Dr Sean Coakley

Senior Research Fellow

School of Biomedical Sciences
Faculty of Medicine
+61 7 336 52873


I received my PhD from The University of Queensland in 2014 where I studied axonal regeneration and degeneration in the laboratory of Professor Massimo Hilliard at the Queensland Brain Institute. In 2016 I was awarded an NHMRC-ARC Dementia Research Development Fellowship to pursue postdoctoral research in Professor Hilliard's lab with the aim of discovering novel genes that regulate axonal degeneration in C. elegans. In 2018 I was awarded a UQ Early Career Researcher Grant and a Young Tall Poppy Science Award. In 2019 I was a visiting scholar in the laboratory of Professor Kang Shen in the Department of Biology at Stanford University, where I studied how mechanosensitive channels regulate dendrite branching through Ca2+ signaling during neuronal development. In 2022 I was awarded an NHMRC Ideas Grant and was recruited to the School of Biomedical Sciences at UQ as a Group Leader. My lab focuses on understanding the cellular mechanisms that protect the nervous system from damage.

Research Interests

  • Axonal Degeneration
    Degeneration of the axon, the longest process of a neuron, is a key early pathological hallmark of Neurodegenerative conditions, including motor neuron disease, glaucoma, and Parkinson’s, Huntington’s and Alzheimer’s diseases.  Despite being described more than 100 years ago, we lack a basic understanding of the cellular and molecular mechanisms regulating axonal degeneration. Using the small nematode worm C. elegans, a very powerful genetic model system, we aim to discover molecules with a protective effect on the axon. The results from this study will provide novel and important insights into how axonal degeneration occurs, and how it can be prevented or delayed, potentially leading to the identification of novel molecular targets to treat neurodegenerative disorders.

Research Impacts

My laboratory focuses on how to build and maintain a nervous system for life. We use C. elegans as a model system because we can use sophisticated genetic, imaging and molecular approaches to study the cellular mechanisms of neuroprotection in exquisite detail.

Failure to maintain the integrity of the axon, the longest and most susceptible compartment of a neuron, results in compromised neuronal function, which is characteristic of both injury and neurodegenerative diseases. Virtually every neuron, including those of the central nervous system, is susceptible to different types of strain insults such as protein accumulation, vascular accidents, and trauma, with excessive mechanical strain triggering axonal degeneration and progression of neurodegenerative diseases. The molecular mechanisms that maintain axonal integrity are unknown and will be essential to develop neuroprotective therapies for human disorders and injury.


  • Doctoral Diploma of Neurological Sciences, The University of Queensland


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PhD and MPhil Supervision

Current Supervision

Completed Supervision