Current Vacancies
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Key details
- Location UK DRI at Edinburgh
- Salary: This opportunity is open to UK and international students and provides funding covering stipend and UK level tuition fees. The University of Edinburgh covers the difference between home and international fees meaning that the EASTBIO DTP offers fu
- Lab: Dr Blanca Diaz-Castro, Dr Lorena Arancibia
About the Project
Astrocytes are exceptionally branched cells that tile the brain to maintain its homeostasis1-3. Astrocytes are strategically positioned as a bridge between the brain vasculature and parenchyma4, exhibiting specialised subcellular compartments that interact with distinct brain components5. Around the vasculature, they enwrap ~90% of the brain vascular tree through structures called astrocyte endfeet that mediate important roles such as nutrient and hormone uptake and processing, blood-flow regulation, toxic brain by-products clearance, and blood-brain barrier maintenance2,6,7. Despite the importance of endfoot functions for vasculature-brain interactions, our understanding of the molecules mediating its functions is remarkably limited.
We have developed new tools to define the astrocyte endfoot proteome in the mouse cortex with high level of depth and specificity (Hill, Bravo-Ferrer et al. Nat Comms in Press). This research has opened up new opportunities to better understand the functions of astrocyte endfeet. While we know astrocyte endfeet are molecularly specialised in comparison to other parts of the astrocyte. It remains to be understood the mechanisms that drive this specialisation. In this project we will:
1- Determine which endfoot proteins are locally translated
We will identify if specific types of endfoot proteins are translated in the cell body or locally, in the endfoot, using RNA in situ hybridization, RNA sequencing, and proteomics.
2- Establish if the endfoot protein composition differs between brain regions or vessel types.
Astrocytes are molecularly diverse across brain regions8, and vascular cells differ depending on the vessel type9. It is likely that endfeet are diverse as well, but this has not been directly tested so far. We will perform cell and region specific proteomic to determine if this is the case.
3- Investigate how endfoot diversity correlates with their surrounding environment.
We will define the proteome of vascular cells along the vascular tree and assess if the endfoot functions relate to the ones of their neighbouring vascular counterparts. Moreover, we will assess if endfoot diversity and its potential relationship with the neighbouring cells are affected by acute or chronic insults.
This project will leverage our recent discoveries and generate new methods to better understand astrocyte endfoot diversity and the mechanisms by which astrocyte endfeet become a molecularly specialised compartment.
Training:
The PhD student will be co-supervised by experts in spatial proteomics (Lorena Arancibia Cárcamo) and astrocyte biology and subcellular proteomics (Blanca Díaz Castro) to master highly specialised molecular biology techniques and investigate the mechanisms that determine the astrocyte endfoot molecular composition.
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Key details
- Location UK DRI at UCL
- Salary: £43,981-£52,586
- Lab: Dr Marc Aurel Busche
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.
The Busche Laboratory, based in the UK DRI at UCL, is a highly interactive environment, with strong collaborations across the UK DRI as well as with researchers at UCL and other renowned institutions.
About the role
We are seeking an exceptional individual to join on a cutting-edge research programme aimed at understanding - and ultimately reversing - neuronal and circuit dysfunction in Alzheimer’s disease.
The focus will be on linking early, cell-type-specific molecular alterations to large-scale neural circuit impairments in mouse models. The project will combine spatial omics methods with advanced techniques to record neuronal activity across large populations of cells, such as in vivo two-photon calcium imaging. A variety of experimental and analytical approaches will be applied to interrogate the mechanisms of dysfunction.
This is an outstanding opportunity to work independently on a high impact, state-of-the-art project in a stimulating, vibrant research environment.
The role is available from 01 February 2026 and funded by the UK Dementia Research Institute until 31 January 2028 in the first instance.
Informal enquiries regarding the role can be addressed to Dr Marc Aurel Busche (m.busche@ucl.ac.uk).
About you
You will hold a PhD in neuroscience, engineering, computer science, mathematics, physics, or a related field, and prior practical experience with spatial transcriptomics and related data processing/analysis. Expertise in modern molecular biology techniques such as AAV design and validation, immunostaining and confocal microscopy, single-cell RNA sequencing, quantitative in situ hybridization, and related bioinformatic skills, experience in rodent stereotactic surgery are essential for the role. Excellent interpersonal, collaboration, and communication skills are also required.
This role meets the eligibility requirements for a skilled worker certificate of sponsorship or a global talent visa under UK Visas and Immigration legislation. Therefore, UCL welcomes applications from international applicants who require a visa.
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Key details
- Location UK DRI at UCL
- Salary: £45,103 - £48,679 per annum
- Lab: Professor Catherine Hall
About us
Dementia is the greatest health challenge of our century.
To date there is no way to prevent it or even slow its progression, and there is an urgent need to fill the knowledge gap in our basic understanding of these diseases.
The UK Dementia Research Institute (UK DRI) is the biggest UK initiative supporting research to fill this gap.
Research in the Hall Lab, based in the UK DRI at UCL and the BHF-UK DRI Centre for Vascular Dementia Research, aims to untangle if and how the balance between the brain’s energy supply and demand shapes its activity, and especially how changes in this balance promote the emergence of vascular and Alzheimer’s dementia.
About the role
We are now recruiting a postdoctoral researcher to join the Hall Lab at UCL and work on an exciting projects defining how brain function is affected by a dysfunctional vasculature, and how blood vessels become damaged during dementia. You will interrogate the mechanisms underlying changes in neurovascular function change in the brain during dementia risk, early dementia, and during mild disruptions to the brain’s energy supply. Projects will use physiological, molecular and biochemical approaches to dissect mechanisms producing neurovascular changes observed in models of Alzheimer’s disease and vascular dementia.
The role is available from 01 February 2026 and funded by the British Heart Foundation/UK DRI for two years in the first instance.
Informal enquiries regarding the role can be addressed to Professor Catherine Hall (catherine.hall@ucl.ac.uk)
About you
You’ll have a PhD in neuroscience, life sciences, or a related field, and the ability to develop new ideas and methods, generate research hypotheses, and design experiments to test these. A strong background in statistical analysis and specialist technical expertise in one or more of the experimental methods relevant for the project is essential, as is an understanding of and interest in the research work of the UK DRI, and excellent organisational, interpersonal, and communication skills.
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Key details
- Location UK DRI at UCL
- Salary: The studentship is funded through the Alzheimer’s Research UK (ARUK) for 4 years and will cover UK university tuition fees (home fees only). The studentship will also pay an annual stipend based on the standard ARUK set stipend rate.
- Lab: Dr Soyon Hong
About the Project
Applications are invited for a fully funded PhD studentship in the UK Dementia Research Institute at UCL, UCL Queen Square Institute of Neurology, to start on 28th September 2026.
Project: This PhD project will investigate how astrocytes and microglia contribute to synaptic loss and aggregate pathology in Alzheimer’s disease (AD).
It is becoming increasingly clear that non-neuronal cells critically contribute to region-specific synapse loss and dysfunction in AD. While microglia are emerging as the central cellular mediators of synapse elimination (for e.g., Hong et al., Science 2016, Rueda-Carrasco et al., EMBOJ 2023, De Schepper et al., Nature Neuroscience 2023, Crowley et al., bioRxiv 2024), our recent work suggests that astrocytes may act upstream to confer the region-specific synapse vulnerability (Sokolova et al., bioRxiv 2024). Mechanistically, we find that these astrocytes, which have marked dysfunctional perisynaptic processes, secrete MFG-E8, which then promote microglial synapse engulfment and synapse loss in their local milieu.
The PhD project will build on these findings and aim to uncover astrocyte-microglia crosstalk in AD. The student will dissect molecular mechanisms underlying this cell-cell crosstalk including MFG-E8 using various cutting-edge tools in post-mortem human tissues, human cells and various mouse models including spatial transcriptomics, single-cell transcriptomics, subcellular or secretome proteomics, in vivo manipulation tools, and/or super-resolution microscopy.
Eligibility: Applicants who have or expect to obtain a 1st class honours or an upper 2:1 in their undergraduate degree in neuroscience, neuroimmunology, immunology, molecular biology, biomedical sciences or related disciplines, as well as a significant level of wet-lab research experience in biology or related field. An MSc/MRes is favoured but not a pre-requisite.
Funding Notes
The studentship is funded through the Alzheimer’s Research UK (ARUK) for 4 years and will cover UK university tuition fees (home fees only). The studentship will also pay an annual stipend based on the standard ARUK set stipend rate. Overseas students may apply but will receive funding at Home rates. As such they will need to apply for additional funding or show evidence of their ability to pay the fee shortfall for the full duration of the study.
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Key details
- Location UK DRI at Imperial
- Successful applicants will receive a generous stipend of £23,800 rising by £1,000 each year, and home fees will covered*. Funding is also provided for research expenses, career development and student travel/conference attendance.
About the Project
An opportunity has arisen for a 4-year PhD studentship within the Department of Brain Sciences at Imperial College London, funded by the VIDA DTC. VIDA (Vascular and Immune contributors to DementiA) is a multi-institutional partnership between Alzheimer’s Society and four world-leading research sites: the University of Manchester, University of Edinburgh, Imperial, and City St George’s University of London. With projects focussing on the importance of vascular and immune mechanisms in dementia, VIDA PhD students will become the next generation of much-needed dementia researchers, contributing to breakthroughs in dementia diagnosis and treatment.
VIDA students will embark upon a 4-year fully-funded PhD project at one of the four institutions above, with access to the state-of-the-art research facilities and interdisciplinary training available at all sites. Students at each site will come together as a cohort at several points during the programme, including annual conferences and residential workshop retreats, which will link in with other Alzheimer’s Society Doctoral Training Centres across the UK. Students will also participate in engagement schemes with the Alzheimer’s Society and beyond, sharing the impact of their research in the community. The programme also benefits from built-in opportunities for placements with leading industrial partners, and bespoke training plans including schemes to develop teaching, mentoring, and grant writing skills.
Project Description:
Cerebral small vessel disease (SVD) is a major cause of stroke and vascular dementia, and a key contributor to Alzheimer’s disease (AD). It affects the brain’s smallest blood vessels, arterioles, capillaries, and venules, leading to pathologies such as cerebral amyloid angiopathy (CAA) and arteriolosclerosis. Clinically, SVD is characterised by white matter hyperintensities (WMHs), lacunes, microbleeds, and enlarged perivascular spaces. Early vascular dysfunction, including impaired cerebral blood flow and increased blood–brain barrier (BBB) permeability, is strongly linked to dementia onset and progression. While circulating biomarkers (e.g. VEGF, ICAM1, PDGFB, EDN1) correlate with imaging features of SVD, no single, robust blood biomarker currently exists.
Genome-wide association studies (GWAS) show that both SVD and AD are highly heritable, sharing several genetic loci such as APOE. Most disease-associated variants are noncoding and likely influence gene regulation. Epigenomic analyses have shown that AD heritability is enriched in microglia and myeloid cells, whereas SVD heritability localises to endothelial, mural, and astrocytic cells, which are key components of the neurovascular unit. Moreover, recent multitrait analyses have revealed shared loci between AD and cardiovascular disease, including PLEC and C1Q, implicating overlapping vascular and immune pathways. However, large-scale studies defining gene regulatory mechanisms in SVD and underlying common genetic mechanisms with cardiovascular traits and other dementias remain unexplored.
We hypothesise that integrative multiomic analyses of SVD blood samples will uncover novel molecular mechanisms, biomarkers, and therapeutic targets. Objective 1 will identify gene regulatory mechanisms that are dysregulation in SVD. DNA methylation and RNA-seq will be generated from 147 longitudinally phenotyped SVD blood samples (Mild Stoke Study 2 [MSS2] cohort), with matched genotype, proteomic, and neuroimaging data. Analyses will identify DNA methylation and gene expression changes associated with SVD subtypes, dementia progression, and polygenic risk, including cross-comparison with age-, sex-, and cardiovascular risk-matched controls from the AIRWAVES cohort. Objective 2 will prioritise genetic determinants of SVD. Multitrait analysis with cardiovascular traits, together with quantitative trait locus and Mendelian randomisation analyses will link causal variants to altered gene regulation. Cross-integration with histone modification (CUT&Tag) and single-cell multiomic data alongside plasma proteomics will refine biomarker and drug target prioritisation.
This project will deliver the first integrative map of gene regulatory mechanisms in SVD, linking human genetics to molecular function. These findings will accelerate biomarker discovery and enable genetically validated therapeutic strategies for SVD and vascular dementias.
Application process:
Applicants must hold (or obtain by October 2026) a first or upper-second-class honours degree or equivalent in a neuroscience, computational neuroscience or cardiovascular science or related discipline. A Master’s degree in a related research is highly desirable but not essential.
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Key details
- Location UK DRI at Edinburgh
- Successful applicants will receive a generous stipend of £21,800 rising by £1,000 each year, and home fees will covered.
About the Project
VIDA (Vascular and Immune contributors to DementiA) is a multi-institutional partnership between Alzheimer’s Society and four world-leading research sites: the University of Manchester, University of Edinburgh, Imperial, and City St George’s University of London. With projects focusing on the importance of vascular and immune mechanisms in dementia, VIDA PhD students will become the next generation of much-needed dementia researchers, contributing to breakthroughs in dementia diagnosis and treatment.
PhD studentships
VIDA students will embark upon a 4-year fully-funded PhD project at one of the four institutions above, with access to the state-of-the-art research facilities and interdisciplinary training available at all sites. Students at each site will come together as a cohort at several points during the programme, including annual conferences and residential workshop retreats which will link in with other Alzheimer’s Society Doctoral Training Centres across the UK. Students will also participate in engagement schemes with the Alzheimer’s Society and beyond, sharing the impact of their research in the community. The programme also benefits from built in opportunities for placements with leading industrial partners, and bespoke training plans including schemes to develop teaching, mentoring, and grant writing skills.
How to apply
Candidates must contact the primary supervisor before applying to discuss their interest in the project and assess their suitability.
To submit the email application, you will need:
- CV and/or cover letter
- University transcripts
- Degree certificates (any certificates/transcripts you have not yet received from your current institution can be uploaded at a later date)
- English language certificates (EU/International applicants only)
- Personal statement
- Two references
- Research proposal
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Key details
- Location UK DRI at Edinburgh
- Successful applicants will receive a generous stipend of £21,800 rising by £1,000 each year, and home fees will covered*. Funding is also provided for research expenses, career development and student travel/conference attendance.
About the Project
VIDA (Vascular and Immune contributors to DementiA) is a multi-institutional partnership between Alzheimer’s Society and four world-leading research sites: the University of Manchester, University of Edinburgh, Imperial, and City St George’s University of London. With projects focusing on the importance of vascular and immune mechanisms in dementia, VIDA PhD students will become the next generation of much-needed dementia researchers, contributing to breakthroughs in dementia diagnosis and treatment.
PhD studentships
VIDA students will embark upon a 4-year fully-funded PhD project at one of the four institutions above, with access to the state-of-the-art research facilities and interdisciplinary training available at all sites. Students at each site will come together as a cohort at several points during the programme, including annual conferences and residential workshop retreats which will link in with other Alzheimer’s Society Doctoral Training Centres across the UK. Students will also participate in engagement schemes with the Alzheimer’s Society and beyond, sharing the impact of their research in the community. The programme also benefits from built in opportunities for placements with leading industrial partners, and bespoke training plans including schemes to develop teaching, mentoring, and grant writing skills.
Project Background
Cerebral small vessel disease (SVD) is the leading cause of vascular dementia, and is characterised by white matter damage which correlates closely with the degree of cognitive impairment. SVD can be sporadic or inherited, and the most common inherited form of the disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is caused by a mutation in the NOTCH3 gene. While we have previously shown some of the ways in which vascular changes can affect white matter in both sporadic and inherited SVD, we still don’t fully understand how these changes occur. Additionally, much of this previous work has relied on rodent models of disease, which do not fully recapitulate changes seen in human patients.
In this project, the student will use human induced pluripotent stem cell (iPSC) derived cells to investigate interactions between vascular cells and oligodendrocytes (myelin forming cells in the brain) to better understand white matter damage in vascular dementia. We hypothesise that vascular cells derived from CADASIL patient iPSCs secrete factors which alter oligodendrocyte behaviour and function, including downstream effects of oligodendrocytes on neuronal activity and microglia. By identifying the molecules involved in these interactions, we hope to ultimately be able to disrupt these pathways to prevent disease pathology.
The aims of the project are to:
- Develop a greater understanding of vascular and endothelial dysfunction in CADASIL, including changes in secreted molecules
- Elucidate the mechanisms underlying oligodendrocyte changes in CADASIL
- Identify secreted and other factors involved in mediating vascular induced oligodendrocyte changes in CADASIL, providing possible therapeutic targets to prevent white matter damage
- Elucidate the role of oligodendrocytes in mediating neuronal and immune cell changes in CADASIL
All of these aims will have high translational relevance through use of human patient-derived cells and human post-mortem tissue
The student will be trained in iPSC cultures; differentiation of endothelial cels, mural cells, oligodendrocytes, neurons and microglia from iPSCs; functional characterisation of oligodendrocytes, neurons and microglia (including immunocytochemistry, live cell imaging and image analysis); histology, immunohistochemistry and in situ hybridisation on human post-mortem tissue; and molecular biology techniques (including ELISAs and proteomics). The student will be based primarily in Dr Rajani’s group at the University of Edinburgh, with short amounts of time spent in Prof Wang’s group at the University of Manchester to train in iPSC-mural cell differentiation.
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Key details
- Location UK DRI at Edinburgh
- Salary: The studentship is funded through the Alzheimer’s Research UK (ARUK) for 4 years and will cover UK university tuition fees (home fees only). The studentship will also pay an annual stipend based on the standard ARUK set stipend rate.
About the Project
VIDA (Vascular and Immune contributors to DementiA) is a multi-institutional partnership between Alzheimer’s Society and four world-leading research sites: the University of Manchester, University of Edinburgh, Imperial, and City St George’s University of London. With projects focusing on the importance of vascular and immune mechanisms in dementia, VIDA PhD students will become the next generation of much-needed dementia researchers, contributing to breakthroughs in dementia diagnosis and treatment.
PhD studentships
VIDA students will embark upon a 4-year fully-funded PhD project at one of the four institutions above, with access to the state-of-the-art research facilities and interdisciplinary training available at all sites. Students at each site will come together as a cohort at several points during the programme, including annual conferences and residential workshop retreats which will link in with other Alzheimer’s Society Doctoral Training Centres across the UK. Students will also participate in engagement schemes with the Alzheimer’s Society and beyond, sharing the impact of their research in the community. The programme also benefits from built in opportunities for placements with leading industrial partners, and bespoke training plans including schemes to develop teaching, mentoring, and grant writing skills.
Project Background
Stroke can double the risk for a new diagnosis of dementia and can worsen cognitive trajectories in patients with existing disease (1). Stroke risk factors, the index stroke and recurrent strokes can contribute to post-stroke dementia, however it is also thought that inflammation can contribute to worsened cognitive decline (2). Systemic infections, such as pneumonia, are also a common complication of stroke recovery, and infections that occur up to 76 days after the initial stroke event have been shown to be independently associated with worsened clinical outcomes (3, 4). Infections can also cause delirium, and recurrent or severe episodes of delirium are also strongly linked to accelerated cognitive decline and the development of dementia (5). Together, this suggests that infection following stroke may contribute to increased dementia risk in survivors, however the mechanisms that drive this are poorly understood. This project will use a mouse model of ischemic stroke and induced bacterial pneumonia to investigate the relationship between systemic infection, neuroinflammation and small vessel disease in stroke recovery.
Objectives:
1. Profile the neuroinflammatory response to bacterial pneumonia and its impact on stroke injury recovery
2. Understand the impact of infection on blood brain barrier (BBB) integrity and blood vessel remodelling after stroke
3. Investigate circulating biomarkers associated with infection and worsened cognitive outcomes
Students will be comprehensively trained in all animal work and laboratory techniques and will develop experimental skills including in vivo animal models, flow cytometry, microscopy, microbiology as well as data and image analysis. This project will be carried out at the Institute for Regeneration and Repair (IRR) at the University of Edinburgh where students benefit from an excellent supportive environment with access to cutting edge facilities and both social and career development events through an active postgraduate researcher community.