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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.

The purpose of this study is to investigate whether a near-infrared fluorescence (NIRF) probe, Cy5.5-D-glucosamine (Cy5.5-2DG), can image arthritis in collagen-induced arthritic (CIA) mice. The presence of arthritis was verified by both visual examination and micro-computed tomography (MicroCT) imaging. CIA mice were imaged by a micro-positron emission tomography (MicroPET) scanner one hour after intravenous injection of 2-deoxy-2-[¹⁸F]fluoro-D-glucose ([¹⁸F]FDG). After radioactivity of [¹⁸F]FDG decayed away, Cy5.5-2DG was injected into a lateral tail vein of the mice. Arthritic tissue targeting and retention of Cy5.5-2DG in CIA mice were evaluated and quantified by an optical imaging system. Inflammatory tissue in CIA mice was clearly visualized by [¹⁸F]FDG-MicroPET scan. NIRF imaging of Cy5.5-2DG in the same mice revealed that the pattern of localization of Cy5.5-2DG in the arthritic tissue was very similar to that of [¹⁸F]FDG. Quantification analysis further showed that [¹⁸F]FDG uptake in arthritic tissues at one hour post-injection (p.i.) and Cy5.5-2DG uptakes at different time points p.i. were all well correlated (r² over 0.65). In conclusion, Cy5.5-DG can detect arthritic tissues in living mice. The good correlation between the [¹⁸F]FDG uptake and Cy5.5-2DG accumulation in the same arthritic tissue warrants further investigation of Cy5.5-2DG as an approach for assessment of anti-inflammatory treatments.