Bezafibrate, a pan-peroxisome proliferator-activated receptor (PPAR) agonist, reportedly attenuated tau pathology in a transgenic mouse model of primary tauopathy. Since tau pathology is a neuropathological hallmark of Alzheimer’s disease (AD), bezafibrate may be a potential drug for the treatment of AD. However, no study has investigated its effects in AD models. Thus, we aimed to evaluate whether bezafibrate has neuroprotective effects in a sporadic AD model induced by streptozotocin (STZ) intracerebroventricular (ICV) injection. Rats were administered STZ-ICV (3 mg/kg) followed by bezafibrate (50 mg/kg/day, intraperitoneal) for 4 weeks. Behavior tests and positron emission tomography (PET) were performed to evaluate longitudinal changes in cognitive function, tau pathology, and cerebral glucose metabolism. Immunofluorescence staining was performed to assess neuronal survival and microglial accumulation. STZ-ICV administration induced significant cognitive impairment and substantial neuronal loss, tau pathology, glucose hypometabolism, and microgliosis in the cortex and hippocampus, while bezafibrate effectively attenuated these abnormalities. This study demonstrated that bezafibrate has long-lasting neuroprotective effects in a sporadic AD model. Our data indicate that the neuroprotective effects of bezafibrate might be associated with its ability to ameliorate tau pathology, brain glucose hypometabolism, and neuroinflammation. These findings suggest that bezafibrate is a potential multi-target drug candidate for the treatment of AD.

(1) Background: This study aimed to investigate the association between radioactive iodine (RAI) and long-term cardiovascular disease (CVD) morbidity/mortality in thyroid cancer. (2) Methods: The study was conducted using data from the Taiwan National Health Insurance Database during 2000–2015. Thyroid cancer patients aged ≥20 years were categorized into RAI (thyroidectomy with RAI) and non-RAI (thyroidectomy only) groups. The Cox proportional hazard regression model and Kaplan–Meier method were used for analysis. (3) Results: A total of 13,310 patients were included. Kaplan–Meier analysis demonstrated that the two groups had similar cumulative risks of CVD (log-rank p = 0.72) and CVD-specific mortality (log-rank p = 0.62). On Cox regression analysis of different RAI doses, the risk of CVD was higher in the cumulative dosage >3.7 GBq (hazard ratio = 1.69, 95% confidence interval = 1.24–2.40, p < 0.001). (4) Conclusions: RAI was not associated with an increased risk of CVD in thyroid cancer. However, CVD surveillance is indicated in the patients receiving the cumulative RAI dosage above 3.7 GBq.

Background/Objectives: Subjective cognitive decline (SCD) may serve as an early indicator of Alzheimer’s disease (AD). This study investigates regional cerebral blood flow (rCBF) alterations in individuals with SCD using single photon emission computed tomography (SPECT). To characterize rCBF patterns in SCD patients compared to healthy controls and examine the relationship between rCBF and cognitive function. Methods: We compared rCBF in 20 SCD patients and 20 age- and sex-matched healthy controls using 99mTc-ECD SPECT imaging. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), Clinical Dementia Rating (CDR), Geriatric Depression Scale (GDS), and Cognitive Abilities Screening Instrument (CASI). Results: SCD patients demonstrated significantly reduced rCBF in the right superior temporal gyrus (rSTG) (mean uptake ratio [UR] = 0.864 ± 0.090 vs. 1.030 ± 0.074, p < 0.001) and right caudate (mean UR = 0.783 ± 0.068 vs. 0.947 ± 0.062, p < 0.001) compared to controls. Additionally, negative correlations were observed between rCBF in these regions and CDR scores, particularly in the memory domain (rSTG: r = −0.37, p = 0.016; right caudate: r = −0.39, p = 0.011). Conclusions: Reduced rCBF in the rSTG and right caudate may represent early biomarkers for SCD, which could aid in the early detection of AD. These findings suggest that SPECT imaging might be a valuable tool for identifying individuals at risk of cognitive decline, potentially allowing for earlier intervention and targeted preventive strategies in the management of AD.

Introduction: The biokinetics of radioiodine (RAI) in thyroid cancer patients are complex. This study aims to develop a practical approach for assessing RAI biokinetics to predict patient discharge time and estimate radiation exposure to caregivers. Methods: We retrospectively reviewed data from patients with differentiated thyroid carcinoma undergoing RAI treatment. Serial radiation dose rates were dynamically collected during hospitalization and fitted to a biexponential model to assess the biokinetic features: RAI uptake fraction of thyroid tissue (F_t) and effective half-life of extra-thyroid tissue (T_et). Correlations with ^99mTc thyroid uptake ratio (TcUR), radiation retention ratio (RR), renal function, and body mass index (BMI) were analyzed. Results: Thirty-five patients were enrolled. The derived F_t was 0.08 ± 0.06 and T_et was 7.57 ± 1.45 h. Pearson’s correlation analysis revealed a significant association between F_t and both TcUR and RR (p < 0.05), while T_et correlated with renal function and BMI (p < 0.05). Conclusion: This novel and practical method assessing RAI biokinetics demonstrates consistency with other parameters and related studies, enhancing the model reliability. It shows promise in predicting an appropriate discharge time and estimating radiation exposure to caregivers, allowing for modifications to radiation protection precautions to follow ALARA principle and minimize the potential risks from radiation exposure.

Chemotherapy-induced cognitive impairment (CICI) is a frequently reported complication in lung cancer patients, yet the underlying cerebral metabolic changes remain poorly characterized. This study aimed to evaluate chemotherapy-related alterations in brain glucose metabolism in patients with non-small cell lung cancer (NSCLC) using a longitudinal, within-subject voxel-based ¹⁸F-FDG PET approach. Forty NSCLC patients who underwent both pre- and post-chemotherapy FDG PET imaging were retrospectively enrolled. Voxel-wise comparisons were performed using SPM12 to identify regional metabolic changes. Patients were stratified based on chemotherapy intensity (standard: ≥4 cycles; short-course: 1-3 cycles) and recovery interval (short: <6 months; long: ≥6 months), with subgroup and interaction analyses conducted accordingly. Compared with baseline, post-treatment scans revealed regional metabolic reductions, predominantly in the right thalamus, left frontal lobe, and bilateral temporal regions. Patients receiving standard chemotherapy exhibited more extensive metabolic reductions than those receiving short-course treatment, particularly in the bilateral temporal and cingulate regions. Furthermore, patients scanned within six months post-chemotherapy showed more pronounced reductions than those with longer recovery intervals, suggesting a potential trend of metabolic recovery over time. In contrast, patients with limited initial metabolic changes (i.e., short-course group) exhibited minimal changes across intervals. This within-subject FDG PET study provides longitudinal evidence that chemotherapy independently contributes to brain metabolic alterations in NSCLC patients, predominantly involving the frontal, temporal, and limbic regions. These findings highlight vulnerable neural substrates and underscore the clinical value of functional neuroimaging in cancer survivorship research.