Rabbit anti Human APP (N-terminal, aa 1-14) polyclonal antibody

Chun et al. find that a severe model of reactive astrocytes overproduces hydrogen peroxide, leading to the development of Alzheimer's disease-like pathologies, including neurodegeneration, tauopathy and memory impairment. Although the pathological contributions of reactive astrocytes have been implicated in Alzheimer's disease (AD), their in vivo functions remain elusive due to the lack of appropriate experimental models and precise molecular mechanisms. Here, we show the importance of astrocytic reactivity on the pathogenesis of AD using GiD, a newly developed animal model of reactive astrocytes, where the reactivity of astrocytes can be manipulated as mild (GiDm) or severe (GiDs). Mechanistically, excessive hydrogen peroxide (H2O2) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H2O2 scavenger. These H2O2--induced pathological features of AD in GiDs are consistently recapitulated in a three-dimensional culture AD model, virus-infected APP/PS1 mice and the brains of patients with AD. Our study identifies H2O2 from severe but not mild reactive astrocytes as a key determinant of neurodegeneration in AD.

Purpose It is commonly believed that central hemodynamics is closely associated with the presence of cardiovascular events. However, controversial data exist on the acute response of competitive sports on central hemodynamics. Moreover, the central hemodynamic response to exercise is too transient to be investigated. Therefore, this study aimed to investigate the central hemodynamic response in young basketball athletes and controls after 1 h recovery after exercise. Methods Fifteen young basketball athletes and fifteen aged-matched controls were recruited to perform the Bruce test. Central hemodynamics were measured and calculated, including heart rate (HR), aortic systolic, diastolic, and pulse pressure (ASP, ADP, and APP), ejection duration (ED), sub-endocardial viability ratio (SEVR), central augmentation index (AIx), and AIx@HR75. Intra-group and inter-group differences were analyzed by two-way repeated measures ANOVA. Results ASP significantly decreased at 10 min after exercise in athletes, while it markedly declined at 15 min after exercise in controls (p < 0.01). Additionally, only in the athlete group, ADP significantly decreased at 50 min and at 1 h after exercise. AIx was also significantly reduced at 1-2, 20, 30, and 40 min after exercise (all p < 0.05). Moreover, there were significant differences in the changes of these parameters between the two groups at these measurement points (p < 0.05). SEVR significantly recovered to the baseline level after 30 min, while ED and HR returned to baseline levels at 40 min after exercise in both groups. Conclusion Sustained decrease of aortic BPs was sooner after the cessation of exercise in athletes than in controls, and changes of aortic stiffness were more evident in athletes than those in controls during the 1 h recovery period. Additionally, SEVR returned to the baseline sooner than ED and HR in athletes.