Purpose: The aim of this study was to investigate the differences in early (EOAD) and late (LOAD) onset of Alzheimer´s disease, as well as glucose uptake, regional cerebral blood flow (R1), amyloid depositions, and functional brain connectivity between normal young (YC) and Old Controls (OC).
Methodology: The study included 22 YC (37 ± 5 y), 22 OC (73 ± 5.9 y), 18 patients with EOAD (63 ± 9.5 y), and 18 with LOAD (70.6 ± 7.1 y). Patients underwent FDG and PIB PET/CT. R1 images were obtained from the compartmental analysis of the dynamic PIB acquisitions. Images were analyzed by a voxel-wise and a VOI-based approach. Functional connectivity was studied from the R1 and glucose uptake images.
Results: OC had a significant reduction of R1 and glucose uptake compared to YC, predominantly at the dorsolateral and mesial frontal cortex. EOAD and LOAD vs. OC showed a decreased R1 and glucose uptake at the posterior parietal cortex, precuneus, and posterior cingulum. EOAD vs. LOAD showed a reduction in glucose uptake and R1 at the occipital and parietal cortex and an increased at the mesial frontal and temporal cortex. There was a mild increase in an amyloid deposition at the frontal cortex in LOAD vs. EOAD. YC presented higher connectivity than OC in R1 but lower connectivity considering glucose uptake. Moreover, EOAD and LOAD showed a decreased connectivity compared to controls that were more pronounced in glucose uptake than R1.
Conclusion: Our results demonstrated differences in amyloid deposition and functional imaging between groups and a differential pattern of functional connectivity in R1 and glucose uptake in each clinical condition. These findings provide new insights into the pathophysiological processes of AD and may have an impact on patient diagnostic evaluation.
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http://dx.doi.org/10.2174/1567205018666211116095035 | DOI Listing |
Hypertension, a major cause of cardiomyopathy, is one of the most critical risk factors for heart failure and mortality worldwide. Loss of metabolic flexibility of cardiomyocytes is one of the major causes of heart failure. Although Catestatin (CST) treatment is known to be both hypotensive and cardioprotective, its effect on cardiac metabolism is unknown.
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Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita-shi, Osaka, Japan.
Hypertrophic cardiomyopathy (HCM) is a frequent inherited form of heart failure. The underlying cause of HCM is generally attributed to mutations in genes that encode for sarcomeric proteins, but the pathogenesis of the disease is also influenced by non-genetic factors, which can contribute to diastolic dysfunction and hypertrophic remodeling. Central to the pathogenesis of HCM is hypercontractility, a state that is an antecedent to several key derangements, including increased mitochondrial workload and oxidative stress.
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Turku PET Centre, University of Turku, Turku, Finland.
Anorexia nervosa (AN) is a severe psychiatric disorder, characterized by restricted eating, fear to gain weight, and a distorted body image. Mu-opioid receptor (MOR) functions as a part of complex opioid system and supports both homeostatic and hedonic control of eating behavior. Thirteen patients with AN and thirteen healthy controls (HC) were included in this study.
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Department of Pathogenobiology, College of Basic Medical Sciences, Jilin University, Changchun 130021, Jilin Province, China. Electronic address:
Hepatocellular carcinoma (HCC), known for its high malignancy, exhibits a critical feature in its progression through the alteration of metabolic pathways. Our study initially observed an increase in hyaluronic acid (HA) secretion by HCC cells through ELISA analysis. Further protein-protein interaction (PPI) network analysis highlighted CD44 and HAS2 as critical nodes, suggesting their pivotal roles in HA metabolism.
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Department of Orthopaedics, Nanchang People's Hospital (The Third Hospital of Nanchang), Nanchang City, Jiangxi Province, China.
Reduction of glucose transporter 1 (GLUT1), even deletion, may results in cartilage fibrosis and osteoarthritis. This study aims to investigate the SUMOylation of GLUT1 in osteoarthritis through small ubiquitin-like modifier 1(SUMO1), and explore the role of SUMOylated GLUT1 in glycometabolism, proliferation and apoptosis in chondrocytes. Human chondrocytes were incubated with 10 ng/mL of IL-1β to mimic osteoarthritis in vitro.
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