IN VIVO ASSESSMENT OF AMYLOID AND GLUCOSE SIGNATURES IN SUBJECTIVE COGNITIVE DECLINE SUBJECTS
Abstract
Subjective cognitive decline (SCD), characterized by self-perceived subtle cognitive impairment ahead of the appearance of explicit and measurable cognitive deficits, is regarded as the preclinical manifestation of the pathological change continuum of Alzheimer’s disease (AD). We were committed to exploring the amyloid and glucose metabolic signatures related to imminent brain metabolic changes in SCD subjects. This study included 39 subjects (mean age = 71.9 years; 14 males and 25 females) diagnosed with SCD disease and 39 gender-matched healthy controls (HCs) (mean age = 75.2; 16 males and 23 females) with brain [18F] fluorodeoxyglucose positron emission tomography (PET) images and [18F] florbetapir PET images. The standardized uptake value ratios (SUVRs) of PET images within the regions of interest (ROIs) were calculated. Inter-group SUVR differences were assessed by two-sample t-testing and receiver operating characteristic curve (ROC) analyses. A generalized linear model (GLM) was employed to evaluate the correlations between amyloid and FDG uptake. Compared with HCs, SCD subjects showed significantly increased amyloid SUVR, as well as significantly increased glucose SUVR in the olfactory, amygdala, thalamus, heschl gyrus, superior and middle temporal gyrus and temporal pole (all P<0.05). The amyloid SUVR of thalamus was found to have a better ROC result (area under the curve (AUC): 0.77, 95% confidence interval (CI): 0.66–0.86) in the HC group, as was the case with the glucose SUVR of the middle temporal gyrus (AUC: 0.83, 95% CI: 0.73–0.91). There were significant positive correlations between amyloid and glucose SUVRs (P<0.05). The amyloid SUVR of the thalamus showed a significantly better main effect (odd ratio = 2.91, 95% CI: 1.44–6.7, P<0.001), and the glucose SUVR of the heschl gyrus indicated an enhanced main effect (odd ratio = 5.08, 95% CI: 1.86–18.15, P<0.001). SCD subjects demonstrated significant amyloid accumulation and glucose hypermetabolism in specific brain regions, and amyloid pathology overlapped with regions of glucose abnormality. These findings may advance the understanding of imminent pathological changes in the SCD stage and help to provide clinical guidelines for interventional management.
