PhD Position in “Morphology and mechanisms of brain microvascular defects in Spinal Muscular Atrophy”

Website Aberdeen University

Details

We are pleased to offer an exciting opportunity to join a fully funded, 36-month project commencing in October 2026, supported by an Anatomical Society Prize Studentship. This studentship provides a comprehensive financial package to support your research at the University of Aberdeen, including home tuition fees, a tax-free student stipend (estimated at £21,383 for the 2026/27 academic year), and all associated research costs. The studentship also provides funding for attendance at three Society conferences and one overseas meeting to present your data.

Spinal muscular atrophy (SMA) is a rare and recessive form of motor neuron disease that predominantly affects the infant population. Defined by progressive motor neuron death, SMA results in skeletal muscle wasting and respiratory failure, and was until the advent of therapy, the most common inherited cause of infant death worldwide. There are now four approved therapies for SMA, all designed specifically to alleviate motor neuron loss, which are improving motor abilities and increasing patient survival. However, widespread tissue and organ pathology beyond the neuromuscular system is now described in multiple animal models and in patient tissues. Much of this work has been carried out in our laboratory (see references).

Systemic manifestations of SMA were largely sub-clinical, but they are now much more likely to be revealed as life-span improves following treatment. Chief amongst these are neurodevelopmental and cognitive defects. Our laboratory is particularly interested in the microvascular phenotypes that are present in SMA mouse models and tissue from SMA patients. Recently we have developed a novel mouse model where SMA cellular pathology is driven exclusively in endothelial cells: EndoSMA mouse. This model has a gross and a cellular phenotype, and preliminary data suggests significant developmental defects in specific areas of the brain, including the hippocampus. We hypothesise that the development of the neurovascular niche may be of critical importance in this. This research project will focus on understanding the mechanisms and implications of microvascular pathology in the brain in SMA. This will lead us to potential future combinatorial therapeutic avenues for treated children.

You will initially carry out morphological experiments to describe and quantify brain defects in the EndoSMA mouse. You will also use rare post-mortem tissue from SMA patients to validate changes found. You will then investigate the mechanisms that drive these changes. You will also have access to samples from animals and patients treated with current therapies, allowing you to examine the efficacy of these treatments for microvascular pathology.

Techniques involved in the research include microdissection, tissue preparation, histology: sectioning, staining, and advanced microscopy, identification and quantification of pathophenotypes in mouse tissues and pathology in patient samples; molecular analysis, data analysis and presentation.

The SMA reseach community is active and engaged in improving outcomes for patients. The recent introduction of newborn screening in Scotland, and shortly in England, provides a drive and focus for these efforts. The Parson laboratory has a long tradition of training scientists in morphological investigations, to observe closely, interpret carefully and present in detail the pathology observed in tissues and organ systems. You will be joining a small, but well-connected research laboratory based in the Institute for Medical Sciences at the Foresterhill Healthcare campus of the University of Aberdeen.

Contact simon.parson@abdn.ac.uk with any questions and for further information.

Candidate Background:

An open and enquiring mind and a willingness to develop the skills to work independently. A first degree including morphological or anatomical content such as, but not limited to, zoology, anatomy, neuroscience, biomedical sciences. Completion of a previous research project as well as some experience of histological techniques and wet laboratory research would be useful. 

We also invite applications from those returning from a career break, industry or other roles. We typically require a minimum of a 2:1 UK Honours degree (or equivalent), but exceptions can be made where applicants can demonstrate excellence in alternative ways, including, but not limited to, performance in masters courses, professional placements, internships or employment.

We actively encourage applications from diverse career paths and backgrounds and across all sections of the community, regardless of age, disability, ethnicity, gender, gender expression, sexual orientation and transgender status, amongst other protected characteristics.

Application Procedure

  • cover letter addressed to the supervisor of the project you’re applying for.
  • An up-to-date CV detailing your academic qualifications, employment history, and any other relevant experience. Please ensure your current permanent address is clearly stated, as this will be used to determine your fee status.
  • Clear copies of your degree certificates and transcripts (if available).
  • Evidence of settled or pre-settled status (if applicable).
  • Two academic references. We cannot request references on your behalf. Please either provide us with copies yourself or have your referees email them directly to us. Direct emails from referees must include your full name and the project you are applying for.

Please send your application with documents attached as a single email with the subject line: “Anatomical Society PhD – [Your Name]”

The deadline for applications is 23:59 GMT on 12th July 2026. Please note that incomplete applications will not be considered.

For any enquiries regarding your application or the application process, please contact smmsn-pgrenquiries@abdn.ac.uk

Funding Notes

This 36-month project is supported by a prestigious Anatomical Society Prize Studentship.

The funding package covers Home tuition fees, research costs, and a tax-free student stipend (estimated at £21,383 for the 2026/27 academic year). The studentship also includes funding to present your research at three Anatomical Society conferences and one overseas meeting.

References

General SMA background
• Mercuri, E., Sumner, C.J., Muntoni, F. et al. Spinal muscular atrophy. Nat Rev Dis Primers 8, 52 (2022).
• Yeo CJJ, Darras BT. Yeo and Darras: Extraneuronal Phenotypes of Spinal Muscular Atrophy. Ann Neurol. 2021 Jan;89(1):24-26. doi: 10.1002/ana.25930. Epub 2020 Oct 29.
• Yeo CJJ, Tizzano EF, Darras BT. Challenges and opportunities in spinal muscular atrophy therapeutics. Lancet Neurol. 2024 Feb;23(2):205-218. doi: 10.1016/S1474-4422(23)00419-
Recent relevant Parson Lab papers
• Allardyce H, Lanz H, Lawrence BD, Crawford TO, Sumner CJ, Parson SH. Microvascular pathology in the spinal cord of severe spinal muscular atrophy patients. Acta Neuropathol Commun. 2026 Feb 15;14(1):65. doi: 10.1186/s40478-026-02232-y.
• Allardyce H, Lawrence BD, Crawford TO, Sumner CJ, Parson SH. A reassessment of spinal cord pathology in severe infantile spinal muscular atrophy: Neuropathol Appl Neurobiol. 2024 Oct;50(5):e13013. doi: 10.1111/nan.13013.
• Zhou H, Hong Y, Scoto M, Thomson A, Pead E, MacGillivray T, Hernandez-Gerez E, Catapano F, Meng J, Zhang Q, Hunter G, Shorrock HK, Ng TK, Hamida A, Sanson M, Baranello G, Howell K, Gillingwater TH, Brogan P, Thompson DA, Parson SH, Muntoni F. Microvasculopathy in spinal muscular atrophy is driven by a reversible autonomous endothelial cell defect. J Clin Invest. 2022 Nov 1;132(21):e153430. doi: 10.1172/JCI153430.
• Allardyce H, Kuhn D, Hernandez-Gerez E, Hensel N, Huang YT, Faller K, Gillingwater TH, Quondamatteo F, Claus P, Parson SH. Renal pathology in a mouse model of severe Spinal Muscular Atrophy is associated with downregulation of Glial Cell-Line Derived Neurotrophic Factor (GDNF). Hum Mol Genet. 2020 Aug 11;29(14):2365-2378. doi: 10.1093/hmg/ddaa126.

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