Strategies for CNS repair following TBI

Aertker, Benjamin M.; Bedi, Supinder S.; Cox, Charles S.

doi:10.1016/j.expneurol.2015.01.008

Cited by 56 publications

(48 citation statements)

References 202 publications

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“…The ongoing brain damage characteristic of secondary injury culminates in notable cell death [24,40,41]. Typically, initial neuronal death following acute brain injury occurs by necrosis, on a time scale of minutes, then, a second wave of delayed cell death occurs mostly by apoptosis [13,[42][43][44][45]. Indeed, this protracted course of cell death following TBI may represent a unique opportunity for therapeutic intervention.…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

“…TBI also involves enhanced glutamatergic activity at extrasynaptic sites due to failure of glutamate uptake, gliotransmission, reverse operation of the glutamate transporters, increase in presynaptic glutamate release or increase in the number and/or stability of glutamatergic receptors [53,62,65,66]. The increase in glutamate levels occurs several minutes after the primary trauma, peaks in about 10 minutes and stays increased for several days [45,64]. Excitotoxicity also causes calcium influx and overload [67,68], resulting in cellular damage due to several mechanisms (i.e.…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

“…In that sense, strategies such as supplementing varying types of trophic factors (i.e. BDNF, VEGF, S100β), manipulating transcriptional regulators, or other pharmacological approaches targeting different aspects of the endogenous neurogenic response have shown promising results improving functional recovery following experimental models of TBI [45,155,161,165]. The potential use of cellular therapies to prevent secondary neural injury and promote recovery of injured tissue in trauma is an area of emerging investigation.…”

Section: Neuroprotective and Neurorestorative Processes In The Traumamentioning

confidence: 99%

“…These factors include activation of resident central nervous system (CNS) immune cells and cerebral infiltration of peripheral immune cells (through a disrupted BBB); these cells mediate inflammatory processes through secretion of a variety of inflammatory cytokines, chemokines, adhesion molecules, ROS, and complement factors [86,87]. Immediately following injury, the levels of various cytokines change drastically in the brain parenchyma and take approximately 48 hours to return to normal [45]. Accordingly, regional, intrathecal, and systemic concentrations of various inflammatory cytokines (interleukin-1, -1β, -6, -8, -10, -12, and tumor necrosis factor-alpha) are altered shortly after TBI in humans and experimental models [88][89][90][91][92][93][94].…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

“…As the major cellular component of the innate immune system in the central nervous system (CNS) and the first line of defense whenever injury or disease occurs, microglia play a critical role in neuroinflammation through the production of various cytokines, proteases, and ROS [45,99]. In the injured brain, microglia can produce neuroprotective factors, clear cellular debris, and orchestrate neurorestorative processes that are beneficial for neurological recovery after TBI [100,101].…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

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Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Understanding the pathophysiology of TBI is crucial for the development of more effective therapeutic strategies. At the moment of the traumatic impact, transfer of kinetic forces causes neurologic damage; this primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, called secondary neural injury. These areas of ongoing secondary injury, or areas of "traumatic penumbra," represent crucial targets for therapeutic interventions. This chapter is focused on the interplay between progression of parenchymal injury and the neuroprotective and neurorestorative processes that are emerging and developing subsequently to traumatic impact. Thus, we emphasized the role of traumatic penumbra in TBI pathogenesis and suggested a crucial contribution of the neurovascular units (NVUs) and paracrine effects of exosomes and miRNAs in promoting neurological recovery.

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Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Section: Neuroprotective and Neurorestorative Processes In The Traumamentioning

confidence: 99%

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

See 3 more Smart Citations

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Biomimetic Architectures for Peripheral Nerve Repair: A Review of Biofabrication Strategies

Wieringa

Pinho

Micera

et al. 2018

Adv Healthcare Materials

119

116

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Biofabrication techniques have endeavored to improve the regeneration of the peripheral nervous system (PNS), but nothing has surpassed the performance of current clinical practices. However, these current approaches have intrinsic limitations that compromise patient care. The "gold standard" autograft provides the best outcomes but requires suitable donor material, while implantable hollow nerve guide conduits (NGCs) can only repair small nerve defects. This review places emphasis on approaches that create structural cues within a hollow NGC lumen in order to match or exceed the regenerative performance of the autograft. An overview of the PNS and nerve regeneration is provided. This is followed by an assessment of reported devices, divided into three major categories: isotropic hydrogel fillers, acting as unstructured interluminal support for regenerating nerves; fibrous interluminal fillers, presenting neurites with topographical guidance within the lumen; and patterned interluminal scaffolds, providing 3D support for nerve growth via structures that mimic native PNS tissue. Also presented is a critical framework to evaluate the impact of reported outcomes. While a universal and versatile nerve repair strategy remains elusive, outlined here is a roadmap of past, present, and emerging fabrication techniques to inform and motivate new developments in the field of peripheral nerve regeneration.

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Visual system pathology in humans and animal models of blast injury

DeWalt

Eldred

2017

J of Comparative Neurology

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Injury from blast exposure is becoming a more prevalent cause of death and disability worldwide. The devastating neurological impairments that result from blasts are significant and lifelong. Progress in the development of effective therapies to treat injury has been slowed by its heterogeneous pathology and the dearth of information regarding the cellular mechanisms involved. Within the last decade, a number of studies have documented visual dysfunction following injury. This brief review examines damage to the visual system in both humans and animal models of blast injury. The in vivo use of the retina as a surrogate to evaluate brain injury following exposure to blast is also highlighted.

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Strategies for CNS repair following TBI

Cited by 56 publications

References 202 publications

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Biomimetic Architectures for Peripheral Nerve Repair: A Review of Biofabrication Strategies

Visual system pathology in humans and animal models of blast injury

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