Current Vacancies
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Key details
- Location UK DRI at UCL
- Salary: £36,433-£41,833 per annum
- Lab: Dr Tim Bartels
About us
Research from UK DRI at UCL covers the journey from the patient to the laboratory and back to the patient with improved diagnosis, biomarkers and candidate therapies put to the test. Led by Professor Karen Duff, UK DRI Centre Director, the team will address the key unanswered mechanistic questions that link genetic and lifecourse factors to dysfunction in molecular pathways, in cells and in neural systems during the progression of the dementias. This work will be enhanced by clinical resource to link lab work to the clinic.
About the role
We are recruiting a Research Technician to join the Bartels lab at the UK DRI at UCL and work on a research project involving the analysis of human blood samples and the optimisation of novel antibodies in an ELISA format to develop a novel biomarker of synucleinopathy. Ex vivo protein standards will be purified from human tissue and mammalian cell culture and quality control conducted via SDS-PAGE, aggregation assays, electronmicroscopy, CD spectroscopy. You will assist with protein biochemical and biophysical analysis, as well as protein expression and purification.
The role is available from May 2026 and is funded by the UK Dementia Research Institute until 30 April 2027 in the first instance.
About you
You will have an Honours degree (minimum 2:1) in Biophysics, Biochemisry, Molecular Biology, or a related discipline, as well as experience and knowledge in one or more of the following areas: neurodegeneration, synucleinopathies, biochemical analysis (including detergent extraction and Western Blot) and protein expression and purification. Good IT, communication, and problem-solving skills are essential, as is a proactive approach to your work and an ability to meet deadlines.
This role does not meet the eligibility requirements for a Skilled Worker Visa certificate of sponsorship under UK Visas and Immigration legislation. Therefore UCL will not be able to sponsor individuals who require right to work in the UK to carry out this role.
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Key details
- Location UK DRI at Cardiff
- Salary: This 3.5‑year studentship, funded by the Motor Neurone Disease Association, is available to 'Home' fee status. The award covers tuition fees and provides a maintenance stipend, which is ££21,383, for the 2026/7 academic year
About the Project
This studentship aims to investigate how mutations associated with rare familial forms of motor neurone disease (MND), disrupt lysosomal function in human motor neurons. Using a combination of patient-derived fibroblasts and iPSC-derived motor neurons carrying MND-associated mutations the studentship will characterise the impact of the mutations on lysosomal morphology, acidification, and Ca2+ handling. Quantitative assays, including ratiometric fluorescent imaging and automated confocal analysis, will be used to assess lysosomal morphology, distribution and function. In parallel, we will evaluate downstream consequences such as altered proteolytic activity and lipid accumulation. The student will explore therapeutic rescue of lysosomal defects using small molecule modulators of lysosomal function. Through detailed mechanistic and phenotypic analyses, this studentship seeks to establish how lysosomal dysregulation contributes to MND and to identify potential therapeutic targets relevant to a broader spectrum of MND patients.
Lead Supervisor- Dr Owen Peter
Entry Requirements:
As only one studentship is available and a very high standard of applications is typically received, the successful applicant is likely to have a very good first degree (a First or Upper Second class BSc Honours or equivalent) and/or be distinguished by having relevant research experience.
How to apply:
You can apply online - consideration is automatic on applying for a PhD with an October 2026 start date.
Entry Requirements:
As only one studentship is available and a very high standard of applications is typically received, the successful applicant is likely to have a very good first degree (a First or Upper Second class BSc Honours or equivalent) and/or be distinguished by having relevant research experience.
This 3.5‑year studentship, funded by the Motor Neurone Disease Association, is available to 'Home' fee status applicants and will begin on 1st October 2026. The award covers tuition fees and provides a maintenance stipend, which is ££21,383, for the 2026/27 academic year.
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Key details
- Location UK DRI at Cardiff
- Salary: This Wales Heart Research Institute Cardiovascular Fund studentship is open to Home and EU applicants. The award offered will cover fees and a maintenance stipend (for 26/27 this will be approx. £21,300).
About the Project
Background
Vascular dementia is the second most common type of dementia after Alzheimer’s disease and is caused by impaired blood supply to the brain. A key causative factor in the pathogenesis of vascular dementia is the development of atherosclerosis affecting the small blood vessels within the brain. Other cardiovascular events such as strokes (large and small) are also major contributory events in the development of the disease. Common “lifestyle” risk factors affecting the development of vascular dementia are identical to those identified for cardiovascular disease and include: high blood pressure, high cholesterol, diabetes, obesity, physical inactivity and smoking.
We have previously shown that the complement system, a key component of innate immunity comprising more than 40 different proteins is intimately involved in the development and progression of atherosclerosis. Thus, in developing atherosclerotic plaques complement is activated, causing an inflammatory response that drives the disease. The absence of key complement proteins of the “terminal” pathway ameliorates disease (Lewis et al 2010). More recently we have focused on the mechanisms underlying the genetically proven links between complement and Alzheimer’s Disease (AD). Here again, we have demonstrated that therapeutic blockade of complement activation in a mouse model of AD through the administration of blocking antibodies can slow the development of the disease and improve cognitive performance (Zelek W.M. et al 2024).
Modelling Dementia in animals relies largely on genetically altered mice carrying the human transgenes responsible for familial AD. This is not ideal since familial AD comprises only a small percentage of dementia cases. Recent publications have described, more relevant models to address the pathology of vascular dementia (Sweetat S. et al 2024, Kruyer A. et al 2015). Given the vascular damage and inflammation that has been documented in these new models we hypothesise that complement will be activated and play a significant contributory role in driving disease.
Aims
To test our hypothesis, we shall use the published ovariectomised model of vascular dementia where female mice are fed a diet high in fat, sugar and salt to mimic post-menopausal ageing together with several of the key risk factors relevant to human vascular dementia. The model will be used in three sets of experimental analyses:
1) We shall assess the extent of complement activation in these model mice. This will be carried out through the use of in-house ELISA-based assays and immunohistochemistry in the serum and brain tissues of these animals respectively.
2) We shall utilise in-house complement deficient strains (eg C7-/-; C3-/- and CD59) to understand the effect of deleting key complement genes in this model of vascular dementia.
3) We shall administer our previously validated anti-complement antibodies (anti C7) to determine whether complement blockade is a viable therapeutic approach to vascular dementia in this model.
Methodologies Employed
A range of techniques will be employed throughout this project to assess disease and test the effectiveness of our therapeutic approach. Thus, ELISA based assays, behavioural tests and immunohistochemistry staining for a range of markers in the brain tissues of these mice including (C3b; MAC; amyloid; tau; Iba-1; GFAP) will be utilised in all three aims. These will validate the model in our hands and allow assessment of the activation of complement. Furthermore, In the serum of model animals, Cytokines, Cholesterol, triglycerides, glucose and liver enzyme function will be assessed at baseline, during and at the end of each experiment. Where needed we shall confirm these findings by ELISA based analyses of total brain homogenates. RNA will be isolated and used in qPCR assessment of specific gene sets relevant to vascular dementia, neuroinflammation and complement. Supporting methodologies will include cell culture, protein purification and complement haemolysis assays to produce, purify and test the therapeutic antibodies that we will employ.
Potential Impact
This project will establish the extent of complement activation and its role in driving the progression of vascular dementia in a newly emerging relevant model of the vascular dementia. Data obtained will allow an assessment of the efficacy of inhibiting complement during the disease as a therapeutic approach. These outcomes could have important implications for how the second most common form of dementia is measured, and open new directions for therapeutic development.
How to apply:
Please use our online application service at: https://www.cardiff.ac.uk/study/postgraduate/research/programmes/programme/pharmacy
and specify in the funding section that you wish to be considered for WHRI funding.
Please also specify the project title and supervisor
The closing date for applications is 6th March 2026 and we expect interviews to be held in April
The successful applicant is likely to have a very good first degree (a First or Upper Second class Honours or equivalent)
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Key details
- Location UK DRI at Cardiff
- Salary: This Wales Heart Research Institute Cardiovascular Fund studentship is open to Home and EU applicants. The award offered will cover fees and a maintenance stipend (for 26/27 this will be approx. £21,300).
About the Project
Project summary:
Shock is a severe, life-threatening condition caused by critically reduced blood flow to tissues and organs and remains a major cause of death and disability in intensive care. A central feature of shock is endothelial dysfunction, leading to vascular leakage, tissue oedema, and multi-organ failure. Emerging evidence indicates that dysregulation of the complement system, a key component of innate immunity, contributes to this process by driving inflammation, amplifying coagulation, and promoting vascular injury. However, the precise complement pathways involved in cardiogenic shock (CS) and the prognostic value of circulating complement biomarkers remain unclear. This project will address these gaps by profiling complement dysregulation in CS using a comprehensive biomarker panel. The work will define the complement pathways driving vascular injury, identify predictive biomarker signatures, and highlight novel therapeutic targets to improve outcomes in critically ill patients.
Research plan
The student will analyse complement dysregulation in shock with the following aims:
Aim 1: Quantify complement components, regulators, and activation markers using 25 in-house complement assays (ELISA and/or MSD) in plasma from a unique cohort of >350 patients with cardiovascular shock, collected at Barts Health NHS Trust (Barts), alongside matched healthy controls.
Aim 2: Integrate complement biomarker data with clinical outcomes and biochemical measures (e.g. troponin, lactate, syndecan-1, vascular cell adhesion molecule-1 (VCAM-1)) to identify signatures associated with endothelial dysfunction and disease severity.
Aim 3: Develop predictive biomarker models using statistical and pathway analyses to identify marker sets associated with mortality, prolonged intensive care unit (ICU) stay, persistent organ dysfunction, and where longitudinal data permit (vascular cognitive impairment and vascular dementia) relevant outcomes, forming the basis for future vascular dementia; focused biomarker and therapeutic studies.
Techniques and training
The student will receive technique-rich training in complement immunoassays (ELISA, MSD), biomarker discovery pipelines, and translational cardiovascular immunology. They will gain experience in advanced biostatistics and machine-learning approaches (e.g. PCA, clustering, random forest) using R and Python, alongside assay development to industry standards, including analytical validation, quality control, and exposure to regulatory frameworks (ISO13485, IVDR principles). The student will be embedded within the Division of Infection and Immunity and the Cardiff Dementia Research Institute (DRI), a highly collaborative environment with a strong ECR network. They will be registered in the School of Medicine and supported by cross-school supervision and collaboration with the School of Biosciences, providing access to complementary expertise, facilities, and training opportunities.
Supervision and environment
The project will be jointly supervised by experts in complement biology, cardiovascular science, and data science:
Impact and career development
This project offers excellent interdisciplinary training at the interface of academic science, clinical medicine, and industry. It is well positioned to generate high-quality pilot data suitable for future BHF or NIHR applications and to deliver impactful research outputs relevant to cardiovascular and immunology research. The student will develop a robust skillset spanning complement biology, vascular inflammation, quantitative biomarker science, and statistical modelling, providing a strong foundation for a career in academia, translational research, or the biotech/pharmaceutical sector.
How to apply:
You can apply online - consideration is automatic on applying for a PhD with an October 2026 start date.
Please use our online application service at: https://www.cardiff.ac.uk/study/postgraduate/research/programmes/programme/pharmacy