First Aid (Level 2) Officer
Accredited Mental Health First Aider
Dr Brent Neumann
Dr Brent Neumann obtained his BSc (Honours) at the University of South Australia and completed his PhD in Prof Tom Gonda's lab at The University Of Queensland's Diamantina Institute. In 2008 he joined A/Prof Massimo Hilliard's lab at the Queensland Brain Institute studying the mechanisms of degeneration and regeneration in the nervous system. In April, 2015 Brent established the Nervous System Development and Repair laboratory within the Neuroscience Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology at Monash University.
Brent also serves two volunteer positions:
- Australian Academy of Science's National Committee for Cellular and Developmental Biology
- Director for the Australian Society for Medical Research (ASMR)
Google scholar page.
HONOURS AND AWARDs
2016-2018: NHMRC Project Grant CIA: APP1101974 - The role of membrane phospholipids in regenerative axonal fusion; total budget $571,950.
2016-2018: NHMRC Project Grant sole CI: APP1099690 - Uncovering the molecular mechanisms behind Charcot-Marie-Tooth disease; total budget $320,967.
2015-2016: CMTAA Research Grant, sole CI: To generate strains of C. elegans carrying specific mutations in Mfn2/fzo-1 that have been identified in CMT patients; total budget $12,500.
2018: Grant Review Panel member for the National Health and Medical Research Council (NHMRC) Project Grants.
2017: Invited to join the Board of Directors for the Australian Society for Medical Research (ASMR) for a two-year term
2016: Paxinos-Watson Award from the Australasian Neuroscience Society.
2016: Nominated by The Australian Academy of Science as an Early–Mid Career Researcher member for the National Committee for Cellular and Developmental Biology.
2016: Featured with a ‘New Faculty Profile’ by the Genetics Society of America.
2016: Young Investigator Award for the 14th Meeting of The Asian-Pacific Society for Neurochemistry (APSN2016), Kuala Lumpur, Malaysia.
2016: Monash University Biomedicine Discovery Institute Travel Award ($2,500).
2015: Best Queensland Brain Institute Publication Prize
2014: Best Queensland Brain Institute Publication Prize
2014: Brisbane Cell and Developmental Biology Meeting oral presentation prize, Brisbane.
2012: EMBL Conference Series C. elegans Neurobiology meeting poster prize, Heidelberg, Germany.
2012: EMBL Corporate Partnership registration fee fellowship, Heidelberg, Germany.
2010: Conference registration fee fellowship, Madison, USA.
2005: ASMR Postgraduate Student Conference poster prize, Brisbane.
Injuries to the nervous system can cause lifelong disabilities due to ineffective repair. Understanding the basic molecular mechanisms regulating axonal regeneration is therefore essential for the development of effective therapies. As a postdoctoral fellow with Massimo Hilliard, Brent identified a mechanism of repair known as axonal fusion in the nematode Caenorhabditis elegans (Dev Dyn 2011). This highly efficient means of nervous system repair occurs such that severed axons spontaneously repair themselves by regrowing, reconnecting and fusing with their separated counterparts.
Analysis of a novel mutation causing hyper-stabilisation of the axonal microtubules revealed that the microtubules play a key role in the axonal fusion process, with their disruption inhibiting the success rate for this repair mechanism (Mol Biol Cell 2013). Through a detailed molecular charaterisation of the process, Brent discovered that regenerative axonal fusion shares much of its molecular machinery with the process of apoptosis (Nature 2015). Following injury, the composition of the axonal membrane is altered, such that the phospholipid phosphatidylserine is exposed on the external surface to serve as a recognition, or ‘save-me’ signal for the regrowing axon. This ‘save-me’ signal is recognized by secreted ligands and receptors on the regrowing axon to allow recognition between the two axon segments. Understanding precisely how axonal fusion occurs in C. elegans may allow it to be applied to other organisms and potentially allow similar mechanisms of nervous system repair to be induced in a clinical setting.
Brent’s research also focuses on axonal degeneration, which can occur as a result of nerve injury or through the disruption of neuronal maintenance mechanisms, and is a common hallmark among many neurodegenerative disorders including motor neuron, Alzheimer’s, and Charcot-Marie-Tooth (CMT) diseases. We lack a complete understanding of the mechanisms employed by neurons to preserve their axons over a lifetime, which has hampered the development of effective therapies.
From a genetic screening method aimed at identifying molecules that cause axonal degeneration when they become inactive through genetic mutations, Brent found that mutation of the α-tubulin acetyltransferase protein, MEC-17/ATAT1 led to spontaneous, adult onset and progressive axonal degeneration (Cell Rep 2014). MEC-17 is highly conserved across species and normally protects against degeneration by stabilising the cytoskeletal structure. Brent’s laboratory in the Department of Anatomy and Developmental Biology aims to identify and characterise additional cellular mechanisms necessary for the maintenance of axonal structure, and also uses C. elegans to model CMT, the most common inherited disorder of the peripheral nervous system, affecting up to 1 in 1,200 people. The disease is characterised by a progressive motor and sensory neuropathy, resulting in muscle weakness and mobility impairments. By modelling the disease in C. elegans, novel information about how the disease develops can be identified, and a better understanding of the disease provided to offer valuable insight for the future generation of therapeutics.
Prior to his current research interests in neurobiology, Brent completed his PhD in molecular biology and biochemistry focusing on a family of genes, known as the Schlafens. The function of these genes were previously unknown, but were linked to the MYB oncogene, which is itself implicated in several types of cancer, including leukaemia and breast cancer. Brent sought to discover the function of the Schlafen genes, performing yeast two-hybrid screening to identify the molecules with which the Schlafens interact, providing a detailed characterisation of where each family member localises within the cell (BBRC 2008), and their role in cellular proliferation (BCMD 2008).