From the Editor's Perspective: Aquaporins to Apoptosis

Our objective for Current Neurovascular Research is to consistently provide a broad platform for leading scientific inquiry of both neuronal and vascular origins in neuroscience. To this end, our current issue is no exception to this rule and offers the opinions and hypotheses of scientific leaders from a broad spectrum of investigative fields. In this issue, the initial article by Lehmann et al. outlines the function of cellular water-selective channels in the central nervous system, termed aquaporins, and the unique role that these channels play in water transport during disorders such as cerebral ischemia, trauma, and neoplasms. Subsequently, the next series of articles in this issue highlight novel therapeutic strategies for a variety of nervous system disorders. Sakamaki presents the molecular mechanisms that can determine vascular endothelial cell injury in conjunction with the cellular and environmental factors that can repair damaged vascular cells and foster new endothelial cell growth during angiogenesis. In another article by Panchal et al., cellular mediators of abnormal peptide metabolism are identified in Alzheimer's disease. Employing current knowledge of the pathways involved in β-amyloid catabolism, potential treatment strategies that would pursue prevention of toxic β-amyloid generation, improve β-amyloid clearance from the brain, and target the modulation of peptidases to degrade β-amyloid in the brain are examined. Further work by Mouzaki et al., Greco and Minghetti, and Ekshyyan and Aw complements such novel therapeutic strategies and describe the use of cytokine modulation and peptide analogs of myelin epitopes for the treatment of demyelinating disease, the biological tracking of cellular oxidative stress through the use of isoprostanes, and the elucidation of molecular programs that lead to cellular suicide in an effort to develop new therapeutic avenues for a host of neurodegenerative disorders. Kuwabara and Misawa extend this work with their discussion of the ionic disturbances and altered membrane excitability that precipitate peripheral neuropathies and motor neuron degeneration. Interestingly, in the manuscript by Holthoff, similar ionic cellular mechanisms that involve membrane excitability also are responsible for regenerative dendrites spikes that may be necessary for the generation of longterm synaptic plasticity. Taken to another level, Brosh and Barkai further describe the sequence of events necessary for learning paradigms that begin with enhanced neuronal excitability and ultimately culminate with enhanced spine density and synaptic connectivity. With this series of articles, we share a glimpse into the varied, but intimately linked cellular mechanisms in the nervous system that can bring apparently diverse topics such as aquaporins and apoptosis to a more common ground.