Professor Simon Parson

Professor Simon Parson
Professor Simon Parson

Professor Simon Parson

FAS

Regius Chair of Anatomy

About

Anatomy Rm 324 Suttie Centre Foresterhill University of Aberdeen Aberdeen AB24 3HF

Biography

BSc Zoology, University of Durham, 1987 

PhD Neuroscience, University of Edinburgh, 1990

Lecturer in Anatomy, University of Leeds, 1995

Senior Lecturer in Anatomy, University of Edinburgh, 2006

Professor of Anatomy, University of Aberdeen, 2013

Regius Chair of Anatomy, 2018

Memberships and Affiliations

Internal Memberships

All aspects relating to Home Office legislation of anatomical teaching and research

College Teaching and Learning Committee

Division of Medical and Dental Education Executive Committee

Year 1-3 Medical Executive Committees

Medicine Curriculum Steering Group

External Memberships

Elected Councillor, Anatomical Society: 2010-2016

Meetings Officer, Anatomical Society: 2011- 2016

IFAA Programme Secretary: 2018 -

Research

Research Overview

Spinal Muscular Atrophy

Systemic involvement in neurodegeneration, espciall the cardiovascular system

Effects of Hypoxia and ischanemia on the nervous system

Current Research

Spinal muscular Atrophy (SMA) is a childhood form of Motor Neurone Disease. It is caused by a defect in a gene which 1:35 of us carry. When two carriers come together there is a 1:4 chance of producing an affected child. SMA is the second most common genetic cause of infant death, affecting between 1:6-10,000 live births Worldwide. The most severely affected children will never sit unaided and will die before their second birthday. The disease is characterised by a loss of motor neurones and resultant muscle weakness and inability to carry out co-ordinated motor tasks including breathing. The genetic defect is well-characterised and attempts to replace or reduce the severe depletion of the key Survival of Motor Neurone (SMN) protein are ongoing. However, even when protein levels in motor neurones are increased and improvements in motor parameters are reported, survival is not increased. 

There is an increasing appreciation that this is not a classical motor neurone disease, but rather a systemic disease in which motor neurones are either most vulnerable or that defects in them are most clinically relevant. 

Our research has pionered significant pre and early symptomatic defects in the cardiovascular system, where the heart, blood vessels and circulating cells are all defective in SMA. We are now particulary interested to determine how this impacts on SMA disease development and progression. This is particularly relevant in the new post-Nusinersen/ Spinraza treatment landscape, as this soleley targets neuronal defects.

We are currenty exploring the extent to which the non-neuronal pathologies described in animal models are also seen in human post-mortem material and are using cellular models to determine the vulnerabilities of SMA cells to hypoxic environments. These will help us to understand and develop novel combinatorial therapies to treat the entirity of SMA pathology in patients. 

Collaborations

Professor Tom Gillingwater: University of Edinburgh

Dr Tom Wishart: Roslin Institute Edinburgh

Dr Lyndsay Murray: University of Edinburgh

Dr's Francesco Muntoni and Haiyan Zhou: UCL, London

Prof Rashmi Kothary: University of Ottawa, Canada

Prof Charlotte Sumner: John Hopkins University, USA

Funding and Grants

SMA Europe 

Anatomical Society 

Tenovus Scotland

Teaching

Teaching Responsibilities

All aspects of Anatomy teaching to Medical and Science students

Publications

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  • Induction of cell stress in neurons from transgenic mice expressing yellow fluorescent protein: implications for neurodegeneration research

    Comley, L. H., Wishart, T. M., Baxter, B., Murray, L. M., Nimmo, A., Thomson, D., Parson, S. H., Gillingwater, T. H.
    PloS ONE, vol. 6, no. 3, e17639
    Contributions to Journals: Articles
  • SMN deficiency disrupts brain development in a mouse model of severe spinal muscular atrophy

    Wishart, T. M., Huang, J. P. -., Murray, L. M., Lamont, D. J., Mutsaers, C. A., Ross, J., Geldsetzer, P., Ansorge, O., Talbot, K., Parson, S. H., Gillingwater, T. H.
    Human Molecular Genetics, vol. 19, no. 21, pp. 4216-4228
    Contributions to Journals: Articles
  • Using mouse cranial muscles to investigate neuromuscular pathology in vivo

    Murray, L. M., Gillingwater, T. H., Parson, S. H.
    Neuromuscular Disorders, vol. 20, no. 11, pp. 740-743
    Contributions to Journals: Articles
  • Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy

    Murray, L. M., Lee, S., Baeumer, D., Parson, S. H., Talbot, K., Gillingwater, T. H.
    Human Molecular Genetics, vol. 19, no. 3, pp. 420-433
    Contributions to Journals: Articles
  • Rapid loss of motor nerve terminals following hypoxia-reperfusion injury occurs via mechanisms distinct from classic Wallerian degeneration

    Baxter, B., Gillingwater, T. H., Parson, S. H.
    Journal of Anatomy, vol. 212, no. 6, pp. 827-835
    Contributions to Journals: Articles
  • Dynamic remodelling of synapses can occur in the absence of the parent cell body

    Bettini, N. L., Moores, T. S., Baxter, B., Deuchars, J., Parson, S. H.
    BMC Neuroscience, vol. 8, 79
    Contributions to Journals: Articles
  • Synaptic vulnerability in neurodegenerative disease

    Wishart, T. M., Parson, S. H., Gillingwater, T. H.
    Journal of Neuropathology and Experimental Neurology, vol. 65, no. 8, pp. 733-739
    Contributions to Journals: Articles
  • Immunohistochemical localisation of the voltage gated potassium ion channel subunit Kv3.3 in the rat medulla oblongata and thoracic spinal cord

    Brooke, R. E., Atkinson, L., Edwards, I., Parson, S. H., Deuchars, J.
    Brain Research, vol. 1070, no. 1, pp. 101-15
    Contributions to Journals: Articles
  • A2A adenosine receptors are located on presynaptic motor nerve terminals in the mouse

    Baxter, R. L., Vega-Riveroll, L. J., Deuchars, J., Parson, S. H.
    Synapse, vol. 57, no. 4, pp. 229-34
    Contributions to Journals: Articles
  • Nonmuscle myosins IIA and IIB are present in adult motor nerve terminals

    Vega-Riveroll, L. J., Wylie, S. R., Loughna, P. T., Parson, S. H., Chantler, P. D.
    Neuroreport, vol. 16, no. 11, pp. 1143-6
    Contributions to Journals: Articles
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