β-Amyloid: The Key Peptide in the Pathogenesis of Alzheimer’s Disease

The amyloid β peptide (Aβ) is a critical initiator that triggers the progression of Alzheimer’s Disease (AD) via accumulation and aggregation, of which the process may be caused by Aβ overproduction or perturbation clearance. Aβ is generated from amyloid precursor protein (APP) through sequential cleavage of β- and γ-secretases while Aβ removal is dependent on the proteolysis and lysosome degradation system. Here, we overviewed the biogenesis and toxicity of Aβ as well as the regulation of Aβ production and clearance. Moreover, we also summarized the animal models correlated with Aβ that are essential in AD research. In addition, we discussed current immunotherapeutic approaches targeting Aβ to give some clues for exploring the more potentially efficient drugs for treatment of AD

Optimum neural tuning curves for information efficiency with rate coding and finite-time window

An important question for neural encoding is what kind of neural systems can convey more information with less energy within a finite time coding window. This paper first proposes a finite-time neural encoding system, where the neurons in the system respond to a stimulus by a sequence of spikes that is assumed to be Poisson process and the external stimuli obey normal distribution. A method for calculating the mutual information of the finite-time neural encoding system is proposed and the definition of information efficiency is introduced. The values of the mutual information and the information efficiency obtained by using Logistic function are compared with those obtained by using other functions and it is found that Logistic function is the best one. It is further found that the parameter representing the steepness of the Logistic function has close relationship with full entropy, and that the parameter representing the translation of the function associates with the energy consumption and noise entropy tightly. The optimum parameter combinations for Logistic function to maximize the information efficiency are calculated when the stimuli and the properties of the encoding system are varied respectively. Some explanations for the results are given. The model and the method we proposed could be useful to study neural encoding system, and the optimum neural tuning curves obtained in this paper might exhibit some characteristics of a real neural system

Polyamine regulates tolerance to water stress in leaves of white clover associated with antioxidant defense and dehydrin genes via involvement in calcium messenger system and hydrogen peroxide signaling

Endogenous polyamine (PA) may play a critical role in tolerance to water stress in plants acting as a signaling molecule activator. Water stress caused increases in endogenous PA content in leaves, including putrescine (Put), spermidine (Spd), and spermine (Spm). Exogenous application of Spd could induce the instantaneous H2O2 burst and accumulation of cytosolic free Ca2+, and activate NADPH oxidase and CDPK gene expression in cells. To a great extent, PA biosynthetic inhibitor reduced the water stress-induced H2O2 accumulation, free cytosolic Ca2+ release, antioxidant enzyme activities and genes expression leading to aggravate water stress-induced oxidative damage, while these suppressing effects were alleviated by the addition of exogenous Spd, indicating PA was involved in water stress-induced H2O2 and cytosolic free Ca2+ production as well as stress tolerance. Dehydrin genes (Y2SK, Y2K, and SK2) were showed to be highly responsive to exogenous Spd. PA-induced antioxidant defense and dehydrin genes expression could be blocked by the scavenger of H2O2 and the inhibitors of H2O2 generation or Ca2+ channels blockers, a calmodulin antagonist, as well as the inhibitor of CDPK. These findings suggested that PA regulated tolerance to water stress in white clover associated with antioxidant defenses and dehydrins via involvement in the calcium messenger system and H2O2 signaling pathways. PA-induced H2O2 production required Ca2+ release, while PA-induced Ca2+ release was also essential for H2O2 production, suggesting an interaction between PA-induced H2O2 and Ca2+ signaling