The Lady Edith Wolfson Fellowship Programme attracts and develops the careers of outstanding young Clinical and Non-Clinical researchers in order to create the future scientific leaders in the field of MND Research. Find out more about our current fellows below.
Clinical Research Fellowships
The first Clinical Fellowship was awarded to Professor Martin Turner (who was Dr Martin Turner at the time) from the University of Oxford in 2008. The Clinical Fellowships are funded in a partnership with the Medical Research Council (MRC).
Dr Fratta received his initial Training Fellowship through the Lady Edith Wolfson Programme in 2010. Starting on 1 February 2015, Dr Fratta was awarded a Clinician Scientist Fellowship to continue his research into MND, where he investigates how mistakes in RNA impact on motor neurone axons, the long processes that connect our spinal cord to the muscles and that degenerate in MND.
April 2015 - March 2019
Dr Feneberg is undertaking her PhD at the University of Oxford, where she is developing a diagnostic and prognostic biomarker based on investigating TDP-43 aggregates found in motor neurones and glial cells of people with MND. This biomarker will have the potential to speed up the development of disease-modifying therapy.
September 2017 - August 2019
Dr Bashford is using high-density surface electromyography to investigate fasciculations in people with MND. Reliable and detailed measures of these could potentially act as an MND biomarker and help with diagnosis and tracking progression of the disease.
October 2016 - September 2019
Dr Mehta, a neurology registrar from Oxford, is undertaking his PhD at the University of Edinburgh. His project will examine the C9orf72 genetic mutation and use patient-derived stem cells and gene editing to better understand the molecular mechanisms underlying MND.
August 2017 - July 2020
Dr Patani’s lab will use human induced pluripotent stem cells (iPSCs) to generate neuronal and glial cells from patients with ALS and healthy volunteers, to work out the earliest molecular events of the disease. Rickie's group specifically focuses on three main areas: i) how abnormalities in RNA transcript structure lead to abnormal RNA-protein interactions to cause ALS; ii) how glial cells of the brain – known as astrocytes – contribute to motor neuron degeneration and iii) how cellular ageing interfaces with the disease process.
January 2019 - December 2023
Our previous Clinical Research Fellows included:
Prof Martin Turner (University of Oxford) | August 2008 - July 2013 and August 2013 - August 2018
Dr Jemeen Sreedharan (Babraham Institute and King's College London) | June 2013 - February 2018
Dr Johnathan Cooper-Knock (University of Sheffield) | September 2012 - September 2015
Dr Jakub Scaber (University of Oxford) | August 2013 - August 2016
Dr Ceryl Harwood (University of Sheffield) | April 2009 - March 2012
Dr Robin Highley (University of Sheffield) | February 2009 - January 2012
The first Non-Clinical Fellowship was awarded to Dr Russell McLaughlin from Trinity College Dublin in 2016. The Non-Clinical Fellowships are funded solely by the MND Association.
In MND, the way that cells use nutrients and generate energy from them is likely to be altered, leading to weight loss. Dr Allen’s research is aiming to improve our understanding of how MND alters the cells’ ability to use energy sources such as carbohydrates and fats. This research should reveal which pathways in the cell are being disrupted and investigate if nutritional supplementation can help restore these cellular pathways.
January 2016 - March 2019
Dr Jones' goal is to identify MND risk genes that have a non-obvious but significant effect in causing MND and to combine his findings with drug-target data to try to identify novel therapies that we could use in MND. He uses new methods to find genes that cause MND that would be ‘invisible’ using traditional methods. This is achieved by using post-mortem brain tissue from donors with MND. It is novel as it not only looks at the underlying genes in these patients but also how the genes are active and what RNA the genes are producing. Dr Jones also works on combining post-mortem analyses with genes important in the development of motor neurons and genes that maintain motor neuron health to understand when the disease likely began in patients.
March 2016 - August 2019
In his PhD project, Dr Gabel applied a mathematical model to MRI data to find the overall sequence of white matter brain changes in MND. In his fellowship, he will build on these ideas using MRI and cognitive data from people with MND from international collaborators.
July 2017 - June 2019
Dr McLaughlin will investigate the impact of ancestry on the development of MND, by sequencing the genetic code of over 1,000 Irish individuals, 700 of whom have MND. Using these sequences, large family trees can be constructed that are likely to link MND patients previously assumed to be unrelated. These ‘superfamilies’ will give researchers a greater chance of identifying rarer gene variants linked to MND development.
January 2016 - September 2019
There is a part of the TDP-43 protein which is heavily linked to the development of TDP-43 deposits - this is called the low-complexity (LC) domain. Dr Hallegger will look at how mutations in the LC domain are linked to MND by studying motor neurones generated from iPSCs. Understanding the ‘knock on’ effects of LC domain mutations, and how these might lead to protein deposits, could enable the development of more targeted therapeutic interventions.
January 2016 - December 2019
Dr Bryson uses stem cells from mice transformed into motor neurones which will be used to create new muscle-neurone connections. These will be implanted back into the mice and observed for how well the neurones connect with muscles. The researchers will then identify the chemicals that promote successful innervation. This study has the potential to contribute to the development of a new therapy by replacing damaged motor neurones and restoring lost muscle function.
August 2017 - July 2020
A number of adverse processes in MND are caused by inadequate communication between two cellular structures – mitochondria and endoplasmic reticulum (ER). A lack of contact between these structures in certain types of MND can then lead to selective death of motor neurones. Dr Gomez-Suaga will investigate whether abnormalities in the C9ORF72 gene cause damage to the communication between mitochondria and ER, potentially establishing a target for intervention.
May 2018 - April 2021
An RNA molecule called NEAT1 forms the scaffolding of small compartments in a cell’s nucleus (the paraspeckle). It has been suggested the way NEAT1 is created may be altered and that these changes might be common to both sporadic and familial MND, and differentiate them from frontotemporal dementia. 'Dr Shelkovnikova's project will model changes in NEAT1 in neurones and observe how such neurones respond to stress and toxicity.
September 2018 - August 2022
Recently the team at the University of Nottingham discovered an interaction or ‘molecular handshake’ between TDP-43, a protein that builds-up and is toxic to motor neurones, and another protein called p62, which controls key cellular ‘waste-disposal’ systems. Preliminary findings indicate that this handshake could be harmful and in fact be responsible for the accumulation of ‘cellular waste’ that is commonly seen in affected individuals. Dr Scott will aim to understand the effect this dysfunctional interaction has on motor neurones, and will concurrently investigate the utility of targeting p62 to prevent the build-up of TDP-43.
August 2019 - December 2022
Dr Wright will search for drug molecules that help SOD1 protein fold properly and create synthetic proteins that destroy misfolded SOD1 using the cellular recycling system. Ultimately, the project will help us understand what causes those instances of MND where SOD1 misfolding is present, and find new ways to remove it.
April 2019 - March 2023