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You will be updated with latest job alerts via email£ 33002 - 35608
1 Vacancy
Salary:33002.00 - 35608.00 per annum
Newcastle University is a great place to work with excellent benefits. We have a generous holiday package; plus the opportunity to buy more great pension schemes and a number of health and wellbeing initiatives to support you.
Closing Date: 08 October 2025
The Role
Type I interferons (IFN-I) are best known as an essential mediator of antiviral immunity yet their neurotoxic potential is increasingly acknowledged. A common signature of dysregulated IFN-I signalling has been identified across a diverse range of neurological disease states including Alzheimers and Parkinsons diseases as well as aging and vascular diseases of the CNS.
Identification of shared pathomechanism in these disorders would offer an efficient route to therapy. Dementias alone cost the UK economy more than 17 billion according to UK government estimates. The burden of disease is expected to rise as populations age with projections suggesting 25% of the European population will be aged over 65 in 2030. Yet fundamental questions remain unanswered concerning the possible involvement of IFN-I in neurological disease foremost among them whether IFN-I contributes directly to CNS disease or is induced as a consequence of neurological damage.
Arguably the strongest evidence for a directly causal role in neuropathology comes from a group of rare inborn errors of immunity termed type I interferonopathies PMID: . Our group previously identified a type I interferonopathy associated with homozygous mutation of STAT2 PMID: . We have generated a mouse model of this disorder in which neurological disease is recapitulated and where multiple CNS cell types including microglia neurones and endothelial cells exhibit pathological effects (unpublished). This project explores the cellular drivers of IFN-mediated pathology using conditional in vivo expression of the pathogenic allele in individual cell types allied with human induced pluripotent stem cell (hiPSC) models of the corresponding cell types in vitro. We will also assess novel IFN-I inhibitors developed in partnership with medicinal chemistry collaborators. This project will shed light on direct and indirect pathogenic properities of IFN-I in the CNS providing a framework for interpreting pathomechanism in neurological disease.
This post is funded by the UK Medical Research Council and is fixed term until 10th July 2027
For informal enquiries contact:
Find out more about the Faculty of Medical Sciences here: out more about our Research Institutes here: Accountabilities
The Person
Knowledge Skills and Experience
Attributes and Behaviour
Qualifications
Newcastle University is a global University where everyone is treated with dignity and respect. As a University of Sanctuary we aim to provide a welcoming place of safety for all offering opportunities to people fleeing violence and persecution.
We are committed to being a fully inclusive university which actively recruits supports and retains colleagues from all sectors of society. We value diversity as well as celebrate support and thrive on the contributions of all of our employees and the communities they represent. We are proud to be an equal opportunities employer and encourage applications from individuals who can complement our existing teams we believe that success is built on having teams whose backgrounds and experiences reflect the diversity of our university and student population.
At Newcastle University we hold a silverAthena Swan award in recognition of our good employment practices for the advancement of gender equality. We also hold a Race Equality Charter Bronze award in recognition of our work towards tackling race inequality in higher education REC. We are a Disability Confident employer and will offer an interview to disabled applicants who meet the essential criteria for the role as part of the offer and interview scheme.
In addition we are a member of the Euraxess initiative supporting researchers in Europe.
Requisition ID: 28625
Required Experience:
IC
Full-Time