Alterations in cerebral glucose metabolism can be indicative of both normal and pathological aging processes. In this retrospective study, we evaluated global and regional neurological glucose metabolism in 73 healthy individuals (mean age: 35.8 ± 13.1 years; 82.5% female) using 18F-Fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT). This population exhibited a low prevalence of comorbidities associated with cerebrovascular risk factors. We utilized ¹⁸F-FDG-PET/CT imaging and quantitative regional analysis to assess cerebral glucose metabolism. A statistically significant negative correlation was found between age and the global standardized uptake value mean (SUVmean) of FDG uptake (p = 0.000795), indicating a decrease in whole-brain glucose metabolism with aging. Furthermore, region-specific analysis identified significant correlations in four cerebral regions, with positive correlations in the basis pontis, cerebellar hemisphere, and cerebellum and a negative correlation in the lateral orbital gyrus. These results were further confirmed via linear regression analysis. Our findings reveal a nuanced understanding of how aging affects glucose metabolism in the brain, providing insight into normal neurology. The study underscores the utility of ¹⁸F-FDG-PET/CT as a sensitive tool in monitoring these metabolic changes, highlighting its potential for the early detection of neurological diseases and disorders related to aging.

Atherosclerosis, a leading cause of mortality and morbidity worldwide, involves inflammatory processes that result in plaque formation and calcification. The early detection of the molecular changes underlying these processes is crucial for effective disease management. This study utilized positron emission tomography/computed tomography (PET/CT) with [¹⁸F] sodium fluoride (NaF) as a tracer to visualize active calcification and inflammation at the molecular level. Our aim was to investigate the association between cardiovascular risk factors and [¹⁸F] NaF uptake in the left and right common carotid arteries (LCC and RCC). A cohort of 102 subjects, comprising both at-risk individuals and healthy controls, underwent [¹⁸F] NaF PET/CT imaging. The results revealed significant correlations between [¹⁸F] NaF uptake and cardiovascular risk factors such as age (β = 0.005, 95% CI 0.003–0.008, p < 0.01 in LCC and β = 0.006, 95% CI 0.004–0.009, p < 0.01 in RCC), male gender (β = −0.08, 95% CI −0.173–−0.002, p = 0.04 in LCC and β = −0.13, 95% CI −0.21–−0.06, p < 0.01 in RCC), BMI (β = 0.02, 95% CI 0.01–0.03, p < 0.01 in LCC and β = 0.02, 95% CI 0.01–0.03, p < 0.01 in RCC), fibrinogen (β = 0.006, 95% CI 0.0009–0.01, p = 0.02 in LCC and β = 0.005, 95% CI 0.001–0.01, p = 0.01), HDL cholesterol (β = 0.13, 95% CI 0.04–0.21, p < 0.01 in RCC only), and CRP (β = −0.01, 95% CI −0.02–0.001, p = 0.03 in RCC only). Subjects at risk showed a higher [¹⁸F] NaF uptake compared to healthy controls (one-way ANOVA; p = 0.02 in LCC and p = 0.04 in RCC), and uptake increased with estimated cardiovascular risk (one-way ANOVA, p < 0.01 in LCC only). These findings underscore the potential of [¹⁸F] NaF PET/CT as a sensitive tool for the early detection of atherosclerotic plaque, assessment of cardiovascular risk, and monitoring of disease progression. Further research is needed to validate the technique’s predictive value and its potential impact on clinical outcomes.

Cerebrovascular disease (CVD) is a global health concern, and early detection is crucial for effective intervention. This case report presents a 31-year-old male patient with multiple cardiac risk factors who underwent positron emission tomography/computed tomography (PET/CT) with ¹⁸F-sodium fluoride (NaF) and ¹⁸F-fluorodeoxyglucose (FDG) to evaluate for the presence and degree of atherosclerosis in the aorta, carotid arteries, coronary arteries, iliac arteries, and the femoral arteries. Elevated NaF uptake within the bilateral carotid arteries signified substantial ongoing vascular microcalcification. Reduced global brain metabolism and region-specific hypometabolism measured with FDG PET indicated potential cerebrovascular mechanisms that may be influencing neurological function. The findings highlight the potential of emerging PET tracers, such as NaF, to improve the diagnostic accuracy and therapeutic management of CVD. This case emphasizes the importance of a comprehensive diagnostic approach as well as continued investigation into CVD pathophysiology using PET-based techniques, which may guide the development of innovative therapeutic strategies.

Background: Cardiovascular disease is a leading cause of illness and death globally, primarily due to atherosclerosis. This disease reduces blood flow and oxygen delivery to organs, and when it affects the carotid arteries, it can lead to cognitive impairment and dementia. In a population of 104 individuals, comprising both healthy controls and individuals at elevated risk for developing cardiovascular diseases (CVD) due to identified risk factors, we used PET imaging with ¹⁸F-fluorodeoxyglucose (FDG) to assess cerebral glucose metabolism and ¹⁸F-sodium fluoride (NaF) to detect atherosclerotic calcification. Our statistical analysis revealed significant differences in metabolic activity between healthy and at-risk individuals in specific brain regions. ¹⁸F-FDG uptake in the brain varied inversely with respect to the clinical assessment of cardiovascular risk in regions such as the cuneus (β = −0.030, SE = 0.014, p = 0.035), middle occipital gyrus (β = −0.032, SE = 0.011, p = 0.005), and posterior cingulate gyrus (β = −0.032, SE = 0.015, p = 0.044). In contrast, areas including the basis pontis (β = 0.025, SE = 0.012, p = 0.038) and the pons (β = 0.034, SE = 0.013, p = 0.008) exhibited direct correlations. Notably, carotid ¹⁸F-NaF uptake had inverse associations with ¹⁸F-FDG uptake in the cerebellum (β = −0.825, SE = 0.354, p = 0.021), medulla (β = −0.888, SE = 0.405, p = 0.029), and posterior cingulate gyrus (β = −1.253, SE = 0.567, p = 0.028), while increased carotid calcification influenced metabolic activity in the fusiform gyrus (β = 1.660, SE = 0.498, p = 0.001) and globus pallidus (β = 1.505, SE = 0.571, p = 0.009). We observed that atherosclerotic plaque accumulation, especially in the carotid arteries, has potential implications for metabolic changes in brain regions governing cognition, emotion, sensory perception, and motor activities. Our findings underscore the possible early interventions that can be used to preempt or delay cognitive deterioration linked with cardiovascular ailments.

Background: Hepatocellular carcinoma (HCC) is a prevalent type of primary liver cancer and one of the leading causes of cancer-related mortality worldwide. Antivascular Ultrasound (AVUS) is a novel therapy approach that utilizes the mechanical and thermal interactions between ultrasound and microbubbles to disrupt tumor vasculature or potentiate effects of chemotherapy or radiation therapy in a dose-dependent fashion. In this review, we aim to illustrate the mechanisms of AVUS, focusing on the preclinical and clinical evidence of AVUS applications in HCC. Methods: Peer-reviewed publications pertaining to the use of AVUS in HCC were collected and analyzed. Results: 12 preclinical studies and 1 clinical trial were analyzed. At lower energy levels, AVUS can enhance tumor perfusion, facilitating the delivery of chemotherapy agents and resulting in improved therapeutic outcomes. Conversely, at higher energy levels, AVUS can disrupt tumor perfusion, leading to ischemic damage of the tumors. Combining AVUS with other therapeutic approaches, such as chemotherapy, radiation therapy, and transarterial radioembolization (TARE), can synergistically enhance therapeutic outcomes. Conclusions: AVUS is a promising novel treatment modality for HCC. Current evidence suggests that AVUS exhibits a dose-dependent nature, making it a versatile approach that can be effectively combined with other therapeutic regimens. Further clinical studies and long-term follow-ups are needed to establish the optimal clinical protocol and safety profile of AVUS.