Background: Factors necessitating the propensity of adults with upper body fat deposition (UBFD) for developing insulin resistance and cardiovascular diseases (CVDs) are poorly understood. Therefore, understanding the roles of adipocytokines in the development of UBFD-associated pathologies could be of clinical importance.
Aim: To assess the levels of selected adipocytokines in males with nuchal fat fold (NFF).
Methodology: Eighty-six males (43 with NFF and 43 without NFF) were enrolled into this study. Serum levels of tumour necrosis factor-alpha (TNF-α), resistin and adiponectin were determined using ELISA.
Results: Adiponectin level was significantly higher while resistin and TNF-α levels were significantly lower in NFF compared with the controls. TNF-α had significant positive correlation with systolic blood pressure (SBP) while adiponectin had significant positive correlation with the waist-hip ratio (WHR). Stratifying based on the obesity status, the mean body weight, BMI, waist circumference (WC), hip circumference (HC), WHR, neck circumference (NC), NFF and diastolic BP were significantly higher in NFF with obesity compared with those without obesity. However, levels of TNF-α, resistin and adiponectin were similar between the two groups.
Conclusions: NFF is associated with elevation in adiponectin level and increased CVD risk. NFF can therefore, serve as an index of early onset of cardiometabolic diseases.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.dsx.2021.102214 | DOI Listing |
Background: Lecanemab is a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils. In two clinical studies (phase 2, NCT01767311 and phase 3 ClarityAD, NCT03887455) in early Alzheimer's disease, lecanemab substantially reduced amyloid PET and significantly slowed clinical decline on multiple measures of cognition and function, including CDR-SB at 18 months. Models describing the change in amyloid PET and CDR-SB in response to lecanemab treatment were used to explore the impact of changing from the initial dosage regimen (10 mg/kg every 2 weeks [Q2W]) to a less intensive maintenance dosing regimen (10 mg/kg every 4 weeks [Q4W]) on clinical efficacy, and to explore the optimal duration of the initial dosing regimen.
View Article and Find Full Text PDFBackground: Senile dementia (SD) is a deteriorative organic brain disorder and it comprises Alzheimer's disease (AD) as a major variant. SD is shown impairment of mental capacities whereas AD is degeneration of neurons. According to World Health Organization (WHO) report; more than 55 million peoples have dementia and it is raising 10 million new cases every year.
View Article and Find Full Text PDFBackground: Previously, we demonstrated therapeutic benefits following intraperitoneal delivery of the TGR5 agonist HY209 in 5xFAD, a transgenic mouse model of Alzheimer's Disease (AD). Given the desirability of a more acceptable administration route for prolonged AD treatment, we assessed the efficacy of HY209 via oral delivery. This study aims to elucidate the therapeutic potential of NuCerin, an oral formulation of HY209, in the aforementioned AD model, while simultaneously identifying potential blood biomarkers indicative of NuCerin's therapeutic action.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
L & J Bio, Co., Ltd, Seoul, Songpa-Gu, Korea, Republic of (South).
Background: Neurofibrillary tangles (NFTs), along with amyloid beta plaque, are neuropathological aggregates of Alzheimer's Disease (AD). Hyperphosphorylated tau is responsible for the NFTs formation and further neurodegeneration in AD. The hippocampal region and the entorhinal cortex (EC) have been a major focus of AD research because the deposits of hyperphosphorylated tau protein and NFT in these regions are correlated with memory deficits.
View Article and Find Full Text PDFBackground: VY-TAU01 is a recombinant humanized IgG4 monoclonal antibody (mAb) directed against pathological tau for the treatment of patients with mild dementia or mild cognitive impairment due to Alzheimer's disease (AD). Both VY-TAU01 and its parental mouse IgG1 mAb Ab-01 target an epitope in the C-terminus of tau, bind pathological tau with high affinity and selectivity over wild-type tau, block paired helical filament seed-induced tau aggregates in vitro, and selectively stain tau tangles in AD and P301S mouse (C57/B6J-Tg[Thy1-MAPT*P301S]2541Godt) brain. Ab-01 robustly inhibits seeding and propagation of pathological tau in a P301S mouse seeding model.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!