Abstract
The recent years saw the advent of promising preclinical strategies that combat the devastating effects of a spinal cord injury (SCI) that are progressing towards clinical trials. However, individually, these treatments produce only modest levels of recovery in animal models of SCI that could hamper their implementation into therapeutic strategies in spinal cord injured humans. Combinational strategies have demonstrated greater beneficial outcomes than their individual components alone by addressing multiple aspects of SCI pathology. Clinical trial designs in the future will eventually also need to align with this notion. The scenario will become increasingly complex as this happens and conversations between basic researchers and clinicians are required to ensure accurate study designs and functional readouts.
Highlights
Miller, 2004; Geoffroy & Zheng, 2014; Worzfeld & Offermanns, 2014)
Lentiviral vector (LV) gene delivery was used to achieve long-term expression of this “mammalianised” Chondroitinase ABC (ChABC) gene in the contused rat spinal cord which resulted in large-scale Chondroitin sulphate proteoglycans (CSPGs) degradation and improved behavioural scores following thoracic injury (Bartus et al, 2014)
spinal cord injury (SCI) results in many problems that need to be addressed in order to discover a cure for the condition
Summary
2004; Geoffroy & Zheng, 2014; Worzfeld & Offermanns, 2014). Yet even when provided with a growth-permissive environment, central neurons regenerate feebly compared to their peripheral or immature CNS counterparts, indicating that they have intrinsic growth limiting factors (Hilton & Bradke, 2017). Seven therapeutic targets are present which can improve functional recovery after SCI: neuroprotective strategies to limit ongoing secondary damage resulting in spared tissue; tissue and cellular transplants to replace lost cells and may provide trophic or growth-permissive environments; removal of inhibitory factors such as CSPGs to allow for enhanced axonal growth; targeting neuron-intrinsic mechanisms to enhance intrinsic regenerative response which could be directed through the resupply of trophic support; and remyelination of demyelinated axons may improve axonal conduction. Lentiviral vector (LV) gene delivery was used to achieve long-term expression of this “mammalianised” ChABC (mChABC) gene in the contused rat spinal cord which resulted in large-scale CSPG degradation and improved behavioural scores following thoracic injury (Bartus et al, 2014) These findings were replicated in the functional restoration of upper limb function and the strategy further developed to control gene expression (James et al, 2015). Adult male Lister Hooded rats 250–300 g C4 dorsal funiculus cut Acute ChABC treatment
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