Dr Brent Neumann, Group Leader
Dr Brent Neumann
T: 61 3 9905 0670
The major research questions we aim to address are:
- How can the nervous system be repaired after traumatic injury?
- What molecular mechanisms lead to Charcot-Marie-Tooth disease?
- How is the nervous system normally maintained over an organism's lifetime?
To understand these questions in neurobiology, we use the nematode C. elegans as our model system due its simplified and exceptionally well-characterised nervous system.
- Dr Ming Soh
- Dr Gursimran Chandhok (visa pending)
- Mr Joseph Byrne
- Ms Michelle Wong
- Mr Jean Teoh
- Ms Nethmi Yapa
Applications from postdoctoral researchers, PhD students and honours students are encouraged. If you are interested in joining our team, please feel free to contact firstname.lastname@example.org via email.
Cellular and molecular mechanisms of axonal regeneration
Injuries to the nervous system can cause lifelong disabilities due to ineffective repair of the damaged nerve fibres and thus, understanding the basic molecular mechanisms regulating axonal regeneration is essential for the development of effective therapies. Using UV-laser axotomy, we are able to sever individual axons in C. elegans to study their responses to injury. We study a highly efficient mechanism of axonal regeneration known as axonal fusion, whereby a regenerating axon is able to reconnect and fuse with its detached segment to restore the original axonal tract and re-establish connection with its target tissue.
We have demonstrated that molecules previously found to function in the recognition of dying cells by phagocytes, also mediate the reconnection between a regrowing axon and its separated segment. We are now studying the precise mechanisms of this recognition process to complete a full molecular description of axonal fusion.
Molecular mechanisms of Charcot-Marie-Tooth disease
Charcot-Marie-Tooth disease (CMT) is the most common inherited disorder of the peripheral nervous system, affecting up to 1 in 2,500 people. The disease is characterized by a progressive motor and sensory neuropathy, resulting in muscle weakness and atrophy, sensory loss, slowed reflexes, foot deformities, and mobility impairments. There is no cure for CMT, and patients frequently suffer lifelong disabilities.
We aim to model CMT in C. elegans in order to uncover novel information about how the disease develops, and provide a better understanding of the disease to offer valuable insight for the future generation of therapeutics. Our research focuses on axonal forms of CMT (classified as CMT2), and in particular on the most common axonal form, CMT2A, which is caused by mutations in Mitofusin 2, a protein critical for normal mitochondrial functioning.
Maintenance of nervous system structure over time
Axonal degeneration can occur as a result of nerve injury or through the disruption of neuronal maintenance mechanisms, and is a hallmark of neurodegenerative disorders such as motor neuron, Alzheimer's, Parkinson's, and Charcot-Marie-Tooth diseases. Despite the importance of this process, we lack a complete understanding of the molecules and mechanisms employed by neurons to preserve their axons over a lifetime, which has hampered the development of effective therapies.
We aim to identify and characterise the cellular mechanisms necessary for the maintenance of axonal structure over an animals' lifetime using candidate gene approaches and forward genetic screening techniques in C. elegans.