Peter G. Noakes is investigating the cell and molecular mechanisms that underlie the development and breakdown of the neuro-motor system. His lab works on the following: 1) cell and molecular mechanisms surrounding the establishment of neuromuscular and motor neuron (CNS) synapses, including electrophysiology. 2) The generation and development of motoneurons in health and in disease (e.g. motor neuron disease {ALS}, using stem cells to create motor neurons and muscle. 3) The role of inflammation in neuromuscular disorders such as motor neuron disease, muscular dystrophy, and myasthenia gravis. His lab employs biochemistry, immuno-histology, electrophysiology, live cell imaging, behaviour, cell and molecular biology to study these issues.

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The Noakes lab has a number of research projects that are suitable for SCIE, Advanced Science, Honours, MSc (lab Rotations), and PhD students, within the following research areas.

1) Motor Neuron Disease (MND)which covers a group of neuromuscular diseases including Amyotrophic Lateral Sclerosis (ALS), and Spinal Muscle Atrophy (SMA). The Noakes lab works with animal models and with human derived stem cells to investigate the cellular and molecular mechanisms of these diseases.We are also embarking upon using AAV viral vectors to help enhance motor nerve muscle signalling.

2) Neuromuscular disorders and inflammation, in this area we are working with chemists that are creating compounds that act to dampen inflammation within muscle and the central nervous system. 

3)Neuromuscular connections - formation, function and stability in development and disease. This also includes the motor neurons regulation of its excitability and its pre-synaptic connections.

Visit eSpace for a full list of publications

  1. Size-dependent dendritic maladaptations of hypoglossal motor neurons in SOD1G93A mice. Fogarty MJ, Mu EWH, Lavidis NA,Noakes PG, Bellingham MC. Anat Rec (Hoboken). 2020 Oct 25. doi: 10.1002/ar.24542.
  2. Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs in Drosophila. Karunanithi S, Lin YQ, Odierna GL, Menon H, Gonzalez JM, Neely GG, Noakes PG, Lavidis NA, Moorhouse AJ, van Swinderen B. J Neurosci. 2020 Oct 14;40(42):8025-8041. doi: 10.1523/JNEUROSCI.0349-20.2020. Epub 2020 Sep 14.
  3. The Role of Altered BDNF/TrkB Signaling in Amyotrophic Lateral Sclerosis. Pradhan J, Noakes PG, Bellingham MC. Front Cell Neurosci. 2019 Aug 13;13:368. doi: 10.3389/fncel.2019.00368. eCollection 2019.PMID: 31456666
  4. Complement components are upregulated and correlate with disease progression in the TDP-43Q331K mouse model of amyotrophic lateral sclerosis. Lee JD, Levin SC, Willis EF, Li R, Woodruff TM, Noakes PG. J Neuroinflammation. 2018 Jun 1;15(1):171. doi: 10.1186/s12974-018-1217-2.
  5. Defects in synaptic transmission at the neuromuscular junction precede motor deficits in a TDP-43Q331K transgenic mouse model of amyotrophic lateral sclerosis. Chand KK, Lee KM, Lee JD, Qiu H, Willis EF, Lavidis NA, Hilliard MA, Noakes PG. FASEB J. 2018 May;32(5):2676-2689. doi: 10.1096/fj.201700835R. Epub 2018 Jan 2.PMID: 29295857
  6. Functional decline at the aging neuromuscular junction is associated with altered laminin-α4 expression. Lee KM, Chand KK, Hammond LA, Lavidis NA, Noakes PG. Aging (Albany NY). 2017 Mar 14;9(3):880-899. doi: 10.18632/aging.101198.
  7. Loss of laminin-α4 results in pre- and postsynaptic modifications at the neuromuscular junction. Chand KK, Lee KM, Lavidis NA, Noakes PG. FASEB J. 2017 Apr;31(4):1323-1336. doi: 10.1096/fj.201600899R. Epub 2016 Dec 20.PMID: 27998908
  8. Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity. Fogarty MJ, Kanjhan R, Bellingham MC, Noakes PG. J Neurosci. 2016 Jan 6;36(1):80-7. doi: 10.1523/JNEUROSCI.1576-15.2016.
  9. Identification of RNA bound to the TDP-43 ribonucleoprotein complex in the adult mouse brain. Narayanan RK, Mangelsdorf M, Panwar A, Butler TJ, Noakes PG, Wallace RH. Amyotroph Lateral Scler Frontotemporal Degener. 2013 May;14(4):252-60. doi: 10.3109/21678421.2012.734520.
  10. Neuregulin-1 potentiates agrin-induced acetylcholine receptor clustering through muscle-specific kinase phosphorylation. Ngo ST, Cole RN, Sunn N, Phillips WD, Noakes PG. J Cell Sci. 2012 Mar 15;125(Pt 6):1531-43. doi: 10.1242/jcs.095109. 
  11. Muscle specific kinase: organiser of synaptic membrane domains. Ghazanfari N, Fernandez KJ, Murata Y, Morsch M, Ngo ST, Reddel SW, Noakes PG, Phillips WD. Int J Biochem Cell Biol. 2011 Mar;43(3):295-8. doi: 10.1016/j.biocel.2010.10.008

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