Profile photo of Staff member

Marco Morsch

Postdoctoral Fellow

Biomedical Sciences, Faculty of Medicine and Health Sciences

Contact Details

Tel: (02) 9850 2787

Email: marco.morsch@mq.edu.au

Level 1, 75 Talavera Road, Macquarie University

I am an early career neuroscientist with a strong focus on advancing our understanding of neuronal communication and cell-cell interactions with a strong expertise in electrophysiology and in vivo imaging approaches.

I received his PhD in 2009 from the University of Bonn, Germany and after moving to Australia I investigated in Prof William Phillips lab at the University of Sydney the signalling mechanisms that sustain or deteriorate the nerve-muscle synapse in ageing and the autoimmune disease myasthenia gravis.

In 2014 I joined Prof Chung’s lab at the MND Research Group at Macquarie University to form my own research niche. Here I developed my own research projects to investigate the basic molecular and cellular mechanisms that define how neurons (in the spinal cord) react to a disease environment and how they get cleared upon death. I am particularly interested in the involvement of glia (microglia and astrocytes) in these processes.

During my young career I made important advances in the biology of neurological disease as well as, more recently, in the underlying principles of neuron-glia interactions in the healthy and stressed nervous system.  I have made recognised contributions to the fields of neurology and neuroscience by carefully investigating the fundamental signalling mechanisms that underpin these interactions in the CNS and the periphery.

Qualifications:

PhD (University of Bonn, Germany)

Research Interests

I have established several independent research projects at Macquarie University that focus on cellular mechanisms in MND and other neurodegenerative diseases:

  • Visualising neuron glia interactions in-vivo using advanced confocal microscopy techniques. We have established a zebrafish model that allows us to track individual protein aggregates and single neurons/glia cells in real time. We use a precise laser ablation and other approaches to selectively stress/kill an individual cell and visualise their fate and interactions specifically in the living fish.
  • Prion like mechanisms of ALS aggregates (TDP-43, SOD1, FUS etc.) in the zebrafish spinal cord (spread of proteins throughout the CNS). Our single cell visualisation and ablation approach allows us to monitor the dispersal of these aggregates throughout the spinal cord. It enables us to carefully investigate the hypothesised prion-like characteristics of these proteins, including the aggregation of these proteins and the impact upon surrounding motor neurons.
  • Neuromuscular junction impairment in ALS (mouse project). The question of where ALS begins has still not been established and we need to better understand the pathophysiology of ALS. There is support for both the “dying-forward” as well as the “dying-back” hypothesis. We will use the recent ALS mouse models (inducible TDP-43) to establish whether it is mainly a disorder of the neurons (dying-forward) or rather begins in the muscle or at the neuromuscular junction.
  • Cannabinoid mediated regulation of neuromuscular transmission (mouse project). Cannabinoids are effective modulators of neuronal communication. They exert dynamic control over many physiological processes including memory formation, cognition and pain perception. However, their role in the periphery and at the NMJ has been curiously neglected. We have strong evidence that neuromuscular transmission is highly regulated by cannabinoids and that they have potential for their treatment of neuromuscular disorders.

Select Publications

  1. M  Morsch, R Radford, A Lee, EK Don, AP Badrock, TE Hall, NJ Cole, R Chung (2015)
  2. In vivo characterization of microglial engulfment of dying neurons in the zebrafish spinal cord.
  3. Front Cell Neurosci. 2015; 9: 321.
  4. Plomp JJ, Morsch M, Phillips WD and Verschuuren JJ (2015)
  5. Electrophysiological analysis of neuromuscular synaptic function in myasthenia gravis patients and animal models.
  6. Experimental Neurology 270:41-54.
  7. RA Radford, M Morsch, SL Rayner, NJ Cole, DL Pountney, RS Chung (2015)
  8. The established and emerging roles of astrocytes and microglia in amyotrophic lateral sclerosis and frontotemporal dementia.
  9. Front Cell Neurosci. 2015; 9: 414.
  10. Reddel,S.W, Morsch,M., and Phillips,W.D. (2014)
  11. Clinical and scientific aspects of MuSK related myasthenia gravis.
  12. Current Opinion in Neurology 27(5):558-65.
  13. Ghazanfari N, Morsch M, Reddel SW, Liang SX & Phillips WD (2014)
  14. Muscle Specific Kinase autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.
  15. Journal of Physiology 592: 2881-97.
  16. Morsch M, Reddel SW, Ghazanfari N, Toyka KV and Phillips WD (2013) Pyridostigmine but not 3,4-diaminopyridine exacerbates ACh receptor loss and myasthenia induced in mice by Muscle Specific Kinase autoantibody. Journal of Physiology 591: 2747-2762.

 Recent Grants

2015    Motor Neurone Research Institute of Australia - Cure for MND Foundation Research Grant (MNDRIA; 2016-2017)

2014     Macquarie University Research Development Grants (MQRDG; 2015-2016)

Back to the top of this page