the46 participants5 individuals were PIB-negative and1 individuals were PIB-positive on both [11C] PIB scans. Ten of the25 individuals (7 females, mean age5.5 ±.3 years), who were PIB-negative at the first [11C] PIB scan, converted to PIB-positive state, with an incidence of conversion of.1% per year. At the second [11C] PIB scan, converters demonstrated substantially greater Aβ deposition in many cortical and subcortical regions compared to PIB-negative individuals. The magnitude of Aβ accumulation was dependent on the duration of follow-up, with greater changes in Aβ levels resulting from longer follow-up. The mean annual rate of change in Aβ deposition in converters was similar to that in individuals PIB-positive at both scans. Seven of the0 converters were APOE4 positive. The incidence of conversion to preclinical AD in APOE4 positive individuals was.0%. The youngest participant to convert was6 years old at the second PIB scan and he was a carrier of two APOE4 alleles. Our findings suggest that conversion to preclinical AD is associated with continuous and widespread progression in AD pathology.