
Professor Simon Parson
FAS
Regius Chair of Anatomy
- About
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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
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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
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Elected Councillor, Anatomical Society: 2010-2016
Meetings Officer, Anatomical Society: 2011- 2016
IFAA Programme Secretary: 2018 -
- Research
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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
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Teaching Responsibilities
All aspects of Anatomy teaching to Medical and Science students
- Publications
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Survival of motor neurone protein is required for normal postnatal development of the spleen
Journal of Anatomy, vol. 230, no. 2, pp. 337–346Contributions to Journals: ArticlesSurvival Motor Neuron (SMN) protein is required for normal mouse liver development
Scientific Reports, vol. 6, 34635Contributions to Journals: Articles- [ONLINE] DOI: https://doi.org/10.1038/srep35898
- [OPEN ACCESS] http://aura.abdn.ac.uk/bitstream/2164/7566/1/srep34635.pdf
- [OPEN ACCESS] http://aura.abdn.ac.uk/bitstream/2164/7566/3/srep35898_1_.pdf
Exploring the microvascular abnormalities in a cohort of paediatric patients with spinal muscular atrophy: P.51
21st International Congress of the World-Muscle-Society, pp. S105Contributions to Journals: Abstracts- [ONLINE] DOI: https://doi.org/10.1016/j.nmd.2016.06.073
Systemic restoration of UBA1 ameliorates disease in spinal muscular atrophy
JCI Insight, vol. 1, no. 11, e87908Contributions to Journals: Articles- [ONLINE] DOI: https://doi.org/10.1172/jci.insight.87908
- [OPEN ACCESS] http://aura.abdn.ac.uk/bitstream/2164/6245/1/JCI_Insight87908.pdf
Histopathological Defects in Intestine in Severe Spinal Muscular Atrophy Mice Are Improved by Systemic Antisense Oligonucleotide Treatment
PloS ONE, vol. 11, no. 5, pp. 1-15Contributions to Journals: ArticlesEvolving student–faculty partnerships in medical education through peer-assisted learning
Medical Education, vol. 50, no. 5, pp. 568-568Contributions to Journals: ArticlesHistological and Histochemical Methods, Theory and Practice, 5th Ed
Journal of Anatomy, vol. 228, no. 5, pp. 887Contributions to Journals: Reviews of Books, Films and Articles- [ONLINE] DOI: https://doi.org/10.1111/joa.12390
- [ONLINE] View publication in Scopus
Vascular Defects and Spinal Cord Hypoxia in Spinal Muscular Atrophy
Annals of Neurology, vol. 79, no. 2, pp. 217-230Contributions to Journals: ArticlesMicrovascular abnormality in spinal muscular atrophy and its response to antisense oligonucleotide therapy
20th International Congress of the World-Muscle-Society, pp. S193Contributions to Journals: Abstracts- [ONLINE] DOI: https://doi.org/10.1016/j.nmd.2015.06.038
An anatomical study of the neurovascular anatomy of the web spaces between the fingers
Journal of hand surgery-European volume, vol. 40, no. 7, pp. 755-757Contributions to Journals: Letters- [ONLINE] DOI: https://doi.org/10.1177/1753193414534382