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UK research brings hope for spinal cord injury treatment

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An existing drug may reduce damage after spinal cord injury by blocking the inflammatory response in the spinal cord, scientists at the University of Birmingham have found.

Their research, published in Clinical and Translational Medicine, demonstrates that AstraZeneca’s AZD1236 can significantly reduce ‘secondary damage’ caused by the body’s response to spinal cord injury (SCI).

Researchers used animal models to demonstrate that the drug can promote significant nerve regeneration, with a 80 per cent preservation in nerve function following spinal cord compression injury.

This translated into an 85 per cent in movement and sensation, the effects observed following three days of treatment with the drug, starting within 24 hours of the injury taking place.

The AZD1236-treated animals showed unprecedented recovery within three weeks, while controls still showed significant deficits at six weeks post-injury.

One of the key drivers of SCI secondary damage is breakdown of the blood-spinal cord barrier (BSCB).

This results in excess fluid build-up around the spinal cord called oedema and triggers an inflammatory response that can hinder the healing process, and lead to nerve cell death.

AZD1236 is a potent and selective inhibitor of enzymes MMP-9 and MMP-12, which are implicated in the inflammatory process.

The researchers demonstrated that AZD1236 halts SCI-induced oedema, and reduces BSCB breakdown and scarring at the site of the injury.

They also examined the effect of AZD1236 dosing on MMP-9 and MMP-12 activity in both the bloodstream and cerebrospinal fluid, which surrounds the spinal cord.

Here they demonstrated significant suppression of enzyme activity after both oral dosing, and intrathecal dosing (injection into the spinal canal).

Oral dosing reduced enzyme activity by 90 per cent in serum, and 69-74 per cent in the cerebrospinal fluid.

Meanwhile, intrathecal injection delivered 88-90 per cent of suppression in the cerebrospinal fluid.

Further studies showed the AZD1236 supressed the formation of pro-inflammatory cytokines (molecules that are known to contribute to the development of long-lasting neuropathic pain, which often follows SCI) by 85-95 per cent.

AZD1236 was also found to be 82 per cent more effective at alleviating SCI-induced neuropathic pain sensitivity to cold, heat and touch when compared to currently used pain medications such as pregabalin (Lyrica) and gabapentin.

Study lead Professor Zubair Ahmed, Professor of Neuroscience and lead for the Neuroscience and Ophthalmology Section at The University’s Institute of Inflammation and Ageing, said:

“There is currently no reparative drug available for SCI patients, treatments only provide symptomatic relief and do not tackle the underlying molecular mechanisms that cause or contribute to oedema and blood-spinal cord barrier breakdown.

“This drug has the potential to be a first-in-class treatment against some of the key pathological drivers of SCI and could revolutionise the prospects for recovery of SCI patients.”

Hitesh Sanganee, Executive Director, Discovery Sciences, AstraZeneca said:

“The work by Professor Ahmed and his team has been supported through our Open Innovation Programme and represents a very successful collaboration between academia and industry to bring about the possibility of real benefits to patients affected by SCI, an area of great medical need.”

University of Birmingham Enterprise is now seeking investors and partners to take the therapeutic to clinical trials.

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