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TBI rehabilitation: Lessons learned from animal studies about mechanisms, timing, and combinatorial approaches
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
These questions are not easy to answer but are being explored in more systematic ways.1 Although there are studies that have attempted to answer some of these questions in clinical populations,2,3 animal models have played a large role. The majority of these questions have primarily been addressed in animal models of stroke and applied to the rehabilitation of both stroke and TBI patients. Recently, however, my laboratory and others are beginning to explore these questions specifically in animal models of TBI. Doing so is demonstrating that the brain following TBI may be less responsive to rehabilitation and less plastic than the brain following stroke. This chapter discusses how examining rehabilitation, neuroplasticity, and adjunctive therapies in animal models of stroke and TBI can help inform studies to address these questions in clinical populations and improve rehabilitation of TBI patients in the clinic.
Statistical Update of Stroke in America
Published in Yanlin Wang-Fischer, Manual of Stroke Models in Rats, 2008
Yanlin Wang-Fischer, Lee Koetzner
Scientists have not given up the search for new approaches to the detrimental consequences of stroke. Research continues to add depth to the overall understanding of the condition, including the discovery of new risk factors, new methods of screening, and most importantly, developing new drugs and improving other treatment regimens. Animal models of stroke fulfill a critical need for those purposes.
Late changes in blood–brain barrier permeability in a rat tMCAO model of stroke detected by gadolinium-enhanced MRI
Published in Neurological Research, 2020
Catherine A. Morgan, Michel Mesquita, Maria Ashioti, John S. Beech, Steve C. R. Williams, Elaine Irving, Diana Cash
After an ischaemic insult the blood–brain barrier (BBB) may be compromised due to an increase in endothelial permeability and a breakdown of basal lamina [1–3]. Disturbance to the function of the blood–brain barrier (BBB) is observed clinically after stroke [4,5], but the large variability of clinical pathology makes it difficult to quantify this disturbance. Many preclinical studies conducted under the more controlled experimental conditions using animal models of stroke have reported increases in BBB permeability. A stroke model in which the middle cerebral artery is temporarily occluded (transient MCAO, tMCAO) is frequently employed in preclinical experiments because of its reproducibility (in terms of infarct size and location [6]) and clinical relevance (the MCA territory is often affected in human cases [7]). The tMCAO model is also thought to provide similar outcomes to those found in human ischaemic stroke with respect to changes in the BBB [8].
Emerging cytoprotective peptide therapies for stroke
Published in Expert Review of Neurotherapeutics, 2020
Bruno P. Meloni, David J. Blacker, Frank L. Mastaglia, Neville W. Knuckey
A large number of different CARPs have now demonstrated neuroprotective efficacy in animal models of stroke [3], providing confidence in the potential of this class of peptides with multimodal cytoprotective mechanisms of action to translate to an effective clinical stroke therapeutic. Indeed, the NA-1 and CN-105 peptides have paved the way in demonstrating the translational process from pre-clinical to clinical studies for ischemic and hemorrhagic stroke, respectively. Even more promising is the first clinical demonstration of a positive effect on clinical outcomes in a subgroup of patients with large artery ischemic stroke treated with the neuroprotective agent NA-1 [8], against which other promising CARPs such as the R18 peptide will now need to be compared [39]. As with any class of drug, the future challenge for CARPs will be to better characterize their neuroprotective mechanisms of action so that the peptide amino acid sequence can be tailored to improve their efficacy, affinity to specific targets and stability, as well as to provide broad spectrum neuroprotection for different stroke subtypes, and possibly other neurological disorders 22.
Phase I/II parallel double-blind randomized controlled clinical trial of perispinal etanercept for chronic stroke: improved mobility and pain alleviation
Published in Expert Opinion on Investigational Drugs, 2020
Stephen J. Ralph, Andrew Weissenberger, Ventzislav Bonev, Liam D. King, Mikaela D. Bonham, Samantha Ferguson, Ashley D. Smith, Adrienne A. Goodman-Jones, Anthony J. Espinet
Putting our findings into the wider evidential context, etanercept has been shown to improve neurological outcomes in six different experimental animal models of stroke (reviewed in [29]). The supportive evidence from animal models together with the findings from this randomized clinical trial and the favorable outcomes from open-label use in over a thousand stroke patients during the past 9 years [32,43]; reviewed in [29]) and the recent case report of immediate resolution of hemispatial neglect and CPSP after perispinal etanercept [31] should arguably justify the availability of perispinal etanercept therapy for chronic stroke being assigned a higher priority. Furthermore, encouragement should be offered promoting further studies to be undertaken so that this treatment gains wider recognition and the acceptance required by the regulatory authorities. The above results in toto provide solid evidential support for the efficacy of perispinal etanercept therapy in improving outcomes with chronic stroke. It also emphasizes the need for further studies to identify in detail how to better exploit this information for alleviating the suffering experienced by stroke victims and to avoid the presently used and often ineffective drugs currently in clinical practice with their higher associated health risks including noted features of sedation and dizziness [83, 84].