What happens to cells in the optic nerve after a head injury that affects sight?

Research details

  • Type of funding: PhD Studentship
  • Grant Holder: Dr Zubair Ahmed
  • Institute: University of Birmingham
  • Region: West Midlands
  • Start date: October 2015
  • End Date: March 2019
  • Priority: Treatment
  • Eye Category: Neuro-ophthalmology


About 8000 people each year in the UK lose their sight after an injury to the head. Sometimes, the optic nerve (which carries visual signals from the eye to the brain) is crushed or cut directly. But more often, a head injury or eye injury leads indirectly to the optic nerve cells dying.

So in this project the student will try to find out more about how a blunt blow or blast injury might lead to cell death. They will compare what happens to retinal ganglion cells (which make up the optic nerve) after different types of injury. They’ll also try to find out whether blocking a particular chain of chemical events inside the cells can prevent them from dying.

If so, the team will seek funds at the end of the project to begin clinical trials. In addition to people with sight loss from head trauma, the project could potentially help people with glaucoma.

  • Scientific summary

    Mechanisms of retinal ganglion cell death in direct and indirect traumatic optic neuropathy

    Traumatic optic neuropathy (TON) is a major cause of visual loss and occurs in 2.3% of head injuries (Pirouzmand 2012), but is also associated with eye injury and the direct nerve injury. Head injury affects 350,000 people in the UK every year (headway.org.uk), giving an estimated 8000 cases of TON secondary to head injury.

    Retinal ganglion cell (RGC) death in TON leads to irreversible and often profound visual loss. RGC death is most commonly studied using the optic nerve crush (ONC) model (direct TON).

    The research team is using two novel models of indirect TON, induced by primary blast injury and blunt ocular trauma to elucidate the cell death mechanisms in indirect TON and compare with direct TON, induced by ONC using in vivo and in vitro assessments of cell death molecules alongside functional and transcriptional analyses. Preliminary data have suggested that caspase-2 may mediate RGC death in experimental TON induced by ONC and blunt ocular trauma and that siRNA inhibition of caspase-2 is likely to preserve visual function.