Professor Simon Parson

Professor Simon Parson
Professor Simon Parson
Professor Simon Parson


Regius Chair of Anatomy

Email Address
Telephone Number
+44 (0)1224 274328
Office Address

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

School of Medicine, Medical Sciences and Nutrition


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 - 2019

President, Anatomical Society 2019-2022


Research Overview

Spinal Muscular Atrophy

Systemic involvement in neurodegeneration, especially of the cardiovascular system

Effects of Hypoxia and ischaemia 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 pioneered 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 particularly interested to determine how this impacts on SMA disease development and progression. This is particularly relevant in the new post- therapeutic landscape, as these were designed to target neuronal defects.

We are currently 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 entirety of SMA pathology in patients. 

Most recently, we are exploring similar non-motor pathologies in ALS/ MNDs.


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 Responsibilities

All aspects of Anatomy teaching to Medical and Science students


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  • Axotomy-dependent and -independent synapse elimination in organ cultures of Wld(s) mutant mouse skeletal muscle

    Parson, S. H., Ribchester, R. R., Davie, N., Gandhi, N. P., Malik, R. Q., Gillingwater, T. H., Thomson, D.
    Journal of neuroscience research, vol. 76, no. 1, pp. 64-75
    Contributions to Journals: Articles
  • Neuronal P2X7 receptors are targeted to presynaptic terminals in the central and peripheral nervous systems

    Deuchars, S. A., Atkinson, L., Brooke, R. E., Musa, H., Milligan, C. J., Batten, T. F., Buckley, N. J., Parson, S. H., Deuchars, J.
    Journal of Neuroscience, vol. 21, no. 18, pp. 7143-52
    Contributions to Journals: Articles
  • Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds)

    Parson, S. H., Mackintosh, C. L., Ribchester, R. R.
    European Journal of Neuroscience, vol. 9, no. 8, pp. 1586-1592
    Contributions to Journals: Articles
  • Loss of myelinated axons is specific to the central nervous system in a mouse model of the fetal alcohol syndrome

    Parson, S. H., Sojitra, N. M.
    Journal of Anatomy, vol. 187 , no. 3, pp. 739-748
    Contributions to Journals: Articles
  • Optic nerve hypoplasia in the fetal alcohol syndrome: a mouse model

    Parson, S. H., Dhillon, B., Findlater, G. S., Kaufman, M. H.
    Journal of Anatomy, vol. 186 , no. 2, pp. 313-320
    Contributions to Journals: Articles
  • Cell viability and laminin-induced neurite outgrowth in cultures of embryonic chick neural tube cells: effects of cytosine-B-D-arabinofuranoside

    Parson, S. H., Price, J. F., Ribchester, R. R.
    Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration, vol. 4, no. 1, pp. 99-106
    Contributions to Journals: Articles
  • Segmental independence and age dependence of neurite outgrowth from embryonic chick sensory neurons

    Parson, S. H., Ribchester, R. R.
    Journal of Neurobiology, vol. 26, no. 1, pp. 1-16
    Contributions to Journals: Articles
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Contributions to Conferences

Contributions to Journals