Treatments

The MND Association funds a number of research projects into potential treatments for MND.

These projects aim to test the effectiveness of potential treatments from the laboratory to clinical trials. A selection of the newest of these projects are highlighted below.

Download our Research we fund information sheet for details of all of the projects we fund.

“The hope is that one day there will be effective therapies to stop the underlying nerve degeneration in MND from occurring.”

– Karen Morrison, Professor of Neurology, Queen Elizabeth Hospital, Birmingham

A selection of the research we fund into developing treatments for MND:

Investigating the efficacy and safety of low-dose interleukin-2 treatment to control neuroinflammation in ALS (MIROCALS)
  • Prof Nigel Leigh
  • University of Sussex
  • £316,440 (Healthcare project) over 3 years
  • Start date: September 2016
  • Our Ref: 80-971-797

The Modifying Immune Response and Outcomes in Amyotrophic Lateral Sclerosis (MIROCALS) study will aim to investigate interleukin-2 as a potential treatment for MND.

Interleukin-2 has been used for many years to treat cancer, however, at low doses it is much safer but still effective against a number of immune diseases. Because the immune system is thought to be involved in causing
damage in MND, the researchers believe it may be beneficial in treating MND too.

This study will aim to start recruiting 216 people living with MND in the UK and France in spring/summer 2017.

Novel therapeutic strategies to prevent toxicity in C9ORF72-related MND
  • Dr Guillaume Hautbergue and Dr Lydia Castelli
  • University of Sheffield
  • £169,358 (Biomedical project) over 2 years
  • Start date: August 2016
  • Our Ref: 846-791

Cells within our body contain a number of separated compartments, each carrying out specific functions. The blueprint for making up thousands of proteins is housed in the form of genes, in a compartment in the centre of the
cell, the nucleus. A copy of the blueprint is created for each protein and is transported into the ‘open plan’ part of the cell, known as the cytoplasm. These copies serve as individual instruction manuals for the building of each
protein. The copies are known as RNA.

Damage to the C9orf72 gene is the commonest cause of inherited MND. The toxicity of the C9orf72 gene is linked to the transport system between the nucleus and the cytoplasm of the motor neurone. Researchers have recently found that a protein called SRSF1/F2 can help reduce this toxicity. In this project, the researchers hope to confirm the role of SRSF1/F2 in the C9orf72 form of MND in fly and human models of the disease. They will also investigate how it might be possible to reduce SRSF1/F2 safely as a possible treatment option.

Correcting the early damage seen in interneurons in zebrafish
  • Dr Johnathan McDearmid, Dr Tennore Ramesh and Prof Dame Pam Shaw
  • University of Leicester and Sheffield Institute for Translational Neuroscience (SITraN)
  • £160,901 (Biomedical project) over three years
  • Start date: September 2015
  • Our Ref: 835-791

Previous research in humans and zebrafish has shown that before symptoms arise in MND, early changes occur in the interneurones (the cells linking between the upper and lower motor neurones).

Using zebrafish, this project will investigate if the early defects that occur in interneurones can be targeted as a potential treatment for MND, in order to slow, or even prevent, the onset of symptoms. These studies will be conducted looking specifically at the electrical activity of the interneurones.

You can read more about this study on our research blog.

Preventing TDP-43 deposits in motor neurones
  • Prof Marcus Rattray and Dr David Hicks
  • University of Bradford
  • £174,965 (Biomedical project) over two years and six months
  • Start date: October 2015
  • Our Ref: 837-791

Deposits of the protein TDP-43 are found within the motor neurones in the majority of cases of MND, and are considered a pathological hallmark of the disease. The events that cause TDP-43 to deposit within the motor neurones are currently unknown.

In previous research, activation of the Unfolded Protein Response (UPR) causes the protein TDP-43 to form abnormal deposits within motor neurones. This project will aim to identify what pathways link the UPR and TDP-43 deposition within the motor neurones and whether reversing the accumulation of TDP-43 has an effect on slowing the progression of MND. The researchers will then aim to screen hundreds of compounds that may potentially reverse this process.

Find out more about their research on our blog.

Protecting against oxidative stress in MND
  • Prof Kaye Davies
  • University of Oxford
  • £95,826 (PhD studentship) over three years
  • Start date: October 2014
  • Our Ref: 869-792

During the early stages of MND it is proposed that motor neurones are more susceptible to an imbalance of oxygen within the cells, known as oxidative stress. Prof Davies has previously shown that increasing the levels of the gene Oxr1 can protect motor neurones from death caused by oxidative stress and delay MND in mice.

The aim of this project is to understand more about the role of Oxr1 in the protection of motor neurones in MND, as well as to determine if increasing levels could be a protective treatment approach.

Read how this research is progressing on our research blog.

 

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