Results from an imaging substudy of the Harvard Aging Brian Study demonstrated associations between subjective cognitive decline (SCD) and region-specific tauopathy, suggesting multiple biologic factors should be considered when assessing SCD in healthy older adults. The study, which was published in JAMA Neurology, examined the associations between SCD and global β-amyloid (Aβ) and tau burdens in regions of interest in healthy older adults.
A total of 133 clinically healthy participants (mean age, 76 years; Clinical Dementia Rating Scale global scores of 0) were enrolled in the study. All participants underwent cross-sectional flortaucipir F 18 positron emission tomography (FTP-PET) imaging for the presence of tau and Pittsburgh compound B carbon 11-labeled PET (PiB-PET) imaging for the presence of Aβ. SCD was assessed via subscales from the Memory Functioning Questionnaire, the Everyday Cognition battery, and a 7-item questionnaire. Aβ levels were based on a summary distribution volume ratio of frontal, lateral temporal and parietal, and retrosplenial PiB-PET tracer uptake. FTP-PET measures were calculated as standardized uptake value ratios.
Overall, 29.3% (39 of 133) of the participants exhibited a high Aβ burden. Greater SCD was significantly associated with increasing entorhinal cortical tau burden (95% CI, 0.19-0.52; P <.001) and Aβ burden (95% CI, 0.08-0.40; P =.005), but not with inferior temporal tau burden (95% CI, −0.08 to 0.28; P =.27). The significant association between entorhinal cortical tau burden and SCD was essentially unchanged after accounting for Aβ burden (95% CI, 0.15-0.58; P =.001).
The investigators concluded that SCD is an important early indicator of abnormal tau and Aβ burden in clinically healthy older adults with multiple underlying pathways. Thus, when evaluating the presence of SCD in these individuals, numerous AD pathologic factors must be taken into account.
Buckley RF, Hanseeuw B, Schultz AP, et al. Region-specific association of subjective cognitive decline with tauopathy independent of global β-amyloid burden [published online October 2, 2017]. JAMA Neurol. doi:10.1001/jamaneurol.2017.2216