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Matthew Young

BBSRC DTP PhD Researcher in Neuroscience, Faculty of Medicine & Health Sciences

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Biography

I'm currently a BBSRC funded DTP PhD Researcher working in the Neuron Function and Axon Biology lab. I previously earned my MRes in Neurosciences from the University of Nottingham, and my BSc in Biomedical Sciences from the Nottingham Trent University.

Supervisors:

Dr Federico Dajas-Bailador

Dr Robert Layfield

Dr Marios Georgiou

Expertise Summary

With a background is in neurodegeneration and the neurobiology of ageing, my current focus is on using standard and microfluidic culture of primary cortical neurons to models autophagy manipulation in axon development and degeneration.

Research Summary

My research looks at how the modulation of a key autophagy protien, P62 and its ALS-associated mutants effects axon function, using primary, mouse cortical neuron microfluidic culture as a model of… read more

Recent Publications

I work with the Nottingham Public Engagement Network as a public engagement with research specialist. I coordinate and advise on public engagement projects and training, with specific expertise on community engagement with researchers in the context of science festivals.

Current Research

My research looks at how the modulation of a key autophagy protien, P62 and its ALS-associated mutants effects axon function, using primary, mouse cortical neuron microfluidic culture as a model of neuronal development and degeneration.

Amyotrophic lateral sclerosis and associated frontotemporal lobe dementia (ALS-FTLD) is a complex, fatal degenerative disease encompassing selective degeneration of the motor neuron network that leads to neuromuscular failure accompanied by dementia-like cognitive defects. Recently, the autophagy protein P62/SQSTM1 has been identified as a component of intracellular protein aggregates typically present in ALS-FTLD affected motor neurons.

Autophagy's role in the long term maintenance of cellular proteostasis is particularly important in long-lived, post-mitotic cells, such as neurons. Mounting evidence has begun to link defects in key autophagy proteins to neurodegenerative diseases like ALS-FTLD, where the presence of protein aggregates and damaged organelles are hallmark pathologies.

P62 sequesters ubiquitin 'tagged' cargoes tagged for degradation within autophagosomal membranes by linking them to acidic autolysosomes for further processing. The L341V mutation is implicated in ALS-FTLD affected motor neurons and impairs the ability of P62 to connect it's cargoes to autophagosomal membranes, reducing autophagy activity.

The proper development and maintenance of axons is vital to proper neuron function. A key conductor in this process is the axon growth cone whose function enables the neuron to respond to various chemotropic cues which guide its axons to pre-synaptic terminals, where they complete neuronal networks.

As a highly specialised cellular compartment, the axon exhibits high levels of finely tuned protein turnover. Therefore, it is becoming increasingly important to understand the mechanisms regulating neuronal autophagy.

School of Life Sciences

University of Nottingham
Medical School
Queen's Medical Centre
Nottingham NG7 2UH

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