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Journal ArticleDOI

Minocycline reduces cell death and improves functional recovery after traumatic spinal cord injury in the rat.

TLDR
Data suggest that minocycline treatment modulated expression of cytokines, attenuated cell death and the size of lesions, and improved functional recovery in the injured rat, suggesting that this approach may provide a therapeutic intervention enabling us to reduce cellDeath and improve functional recovery after SCI.
Abstract
We examined the effects of minocycline, an anti-inflammatory drug, on functional recovery following spinal cord injury (SCI). Rats received a mild, weight-drop contusion injury to the spinal cord and were treated with the vehicle or minocycline at a dose of 90 mg/kg immediately after SCI and then twice at a dose of 45 mg/kg every 12 h. Injecting minocycline after SCI improved hind limb motor function as determined by the Basso-Beattie-Bresnahan (BBB) locomotor open field behavioral rating test. Twenty four to 38 days after SCI, BBB scores were significantly higher in minocycline-treated rats as compared with those in vehicle-treated rats. Morphological analysis showed that lesion size increased progressively in both vehicle-treated and minocycline-treated spinal cords. However, in response to treatment with minocycline, the lesion size was significantly reduced at 21–38 days after SCI when compared to the vehicle control. Minocycline treatment significantly reduced the number of terminal deoxynucleotidyl ...

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Journal ArticleDOI

Traumatic spinal cord injury

TL;DR: Several animal models and complementary behavioural tests of SCI have been developed to mimic this pathological process and form the basis for the development of preclinical and translational neuroprotective and neuroregenerative strategies.
Journal ArticleDOI

Therapeutic interventions after spinal cord injury.

TL;DR: It is predicted that combinations of strategies will lead to improvements in outcome after SCI, and that individual therapies are unlikely to provide a panacea.
Journal ArticleDOI

Role of pro-inflammatory cytokines released from microglia in neurodegenerative diseases.

TL;DR: Current understanding of the involvement of cytokines in neurodegenerative disorders and their potential signaling mechanisms are summarized to suggest that microglial activation and pro-inflammatory cytokines merit interest as targets in the treatment of neurodegnerative disorders.
Journal ArticleDOI

Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury

TL;DR: An important role for activated microglia in the maintenance of chronic central below-level pain after SCI is suggested and the newly emerging role of non-neuronal immune cells as a contributing factor in post-SCI pain is supported.
Journal Article

Secondary injury mechanisms in traumatic spinal cord injury: a nugget of this multiply cascade

TL;DR: This article has cataloged over twenty five identified secondary mechanisms of injury in the spinal cord in an open access portal, and is particularly versatile for starters in spinal cord injury research.
References
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Journal ArticleDOI

A Sensitive and Reliable Locomotor Rating Scale for Open Field Testing in Rats

TL;DR: The data indicate that the BBB scale is a valid and predictive measure of locomotor recovery able to distinguish behavioral outcomes due to different injuries and to predict anatomical alterations at the lesion center.
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Apoptosis in the nervous system

TL;DR: The principal molecular components of the apoptosis programme in neurons include Apaf-1 (apoptotic protease-activating factor 1) and proteins of the Bcl-2 and caspase families, which regulate neuronal apoptosis through the action of critical protein kinase cascades.
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Graded Histological and Locomotor Outcomes after Spinal Cord Contusion Using the NYU Weight-Drop Device versus Transection

TL;DR: Injury reproducibility is an important characteristic of experimental models of spinal cord injuries (SCI) because it limits the variability in locomotor and anatomical outcome measures and spared descending systems appear to modify segmental systems which produce greater behavioral improvements than isolated cord systems.
Journal ArticleDOI

Administration of Methylprednisolone for 24 or 48 Hours or Tirilazad Mesylate for 48 Hours in the Treatment of Acute Spinal Cord Injury Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial

TL;DR: Patients with acute spinal cord injury who receive methylprednisolone within 3 hours of injury should be maintained on the treatment regimen for 24 hours, and patients treated with tirilazad for 48 hours showed motor recovery rates equivalent to patients who received methylpredisonsolone for 24Hours.
Journal ArticleDOI

Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys.

TL;DR: Both secondary degeneration at the site of SCI and the chronic demyelination of tracts away from the injury appear to be due in part to apoptosis, and as cytokines have been shown to mediate oligodendrocyte death in vitro, it seems likely that chronic demYelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.
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