Omarblackburn5754

Current management for spinal cord injury aims to reduce secondary damage and recover sensation and movement. Acute spinal cord injury is often accompanied by spinal cord compartment syndrome. Decompression by durotomy and/or myelotomy attempts to relieve secondary damage by completelyrelieving the compression of the spinal cord, removing the necrotic tissue, decreasing edema, reducing hemorrhage, and improving blood circulation in the spinal cord. However, it is controversial whether durotomy and/or myelotomy after spinal cord injury are beneficial to neurological recovery. This review compares the clinical effects of durotomy with those of myelotomy in the treatment of spinal cord injury. We found that durotomy has been performed more than myelotomy in the clinic, and that durotomy may be safer and more effective than myelotomy. Durotomy performed in humans had positive effects on neurological function in 92.3% of studies in this review, while durotomy in animals had positive effects on neurological function in 83.3% of studies. Myelotomy procedures were effective in 80% of animal studies, but only one clinical study of myelotomy has reported positive results, of motor and sensory improvement, in humans. However, a number of new animal studies have reported that durotomy and myelotomy are ineffective for spinal cord injury. More clinical data, in the form of a randomized controlled study, are needed to understand the effectiveness of durotomy and myelotomy.Activin receptor-like kinase 1 (ALK1) is a transmembrane serine/threonine receptor kinase of the transforming growth factor beta (TGFβ) receptor superfamily. ALK1 is specifically expressed in vascular endothelial cells, and its dynamic changes are closely related to the proliferation of endothelial cells, the recruitment of pericytes to blood vessels, and functional differentiation during embryonic vascular development. The pathophysiology of many cerebrovascular diseases is today understood as a disorder of endothelial cell function and an imbalance in the proportion of vascular cells. Indeed, mutations in ALK1 and its co-receptor endoglin are major genetic risk factors for vascular arteriovenous malformation. Many studies have shown that ALK1 is closely related to the development of cerebral aneurysms, arteriovenous malformations, and cerebral atherosclerosis. In this review, we describe the various roles of ALK1 in the regulation of angiogenesis and in the maintenance of cerebral vascular homeostasis, and we discuss its relationship to functional dysregulation in cerebrovascular diseases. This review should provide new perspectives for basic research on cerebrovascular diseases and offer more effective targets and strategies for clinical diagnosis, treatment, and prevention.For decades visual field defects were considered irreversible because it was thought that in the visual system the regeneration potential of the neuronal tissues is low. Nevertheless, there is always some potential for partial recovery of the visual field defect that can be achieved through induction of neuroplasticity. Neuroplasticity refers to the ability of the brain to change its own functional architecture by modulating synaptic efficacy. It is maintained throughout life and just as neurological rehabilitation can improve motor coordination, visual field defects in glaucoma, diabetic retinopathy or optic neuropathy can be improved by inducing neuroplasticity. STAT5IN1 In ophthalmology many new treatment paradigms have been tested that can induce neuroplastic changes, including non-invasive alternating current stimulation. Treatment with alternating current stimulation (e.g., 30 minutes, daily for 10 days using transorbital electrodes and ~10 Hz) activates the entire retina and parts of the brain. Electroencephalography and functional magnetic resonance imaging studies revealed local activation of the visual cortex, global reorganization of functional brain networks, and enhanced blood flow, which together activate neurons and their networks. The future of low vision is optimistic because vision loss is indeed, partially reversible.The over-activated microglial cells induce neuroinflammation which has the main role in neurological disorders. The over-activated microglia can disturb neuronal function by releasing inflammatory mediators leading to neuronal dysfunctions and death. Thus, inhibition of over-activated microglia may be an effective therapeutic approach for modulating neuroinflammation. Experimental studies have indicated anti-neuroinflammatory effects of flavonoids such as green tea catechins. The current research was aimed to review the effect of green tea catechins in inhibiting microglial cells, inflammatory cascades, and subsequent neurological diseases.Inherited retinal degeneration is a major cause of incurable blindness characterized by loss of retinal photoreceptor cells. Inherited retinal degeneration is characterized by high genetic and phenotypic heterogeneity with several genes mutated in patients affected by these genetic diseases. The high genetic heterogeneity of these diseases hampers the development of effective therapeutic interventions for the cure of a large cohort of patients. Common cell demise mechanisms can be envisioned as targets to treat patients regardless the specific mutation. One of these targets is the increase of intracellular calcium ions, that has been detected in several murine models of inherited retinal degeneration. Recently, neurotrophic factors that favor the efflux of calcium ions to concentrations below toxic levels have been identified as promising molecules that should be evaluated as new treatments for retinal degeneration. Here, we discuss therapeutic options for inherited retinal degeneration and we will focus on neuroprotective approaches, such as the neuroprotective activity of the Pigment epithelium-derived factor. The characterization of specific targets for neuroprotection opens new perspectives together with many questions that require deep analyses to take advantage of this knowledge and develop new therapeutic approaches. We believe that minimizing cell demise by neuroprotection may represent a promising treatment strategy for retinal degeneration.