- Project: Target identification of oxidative stress response-modifying drugs in an ESC-derived motor neuron model of ALS
- Lead Applicant: Professor Kevin Talbot
- Amount funded: £79,991.29
In 2022 we agreed to fund the research project above. This research project has now been completed.
Those with MND need an armoury of drugs NOW to help with disease progression and quality of life. Although a final cure may come from detailed MND research into the forces driving this disease, such as the novel molecular therapy drugs such as Jacifusen and Tofersen, the quickest route to fighting back may be repositioning current drugs that are successful in related or distinct areas of human health. Indeed, this is reflected in the current major initiative termed ‘the EXPERTS-ALS study’ which is to test repositioned drugs quickly and efficiently in MND clinics. A Darby Rimmer MND Foundation funded study directed by Professor Kevin Talbot has demonstrated that common calcium blockers drugs which are used for a number of conditions including hypertension may be an effective treatment of MND. The data which is outlined below has attracted over a further £350,000 from MND Scotland & My Name’5 Doddie Foundation for further investigation as a potentially beneficial treatment for MND. This will hopefully help take the laboratory results to validation in the clinic. It is wonderful to see our supporters’ fundraising efforts helping to take steps towards both a cure and improving quality of life for those with MND
From the Talbot group
Drug development takes years, requires vast amounts of money, and has a very high failure rate. Some drugs that are already licenced for the treatment of other conditions, may also have potential to be beneficial in the treatment of MND. In previous work we identified a drug, called a calcium channel blocker, that is commonly used for lowering blood pressure, that can keep motor neurons alive for longer in one of our laboratory models. In this project we further investigated the effects of calcium channel blockers on additional disease-associated hallmarks in our laboratory models. These hallmarks included looking at how a cell responds to stress and the release of a cell messenger, called calcium. We didn’t find any differences in the levels of calcium between the disease and healthy control laboratory models However, we found that our disease laboratory model showed impaired responses to stress compared to healthy control models. These impairments were rescued following treatment with two of the calcium channel blockers examined. These findings suggest that calcium channel blockers warrant further investigation as a potentially beneficial treatment for MND.
