The Experts below are selected from a list of 28992 Experts worldwide ranked by ideXlab platform
Dale Corbett - One of the best experts on this subject based on the ideXlab platform.
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the effects of poststroke aerobic exercise on Neuroplasticity a systematic review of animal and clinical studies
Translational Stroke Research, 2015Co-Authors: Michelle Ploughman, Mark W Austin, Lindsay Glynn, Dale CorbettAbstract:Aerobic exercise may be a catalyst to promote Neuroplasticity and recovery following stroke; however, the optimal methods to measure Neuroplasticity and the effects of training parameters have not been fully elucidated. We conducted a systematic review and synthesis of clinical trials and studies in animal models to determine (1) the extent to which aerobic exercise influences poststroke markers of Neuroplasticity, (2) the optimal parameters of exercise required to induce beneficial effects, and (3) consistent outcomes in animal models that could help inform the design of future trials. Synthesized findings show that forced exercise at moderate to high intensity increases brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), nerve growth factor (NGF), and synaptogenesis in multiple brain regions. Dendritic branching was most responsive to moderate rather than intense training. Disparity between clinical stroke and stroke models (timing of initiation of exercise, age, gender) and clinically viable methods to measure Neuroplasticity are some of the areas that should be addressed in future research.
Simone Giovanni - One of the best experts on this subject based on the ideXlab platform.
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The translational landscape in spinal cord injury: focus on Neuroplasticity and regeneration
Nature Reviews Neurology, 2019Co-Authors: Thomas H. Hutson, Simone GiovanniAbstract:Spinal cord injury leads to disruption of neural circuitry and connectivity, resulting in permanent neurological disability. Hutson and Di Giovanni assess the clinical potential of emerging strategies that are designed to augment Neuroplasticity and promote sensorimotor recovery after spinal cord injury. Spinal cord injury (SCI) is a complex pathological condition and although several therapeutic approaches have shown potential in preclinical studies, few have progressed to clinical trials. Understanding the spatial and temporal changes in transcription and chromatin accessibility in selected neuronal subpopulations after SCI could help identify key proteins that orchestrate specific changes in Neuroplasticity. The use of chondroitinase ABC and anti-NogoA treatment to reduce inhibitory signalling in the neuronal extrinsic environment after SCI has shown promise in terms of promoting axon sprouting and recovery. Unprecedented long-distance axon regeneration, cell replacement and relay formation have been achieved using spinal cord-derived neural stem cell grafts combined with growth factors. Neuromodulation strategies including electrical epidural stimulation and brain–machine interfaces have demonstrated impressive improvements in voluntary motor function, and wireless systems will further improve the clinical utility of these strategies. Combining mechanism-based biological strategies with targeted technological interventions to augment Neuroplasticity, followed by rehabilitation to direct circuit reorganization, could facilitate clinically meaningful recovery after SCI. Over the past decade, we have witnessed a flourishing of novel strategies to enhance Neuroplasticity and promote axon regeneration following spinal cord injury, and results from preclinical studies suggest that some of these strategies have the potential for clinical translation. Spinal cord injury leads to the disruption of neural circuitry and connectivity, resulting in permanent neurological disability. Recovery of function relies on augmenting Neuroplasticity to potentiate sprouting and regeneration of spared and injured axons, to increase the strength of residual connections and to promote the formation of new connections and circuits. Neuroplasticity can be fostered by exploiting four main biological properties: neuronal intrinsic signalling, the neuronal extrinsic environment, the capacity to reconnect the severed spinal cord via neural stem cell grafts, and modulation of neuronal activity. In this Review, we discuss experimental evidence from rodents, nonhuman primates and patients regarding interventions that target each of these four properties. We then highlight the strengths and challenges of individual and combinatorial approaches with respect to clinical translation. We conclude by considering future developments and providing views on how to bridge the gap between preclinical studies and clinical translation.
Rupert Lanzenberger - One of the best experts on this subject based on the ideXlab platform.
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serotonin and Neuroplasticity links between molecular functional and structural pathophysiology in depression
Neuroscience & Biobehavioral Reviews, 2017Co-Authors: Christoph Kraus, Eero Castren, Siegfried Kasper, Rupert LanzenbergerAbstract:Serotonin modulates Neuroplasticity, especially during early life, and dysfunctions in both systems likewise contribute to pathophysiology of depression. Recent findings demonstrate that serotonin reuptake inhibitors trigger reactivation of juvenile-like Neuroplasticity. How these findings translate to clinical antidepressant treatment in major depressive disorder remains unclear. With this review, we link preclinical with clinical work on serotonin and Neuroplasticity to bring two pathophysiologic models in clinical depression closer together. Dysfunctional developmental plasticity impacts on later-life cognitive and emotional functions, changes of synaptic serotonin levels and receptor levels are coupled with altered synaptic plasticity and neurogenesis. Structural magnetic resonance imaging in patients reveals disease-state-specific reductions of gray matter, a marker of Neuroplasticity, and reversibility upon selective serotonin reuptake inhibitor treatment. Translational evidence from magnetic resonance imaging in animals support that reduced densities and sizes of neurons and reduced hippocampal volumes in depressive patients could be attributable to changes of serotonergic Neuroplasticity. Since ketamine, physical exercise or learning enhance Neuroplasticity, combinatory paradigms with selective serotonin reuptake inhibitors could enhance clinical treatment of depression.
Ronald S. Duman - One of the best experts on this subject based on the ideXlab platform.
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Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms
Neuropsychopharmacology, 2007Co-Authors: Christopher Pittenger, Ronald S. DumanAbstract:Increasing evidence demonstrates that Neuroplasticity, a fundamental mechanism of neuronal adaptation, is disrupted in mood disorders and in animal models of stress. Here we provide an overview of the evidence that chronic stress, which can precipitate or exacerbate depression, disrupts Neuroplasticity, while antidepressant treatment produces opposing effects and can enhance Neuroplasticity. We discuss Neuroplasticity at different levels: structural plasticity (such as plastic changes in spine and dendrite morphology as well as adult neurogenesis), functional synaptic plasticity, and the molecular and cellular mechanisms accompanying such changes. Together, these studies elucidate mechanisms that may contribute to the pathophysiology of depression. Greater appreciation of the convergence of mechanisms between stress, depression, and Neuroplasticity is likely to lead to the identification of novel targets for more efficacious treatments.
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antidepressants and Neuroplasticity
Bipolar Disorders, 2002Co-Authors: Carrol Dsa, Ronald S. DumanAbstract:Objective: We review the literature on the cellular changes that underlie the structural impairments observed in brains of animals exposed to stress and in subjects with depressive disorders. We discuss the molecular, cellular and structural adaptations that underlie the therapeutic responses of different classes of antidepressants and contribute to the adaptive plasticity induced in the brain by these drugs. Methods: We review results from various clinical and basic research studies. Results: Studies demonstrate that chronic antidepressant treatment increases the rate of neurogenesis in the adult hippocampus. Studies also show that antidepressants up-regulate the cyclic adenosine monophosphate (cAMP) and the neurotrophin signaling pathways involved in plasticity and survival. In vitro and in vivo data provide direct evidence that the transcription factor, cAMP response element-binding protein (CREB) and the neurotrophin, brain derived-neurotrophic factor (BDNF) are key mediators of the therapeutic response to antidepressants. Conclusions: These results suggest that depression maybe associated with a disruption of mechanisms that govern cell survival and neural plasticity in the brain. Antidepressants could mediate their effects by increasing neurogenesis and modulating the signaling pathways involved in plasticity and survival.
Chet T. Moritz - One of the best experts on this subject based on the ideXlab platform.
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Now is the Critical Time for Engineered Neuroplasticity
Neurotherapeutics, 2018Co-Authors: Chet T. MoritzAbstract:Recent advances in neuroscience and devices are ushering in a new generation of medical treatments. Engineered biodevices are demonstrating the potential to create long-term changes in neural circuits, termed Neuroplasticity. Thus, the approach of engineering Neuroplasticity is rapidly expanding, building on recent demonstrations of improved quality of life for people with movement disorders, epilepsy, and spinal cord injury. In addition, discovering the fundamental mechanisms of engineered Neuroplasticity by leveraging anatomically well-documented systems like the spinal cord is likely to provide powerful insights into solutions for other neurotraumas, such as stroke and traumatic brain injury, as well as neurodegenerative disorders, such as Alzheimer’s, Parkinson disease, and multiple sclerosis. Now is the time for advancing both the experimental neuroscience, device development, and pioneering human trials to reap the benefits of engineered Neuroplasticity as a therapeutic approach for improving quality of life after spinal cord injury.
