Postgraduate Afternoon 2018

On Monday 14th May 2018, at our ninth annual postgradute symposium, six postgraduate students or postdoctoral researchers presented their work. We also heard fascinating talks from new Centre member Prof Louise Locock from the University of Aberdeen, and invited speaker Prof Ira Leroi from the University of Manchester.

Hampton Awards

Many congratulations to the four winners of this year's Hampton Award - given to PhD students or postdocs who have made exceptional personal contributions in addition to showing academic excellence.   The winners this year were (left to right in the picture): Rachel Kline, Bhuvaneish Selvaraj, Chris Henstridge and Gabrielle King. Well done all!

Postgraduate presentation summaries

Cornelia Roesl (postdoc in Ribchester lab)

"New approaches of labelling human NMJs for confocal endomicroscopy"

Neuromuscular junctions, the interaction point between nerves and muscles, are the first to degrade in motor neurone disease patients, leading to muscle numbness followed by the inability to control muscle movement. My project aims to find new molecules to fluorescently label these junctions. If we find a label we can use confocal endomicroscopy as a new diagnostic tool to get a visual output of these junctions in humans and therefore improve diagnostics.

Natalie Courtney (final year PhD student in Murray lab)

“Motor neurone degeneration and P53 in spinal muscular atrophy”

My research looks at neuromuscular junction (NMJ) breakdown and withdrawal in Spinal Muscular Atrophy. During my PhD, I saw that the point at which the NMJ begins to breaks down and the activation of the P53 signalling pathway appeared to coincide. I found that by knocking out P53 I was able to reduce the amount of denervation within a muscle suggesting that the activation of P53 is causing the NMJ to withdraw from the muscle.

Chris Crockford (PhD student in Abrahams lab - has just submitted his thesis - congratulations!)

“Cognitive and behavioural decline across the ALS disease course”

Our research aimed to explore if cognition (thinking abilities) and behaviour decline as ALS progresses. We found that certain thinking abilities and behaviour do decline over time and this decline is related to disease progression. As such, it is important to consider and monitor the progression of cognition and behaviour in people with ALS.

Arpan Mehta (first year clinical PhD student in Chandran / Hardingham labs)

"Unravelling disease mechanisms in patient-derived motor neurones harbouring the C9orf72 mutation"

Arpan talked about his work on motor neurones derived from stem cells from patients living with motor neurone disease caused by the C9orf72 mutation. He spoke of the valuable contribution of gene editing to stem cell models. This approach has allowed for a comprehensive and unbiased decoding of the motor neurone transcriptome (the cell’s “messages”) in C9orf72. Disease pathways involving defects in the axons (the long processes emanating from the central cell body) and mitochondria (the cellular batteries) have been identified, and work is ongoing to characterise these further.

Rachel Kline (first year PhD student in Wishart lab)

“Identifying conserved regulators of neuronal stability across MNDs”

There are some motor neuron diseases (MNDs) that we know are caused by certain genes, but we still don’t understand what may be causing the majority remainder. However, we have some clues that there are common factors to all MNDs that behave as a “signature” of sorts to produce the typical MND symptoms. My project aims to find out what this common “signature” may be, as we hope to find factors within this “signature” that can be targeted with therapies even if the original disease cause is still unclear.

Jannigje Kok (MSc student supervised by Chris Henstridge in Spires-Jones lab)

“Investigating synaptic changes in a new mouse model of ALS/FTD"

Amyotrophic lateral sclerosis and frontotemporal dementia exist on a spectrum and commonly feature changes in a protein called TDP-43. Mice which have a mutation in the TDP-43 gene exhibit frontotemporal dementia-like behavioural changes. Recently, it was found that these mice also have changes in their brain cell connections which may interfere with the ability of brain cells to communicate, and potentially lead to the behavioural changes observed.