Neuronal cell death in the central nervous system has always been a challenging process to decipher. In normal physiological conditions, neuronal cell death is restricted in the adult brain, even in aged individuals. However, in the pathological conditions of various neurodegenerative diseases, cell death and shrinkage in a specific region of the brain represent a fundamental pathological feature across different neurodegenerative diseases. In this review, we will briefly go through the general pathways of cell death and describe evidence for cell death in the context of individual common neurodegenerative diseases, discussing our current understanding of cell death by connecting with renowned pathogenic proteins, including Tau, amyloid-beta, alpha-synuclein, huntingtin and TDP-43.
Disrupted myelin and impaired myelin repair have been observed in the brains of patients and various mouse models of Alzheimer’s disease (AD). Clemastine, an H1-antihistamine, shows the capability to induce oligodendrocyte precursor cell (OPC) differentiation and myelin formation under different neuropathological conditions featuring demyelination via the antagonism of M1 muscarinic receptor. In this study, we investigated if aged APPSwe/PS1dE9 mice, a model of AD, can benefit from chronic clemastine treatment. We found the treatment reduced brain amyloid-beta deposition and rescued the short-term memory deficit of the mice. The densities of OPCs, oligodendrocytes, and myelin were enhanced upon the treatment, whereas the levels of degraded MBP were reduced, a marker for degenerated myelin. In addition, we also suggest the role of clemastine in preventing OPCs from entering the state of cellular senescence, which was shown recently as an essential causal factor in AD pathogenesis. Thus, clemastine exhibits therapeutic potential in AD via preventing senescence of OPCs.
Abstract-A multi-interface ZigBee building area network (MIZBAN) for a high-traffic advanced metering infrastructure (AMI) for high-rise buildings was developed. This supports meter management functions such as Demand Response for smart grid applications. To cater for the high-traffic communication in these building area networks (BANs), a multi-interface management framework was defined and designed to coordinate the operation between multiple interfaces based on a newly defined tree-based mesh (T-Mesh) ZigBee topology, which supports both mesh and tree routing in a single network. To evaluate MIZBAN, an experiment was set up in a five-floor building. Based on the measured data, simulations were performed to extend the analysis to a 23-floor building. These revealed that MIZBAN yields an improvement in application-layer latency of the backbone and the floor network by 75% and 67%, respectively. This paper provides the design engineer with seven recommendations for a generic MIZBAN design, which will fulfill the requirement for demand response by the U.S. government, i.e. a latency of less than 0.25 s.Index Terms-Advanced Metering Infrastructure (AMI), building area network (BAN), multi-interface, smart grid, ZigBee.
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