Our Fellows

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 2022

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 - May 2023

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 2024

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 - January 2024

Preventing toxic protein aggregates being formed or preventing them causing damage are possible ways to treat MND, and the presence of these aggregates could be used for early disease diagnosis. However, detailed understanding of the shape, size and properties of these aggregates has been hampered by their low abundance and the fact they can form many different types of clumps. Therefore, it remains unclear how well the cellular models used in MND research best represent the real disease. This project will aim to use sensitive imaging techniques to enhance understanding of these aggregates.

July 2021 - June 2023

Healthy motor neurons work by transmitting signals from the brain and spinal cord to muscles to allow us to move, speak and breathe. This relies on a complicated process known as ‘axonal transport’, which refers to the movement of important molecules and organelles (subunits of a cell that have specific functions) up and down motor neuron cells. When people have MND, this transport process doesn’t work as well so the molecules and organelles that cells normally need to survive get stuck in the wrong places. Dr Tosolini’s research, which uses motor neurons developed from people with MND or from mice, will focus on understanding this process, and how it might be restored to normal.

November 2021 - October 2023

MND affects people in different ways, with symptoms emerging and progressing at highly variable, unpredictable rates. Therefore, some treatments may work in some people with MND but not in others. It is now established that those with the disease often experience cognitive and behavioural problems. The aim of this project is to develop ways to measure brain function changes that can predict patient symptoms and improve understanding of the biology of why MND has different effects on different people. This is expected to facilitate earlier, more informative diagnoses and improve detection of effective therapies in clinical trials.

April 2021 - March 2023

FUS is a protein that regulates the production of other proteins and is known to be dysfunctional in MND. This project aims to understand how the disruptions to protein production caused by FUS alter the function of nerve cells and their connection to muscles. Once it is understood how nerve cells are damaged, the project will move on to investigating if it is possible to correct this damage. Understanding the changes to nerve cells in MND is crucial to designing new and effective treatments.

September 2022 - August 2025

Glial cells, a type of cell found in the brain and spinal cord, help to ensure that neurons are functioning correctly and maintain connections between neurons and muscles. In some neurological diseases, glial cells become toxic and consume synapses (connections which enable messages to be sent from one neuron to another to be passed to the muscles) causing these connections to be lost. This project aims to investigate the link between toxic glial cells and synapse loss in MND using cell models and brain tissue to observe the action of the toxic glial cells on synapses. It will provide new insights into the role of glial cells in MND and may potentially highlight ways to delay or prevent synapse loss which could help to slow the progression of the disease.

February 2022 - July 2024

Currently, we do not know the best way to subgroup and classify neurodegenerative diseases since overlapping disease mechanisms are often not taken into account. This project involves reclassifying these diseases based on a combination of biological measures. This will include genetic profile, epigenetics (a system controlling whether genes are switched on or off) and the level of a nerve protein found in the blood called neurofilament. The variations of these three areas will be analysed for both MND and Frontotemporal dementia (FTD) and machine learning will then be used to find patterns that correspond to different subgroups. If this allows for the formation of new subgroups, these can be used group people with MND together for clinical trials and to understand the underlying biology of the conditions.

January 2022 - March 2024

While research into MND has improved our understanding of what is changing within the motor neurons in the disease, current knowledge of why these changes occur is limited. One of these changes is the incorrect processing and placement of a molecule called RNA, which is a photocopy of DNA that is used to make proteins in cells. The main aim of this project is to investigate whether a class of small RNA molecules, known as miRNA, are affected in MND and, if they are, whether they are a cause or consequence of the disease. Identifying the miRNA molecules affected in MND and how they change could help to reveal a potential treatment strategy.

October 2022 - September 2024