An overview of therapies to promote repair of the brain after stroke

Cramer, Steven C.

doi:10.1002/hed.21840

Cited by 19 publications

(12 citation statements)

References 140 publications

(377 reference statements)

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“…Comprehensive reviews of restorative therapies and their purported mechanisms are available [173, 174]. Briefly, several of the above therapies manipulate the peripheral nervous system while others directly stimulate brain matter.…”

Section: Treatment-driven Functional Recovery Mechanismsmentioning

confidence: 99%

Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Cassidy

Cramer

2016

Transl. Stroke Res.

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231

139

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With increasing rates of survival throughout the past several years, stroke remains one of the leading causes of adult disability. Following the onset of stroke, spontaneous mechanisms of recovery at the cellular, molecular, and systems levels ensue. The degree of spontaneous recovery is generally incomplete and variable amongst individuals. Typically, the best recovery outcomes entail the restitution of function in injured but surviving neural matter. An assortment of restorative therapies exists or is under development with the goal of potentiating restitution of function in damaged areas or in nearby ipsilesional regions by fostering neuroplastic changes, which often rely on mechanisms similar to those observed during spontaneous recovery. Advancements in stroke rehabilitation depend on the elucidation of both spontaneous and therapeutic-driven mechanisms of recovery. Further, the implementation of neural biomarkers in research and clinical settings will enable a multimodal approach to probing brain state and predicting the extent of post-stroke functional recovery. This review will discuss spontaneous and therapeutic-induced mechanisms driving post-stroke functional recovery while underscoring several potential restorative therapies and biomarkers.

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Section: Treatment-driven Functional Recovery Mechanismsmentioning

confidence: 99%

Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Cassidy

Cramer

2016

Transl. Stroke Res.

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231

139

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“…Stroke remains as a leading cause of death in the United States in part due to the lack of effective therapeutics for most patients (Cramer, 2011). The complexity of intracellular signaling mechanisms that are triggered in an ischemic event, as well as the variety of cell types that are affected in the brain, have made the search for effective treatments a daunting task.…”

Section: Introductionmentioning

confidence: 99%

Complete transglutaminase 2 ablation results in reduced stroke volumes and astrocytes that exhibit increased survival in response to ischemia

Colak

Johnson

2012

Neurobiology of Disease

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Transglutaminase 2 (TG2) is a very multifunctional protein that is ubiquitously expressed in the body. It is a Ca2+-dependent transamidating enzyme, a GTPase, as well as a scaffolding protein. TG2 is the predominant form of transglutaminase expressed in the mammalian nervous system. Previously, it was shown that TG2 can affect both cell death and cell survival mechanisms depending on the cell type and the stressor. In the case of ischemic stress, TG2 was previously shown to play a protective role in the models used. For example in hTG2 transgenic mice, where TG2 is overexpressed only in neurons, middle cerebral artery ligation (MCAL) resulted in smaller infarct volumes compared to wild type mice. In this study TG2 knock out mice were used to determine how endogenous TG2 affected stroke volumes. Intriguingly, infarct volumes in TG2 knock out mice were significantly smaller compared to wild type mice. As expected, primary neurons isolated from TG2 knock out mice showed decreased viability in response to oxygen-glucose deprivation. However, primary astrocytes that were isolated from TG2 knock out mice were resistant to oxygen-glucose deprivation in situ. Both wild type and knock out neurons were protected against oxygen glucose deprivation when they were co-cultured with astrocytes from TG2 knockout mice. Therefore, the decreased stroke volumes observed in TG2 knock out mice after MCAL, can be correlated with the protective effects of TG2 knock out in astrocytes in response to oxygen glucose deprivation in situ. These findings suggest that neuron-astrocyte crosstalk plays a significant role in mediating ischemic cell death and that TG2 differentially impacts cell survival depending on cell context.

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“…More than 795,000 people in the United States suffer from a stroke each year [3], [4]; this costs the country an estimated $38.6 billion that includes the cost of healthcare services and missed days of work. Computer-assisted technology has a key role in enhancing the traditional physical and occupational therapy, improving healthcare service, and decreasing the associated costs [5], [6].…”

Section: Introductionmentioning

confidence: 99%

An assistive tabletop keyboard for stroke rehabilitation

Khademi

Hondori

Dodakian

et al. 2013

Proceedings of the 2013 ACM International Conference on Interactive Tabletops and Surfaces

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1We propose a tabletop keyboard that assists stroke patients in using computers. Using computers for purposes such as paying bills, managing bank accounts, sending emails, etc., which all include typing, is part of Activities of Daily Living (ADL) that stroke patients wish to recover. To date, stroke rehabilitation research has greatly focused on using computer-assisted technology for rehabilitation. However, working with computers as a skill that patients need to recover has been neglected.The conventional human computer interfaces are mouse and keyboard. Using keyboard stays the main challenge for hemiplegic stroke patients because typing is usually a bimanual task. Therefore, we propose an assistive tabletop keyboard which is not only a novel computer interface that is specially designed to facilitate patient-computer interaction but also a rehab medium through which patients practice the desired arm/hand functions.

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An overview of therapies to promote repair of the brain after stroke

Cited by 19 publications

References 140 publications

Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Complete transglutaminase 2 ablation results in reduced stroke volumes and astrocytes that exhibit increased survival in response to ischemia

An assistive tabletop keyboard for stroke rehabilitation

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