KING'S COLLEGE LONDON

UKRI Gateway to Research · FY 2025 · 2025-11

Cosmic observations emphatically demonstrate that most of the Universe's matter is invisible to light. "Dark matter" (DM) is the scaffold for the Universe, gravitationally attracting ordinary visible matter, and thus is essential to the formation of galaxies, stars, planets and life. Understanding the nature of DM is fundamental to understanding the origin of humanity, but the constituents of DM (particles and interactions) remain a mystery. This is a critical moment when null results for the traditionally-favoured DM candidate (weakly interacting massive particles) are driving an explosion in well-motivated DM theories that urgently need new discovery strategies. We will imminently map the Universe's large-scale structure with unparalleled fidelity in surveys like Rubin. These surveys will provide a new, powerful testbed for microphysical DM models that current direct detection technology cannot probe, but which cause detectable cosmic signatures — if the theoretical modelling challenge is solved. As ERF at the pre-eminent astrostatistics group at Imperial College London, I will solve this challenge to detect or exclude the most compelling DM theories by the distinctive gravitational signatures they imprint in the cosmic web of structure. My vision is, thus, to transform how we search for the nature of dark matter by developing precision cosmological structure formation models for novel DM theories, where cosmological observations provide the most powerful — or often only — way to search for DM candidates. I will definitively detect or exclude wave-like cosmic web effects from ultra-light axion DM (ULDM), whose discovery could point towards a "theory of everything" that seeks to explain all physical phenomena in a single set of laws. I will improve, by a factor of 25, constraints on nuclear/electronic interaction cross sections for light (sub-GeV) particle DM probing novel DM production mechanisms like freeze-in. I pioneered AI techniques to map accurately cosmic constraints from one DM model to another. Using these methods, I will release public likelihood software that will be used to search for other well-motivated DM scenarios like sterile neutrinos, dark photons or complex dark sectors like atomic dark matter. Combining structure information across 12 billion years, I will test for decaying DM signals. Since dark matter doesn't observably emit or absorb light, I will instead look for how different DM candidates change the gravitational clumping of visible objects like galaxies and gas in-between galaxies. I will lead DM searches within transformational telescope surveys (Rubin) so that I robustly mitigate astrophysical and instrumental data effects. I will build on my structure formation modelling expertise that I already used to set world-leading DM limits. To match the coming step-up in data precision, I will build new models of the effect of light, ultra-light and decaying DM on the cosmic web. To scan systematically across DM parameter space, I will combine information from larger-scale (> Mpc) probes like galaxy clustering and their gravitational lensing by DM (Rubin) — with smaller-scale (< Mpc) probes like Lyman-alpha forest absorption and Milky Way stellar stream perturbations (Rubin). The UK has invested hundreds of millions of pounds in next-generation surveys like Rubin. This programme will maximise their impact by developing theoretical and AI models needed to extract precision DM constraints. My results will set the baseline sensitivity and targets for future DM direct detection experiments like the UK-based AION experiment for ULDM and semiconductor/superconductor-based technology (e.g., TESSERACT) to search for sub-GeV particle DM.

UKRI Gateway to Research · FY 2025 · 2025-11

Context Reproduction is essential for human and animal survival yet is exquisitely sensitive to perturbations. Reproductive problems, including stress-related infertility, have enormous socioeconomic impact and understanding underlying mechanisms will facilitate innovative treatments and enhance wellbeing. Challenge Successful reproduction requires normal function of a neural oscillator, the gonadotrophin-releasing-hormone (GnRH) pulse generator, which drives pulsatile release of gonadotrophic-hormones (LH/FSH) to control ovulation and spermatogenesis. This oscillator comprises hypothalamic Kisspeptin neurones co-expressing Neurokinin-B (NKB) and Dynorphin (acronym-KNDy). Despite recent insights into the KNDy neural network, major questions remain unanswered. How do NKB and dynorphin, and intrinsic-glutamatergic neurotransmission collectively orchestrate the intermittent synchronisation of KNDy neurones which underlie GnRH pulsatility? How does stress suppress this synchronisation to cause infertility? Our preliminary work using real-time monitoring of single-KNDy neurones in-situ has revealed for the first-time a complex repertoire of mini-synchronised events (mSEs; synchronisation between 2-or-more neurones) building up to the full-blown SEs characteristic of LH pulses. Through computational modelling we have begun to uncover the precise role of the key neurotransmitters (NKB, dynorphin and glutamate) in orchestrating the emergence of these mSEs that somehow contrive to facilitate synchronisation, as well as understanding how this system collapses under stress. This insight provides a unique opportunity to establish how individual KNDy neurones entrain and synchronise to produce the dynamic SE architecture underlying normal-reproduction and stress-related conditions. To further scrutinise the system, we will integrate our in-silico modelling of the biophysical mechanisms with cutting-edge in-vivo GRadient-INdex-(GRIN)-lens miniendoscopy and electrophysiology, and use the latest in-vivo CRISPR-Cas9-gene-editing methods to selectively knockdown glutamate, NKB, or dynorphin expression in KNDy neurones. Aims and Objectives Hypothesis: Synchronisation in the KNDy neural network is a dynamic phenomenon driven by mini-synchronisation events (mSEs) involving intricate interactions between glutamate, neurokinin-B, and dynorphin signalling, which collectively orchestrate GnRH pulse generation required for successful reproduction. These mSEs vary across the ovarian-cycle influencing the network’s predisposition to synchronisation, while stress-related inputs disrupt synchronisation patterns, dampen pulse generation and impact on fertility. Objective-1: Using in-vivo GRIN-lens and electrophysiological data from single-KNDy neurones across the female ovarian-cycle and in males, to develop a mathematical framework to capture the transient dynamics leading to synchronisation in the KNDy-network, and predict the balance of neuropeptide and neurotransmitter signalling in the synchronisation process. Objective-2: Using CRISPR-Cas9 mutagenesis, and leveraging in-silico insights from Objective-1, to interrogate the integrative role of neurokinin-B, dynorphin and glutamate transmission in synchronising the KNDy-network to initiate and sustain pulsatile dynamics of the GnRH pulse generator. Objective-3: Using in-vivo and in-silico approaches, to develop a quantitative understanding of how stress-activated external inputs to the KNDy-network of female and male mice influence single-neurone and network activity, leading to dysregulation of GnRH pulse generator frequency. Beneficiaries Outcomes from this research will characterise mechanisms fundamental to the control of the GnRH pulse generator. Primarily the livestock industry is a likely beneficiary through improved fertility, quality and productivity. Also, millions of people may benefit from development of novel-therapeutics for infertility, and other reproductive disorders including PCOS and delayed puberty. Academics, clinicians and industry also stand to gain, as our approach aligns with the BBSRC Strategic Delivery Plan objectives “Capacity and Capability in Core-Bioscience Disciplines” by combining in-silico modelling and experimental science, “Understanding the rules-of-life”, relating to human and animal health and wellbeing, and “Enabling world-leading bioscience, and its transition into economic and societal benefits”.  

UKRI Gateway to Research · FY 2025 · 2025-11

This project sits within the realm of Diophantine equations, an ancient area of mathematics containing problems that have remained unsolved for thousands of years. Mathematicians working in this field study the integer (i.e. whole number) solutions of polynomial equations. Given such an equation, the first question one might ask is whether any integer or rational solutions exist. In fact, this can be a very hard problem: even with the most powerful computers in the world, we cannot check all the infinitely many possibilities to see whether they are solutions. In 1900, Hilbert challenged mathematicians to come up with an algorithm that can determine whether a polynomial equation has an integer solution. Seventy years later, building on work of Robinson, Davis and Putnam, Matiyasevich showed that no such general algorithm exists! Nevertheless, the study of these equations remains a thriving area of current research and they underlie cryptographic schemes protecting our data in many aspects of modern life, e.g. online shopping. Modern methods for tackling Diophantine equations proceed via the local-global method. One first checks whether the equation has an integer solution everywhere locally. This is a finite computation, thanks to the Lang—Weil bounds. The challenging part is deciding whether these local solutions patch together to form a global integer solution. For some types of equations, such as quadratic forms, this always works. This is what it means to say that the Hasse principle (the primary example of a local-global principle) holds for quadratic forms. But for equations of higher degree, such as cubic equations, the Hasse principle can fail. Understanding why and how often local-global principles fail is key to unravelling the mysteries of Diophantine equations, and is the focus of this research project. A common explanation for the failure of local-global principles comes from the so-called Brauer—Manin obstruction. Skorobogatov has conjectured that the Brauer—Manin obstruction explains all failures of the Hasse principle for equations defining K3 surfaces. These surfaces are of interest for several reasons: they sit at the boundary of what is known about Diophantine equations, have been used as a testing ground for important conjectures (e.g. Deligne’s proof of the Weil conjectures), and also crop up in mirror symmetry and string theory. The first strand of my project concerns Brauer—Manin obstructions on K3 surfaces. In certain cases of interest, I will calculate the relevant Brauer groups and from there compute Brauer—Manin obstructions by evaluating Brauer group elements at collections of local points and investigating how these evaluations vary as one changes the local points. The second strand of my project takes a statistical approach and studies whole families of mathematical objects. For example, I will study a certain family of Diophantine equations that define geometric objects called elliptic curves and aim to determine how often their solution sets are finite as opposed to infinite. Equations defining elliptic curves rightfully command a great deal of attention. They are noted for the rich structure of their sets of solutions in which one can build new solutions from old, their connection to ancient problems (such as the still unsolved Congruent Number Problem that dates back to at least the 10th century), their crucial role in Wiles’ famous proof of Fermat’s Last Theorem, and their use in elliptic curve cryptography.

UKRI Gateway to Research · FY 2025 · 2025-11

Food allergies are increasing, affect 8% of children and 10% of adults and can be life-threatening. With no cure, patients must avoid allergens and carry emergency medication, leading to restricted social lives and anxiety. While immunotherapy can raise the reaction threshold, it does not eliminate life-style limitations and risk of reactions. Urgent action is needed to develop definitive treatments for food allergies. Exposure to food allergens through the gastrointestinal tract is tolerogenic. Peanut consumption from the first year of life reduced peanut allergy by 81% in a randomised-controlled trial. This impressive effect was allergen-specific and sustained over time. However, the underlying immune mechanisms of oral tolerance induction to peanut are not well understood. This is due to limited access to the tissue where oral tolerance develops: the gut. We have developed a novel in vitro model using human gut organoids populated with blood immune cells, which mimics children’s intestinal environment and allows us to explore immune mechanisms of oral tolerance and food allergy in humans. Oral tolerance to food antigens occurs in the duodenum and involves various immune cell populations to actively suppress allergic responses, locally and systemically. Revealing the mechanisms that initiate this process will identify targets to halt food allergy. Innate lymphoid cells (ILC) are crucial first responders. In murine models, ILC2 have been implicated in the inception of food allergy mainly through secretion of Th2 cytokines. Conversely, ILC3 have been shown to be important in tolerance to gut commensals, namely through the induction of regulatory T cells. Overall, this evidence led us to hypothesise that ILC2 drive food allergic responses whilst ILC3 drive oral tolerance to food allergens in humans. ILC closely interact with the intestinal epithelium in a bidirectional mode and thus these immune mechanisms may likely be influenced by the epithelium. In this research programme, we will use unique samples from young children undergoing their first oral exposure to peanut and our novel co-culture of human gut organoid models with patients’ immune cells. This will allow us to pinpoint key pathways involved in establishing oral tolerance to food allergens and explore how they can be modulated to develop curative treatments for food allergies. Specifically, we will compare peanut-specific immune responses between peanut-allergic and peanut-sensitised-tolerant children during their first oral exposure to peanuts via oral food challenge (OFC). Blood samples collected before and after the OFC will be used to analyse systemic immunological changes (Aim 1). Gut organoids and duodenal tissue will be utilised to examine how intestinal ILCs are altered following exposure to peanut allergens (Aim 2). We will investigate the direct effects of peanut allergens on the intestinal barrier and ILC-epithelium interactions (Aim 3), as well as gut ILC-T cell interactions (Aim 4). Finally, we will identify key immune pathways activated or suppressed by peanut allergens and explore their pharmacological modulation using blood samples from peanut-allergic children and adults to assess whether the allergic response can be suppressed and oral tolerance induced (Aim 5). By the end of this research programme, we will have fundamentally changed our understanding immune responses to food allergens in the human gut and will have identified specific targets for the much-needed curative treatment of food allergy. This will benefit food allergic patients and their families, the food industry and academic-industry partnerships to pursue identified targeted therapies.  

UKRI Gateway to Research · FY 2025 · 2025-11

Medicine and the Making of Race examines the role of European medical practice in the early transatlantic slave trade and the way it shaped developing ideas about race. In the first three years of our project we have explored archives across the UK, the Netherlands, Barbados, Spain, and the Canary Islands, together with a wide-ranging programme of research into travel narratives, manuscript culture and correspondence, and medical publications. Fully integrating our research into the history of Europe, rather than seeing it as a fundamentally colonial or North American preoccupation, our work has helped to shape a new understanding of the participation of medical practitioners from all over Europe in constructing systems of slavery; challenging the interpretation of the 'triangular slave trade' as a transnational force shaped by macroeconomic developments, and conceptualising it instead as created and shaped by many thousands of personal interactions. In its renewal phase, MMoR will shift our focus from people to medical practices – specifically diagnosis, pharmaceutical treatment, and postmortem dissections, and their increasingly racialised performance on the bodies of enslaved individuals. We will explore the local practices that European medical writers encountered on the west coast of Africa, with an explicit focus on their engagement with western African “plantworlds”, a relational concept in which plants link ecology and human behaviour. Thousands of west African plants were recorded, and sometimes sent by medical practitioners from all over the west coast of Africa. Stripped from their context, they were noted in scientific sources simply as botanical specimens, but elsewhere, through inquisition records, correspondence, and early ethnography, we can recover traces of the complex practices which surrounded them.  Drawing on the innovations of postcolonial and Black feminist historians of slavery who have developed novel methodologies of reading colonial sources ‘along the biased grain’ to theorise human agency, we seek to use these records as resources for a reparative recovery of knowledge. To carry out this work, we are also turning to a new body of sources: the “detached” papers of the Royal African Company, the “other (overige)” files of the Middelburg company, and the “miscellaneous” records of the Brandenburg company. Deemed insignificant by their original archivists, and largely uncatalogued on a per item basis, they contain vast quantities of unstudied information, from letters of application, to complaints between provisioners, to examine how medical practices and knowledge moved across different geographical regions, and across increasingly solidified racial lines. The role of medicine we suggest, offers a case study of the ordinary, transactional and everyday ways in which regimes of slavery were enacted and integrated within the metropolitan centres of Europe, and affords insight into the ad-hoc, unsystematic way in which racialised knowledge was made. Foregrounding interpersonal encounters and embodied practices, our work offers a new way to think about one of the most fundamental problems in historical scholarship: how ideas of race came to frame Western thinking about the world.    

UKRI Gateway to Research · FY 2025 · 2025-10

Visual snow syndrome (VSS) is a neurological condition that affects how people see the world. Those with VSS constantly experience visual disturbances, such as static-like vision, finding light painful or bothersome, floaters, and lingering afterimages. Further, patients with VSS often have concomitant migraine disorder and continuous tinnitus, which can be very difficult to manage. While visual snow can vary in severity, countless patients are profoundly impacted in their daily lives by the condition, with epidemiological studies showing that VSS affects around 2% of the population. VSS was only recognized as a medical condition ten years ago, and very little is known about what causes it and how best to treat it. In addition, the relationship of VSS with migraine, a frequent and highly disabling disease with which it shares biological similarities, is unclear. Comorbid migraine is linked to greater severity of VSS, with brain mechanisms such as cortical hyperexcitability and hyperresponsivity—particularly in visual regions—implicated in both conditions. Gaining deeper insight into the shared and distinct neural mechanisms of these disorders will enhance our knowledge and improve clinical recognition and differentiation between the two. In this fellowship I aim to better understand the mechanisms underlying VSS, and to identify brain biomarkers specific to VSS. This research will expand our understanding of the condition and lay the groundwork for developing targeted treatments for patients in the future. I will also explore how VSS differs from migraine, providing invaluable information for large groups of patients. My specific objectives are: To determine and quantify the neurotransmitters involved in VSS, and specifically to disentangle glutamate and GABA activity in the visual cortex. To study the brain mechanisms that determine VSS by measuring cortical excitability, inhibitory mechanisms, and excitation/inhibition balance within the visual system, and how these aspects influence visual processing and symptom generation in VSS. To differentiate the neurobiology of VSS from that of migraine, determining differences in habituation, visual processing, metabolic changes and cortical connectivity. To accomplish these goals, I will employ cutting-edge techniques that have never been applied to the study of this condition. In particular, I will use 7 Tesla magnetic resonance (MR) spectroscopy—the most powerful MR technology available for human research—to investigate changes in visual brain function and metabolism in patients with VSS, both at rest and during an active brain state. I will complement this approach with innovative methods for measuring brain activity, designed to stimulate and detect subtle changes in brain cortical nerve cells. Finally, I will employ drugs that modulate nerve cell signalling within these circuits, to establish a pharmacological model of VSS that enables direct and detailed investigation of the condition. In summary, this project will allow me to explore changes in brain function in patients with VSS, and, in the long term, to discover ways to improve outcomes for patients living with this disabling disorder. It will also deepen our knowledge of the neural mechanisms underlying abnormal sensory processing through a multidisciplinary approach, potentially influencing a wide range of disorders characterized by similar alterations.

UKRI Gateway to Research · FY 2025 · 2025-10

GLOW-in-a-BOX: a pioneering social venture addressing the critical underrepresentation of gender-diverse creators in creative technology through the world's first touring exhibition platform. Building on proven demand from successful GLOW events [https://www.kcl.ac.uk/events/series/glow-illuminating-innovation], and a recognisable brand identity, it creates sustainable revenue streams by connecting creators with venues and audiences nationwide. With trademark protection secured and a scalable touring model, GLOW-in-a-BOX transforms cultural support into commercially viable programming while urgently addressing gender inequity in emerging technologies. GLOW-in-a-BOX addresses two interconnected problems: critical underrepresentation of women, non-binary and trans individuals in creative technology (women represent only 19% of the tech sector despite being 49% of the workforce), and fragmented distribution models for immersive exhibitions. With the immersive technology market projected to reach $228 billion by 2028, marginalised creators lack sustainable platforms for showcasing work. This creates barriers to funding, recognition, and career advancement, limiting innovation in the rapidly expanding creative economy.

UKRI Gateway to Research · FY 2025 · 2025-10

Why is research needed in this area? Eczema is a very common skin condition that causes redness, dryness and itch over the body. It affects physical and psychological well-being, profoundly impacting quality of life. New, potent tablet and injection treatments that affect the immune system are effective at controlling the symptoms of eczema, but are typically started too late. Once treatment is started, it is expected to be continued lifelong, carrying risks of side effects and healthcare costs. In other similar conditions caused by abnormal immune system activity such as rheumatoid arthritis and psoriasis, there is evidence that earlier treatment leads to better outcomes for patients. However, we do not fully understand the mechanisms underlying why early intervention is beneficial. Once diseases such as eczema are successfully treated, abnormal cells or molecules may remain in affected body sites such as the skin – known as an ‘inflammatory memory’. These may ‘reactivate’ in the future, causing disease to recur in the same sites. We currently do not understand much about these processes, and whether early treatment is effective because it reduces the build-up of inflammatory memory. With better understanding, we may identify new treatment strategies for eczema that target the inflammatory memory, with potential for progressing towards a cure. This knowledge may also be applicable to other inflammatory conditions.   How will this research be conducted? This research is a distinct project that will use data from the ongoing mySkinomics study, which involves the collection of skin samples from patients participating in a clinical trial called BEACON (which is comparing how effective and safe various tablet and injection treatments are for adults with eczema). Skin samples are being collected before and after patients start an injection treatment called dupilumab, and examined using state-of-the-art scientific techniques. I will establish the features of inflammatory memory in eczema skin and perform experiments on cells grown in the laboratory to find out how different cells interact to form this inflammatory memory. Next, I will explore whether the duration of severe disease influences the features of inflammatory memory in eczema skin. Finally, I will investigate how these features change over time after dupilumab treatment is started, and determine whether earlier treatment is more effective at reducing or reversing the inflammatory memory in eczema skin.   What does this research hope to achieve? This research aims to advance our understanding of inflammatory memory in eczema, and the effect of early treatment. This will shed light on the changes in the cells and molecules in the skin that make up inflammatory memory, and hopefully reveal why earlier treatment is more effective at correcting these abnormalities. This research will reveal valuable insights into disease processes that will be relevant to other inflammatory conditions beyond eczema, and may help us identify new treatments that target the inflammatory memory so that patients can remain disease-free and drug-free long-term. We may also gain supporting evidence to influence health policy decisions, to enable access to earlier treatment as a priority for eczema and other inflammatory conditions.

UKRI Gateway to Research · FY 2025 · 2025-10

Context and challenge. Molecular interactions between proteins and RNA sustain life. RNA-binding proteins (RBPs) are enriched for intrinsically disordered regions (IDRs) which, unlike folded domains, exist in a dynamic ensemble of interconverting conformations. Despite the lack of stable structure, these IDRs are now recognised as key mediators of various types of protein-RNA activities, thereby dictating the cellular functions of RBPs. Yet, because of several challenges specific to flexible and disordered regions, the functional characterisation of IDRs has lagged. Hence, the big question of how the majority of RBPs selectively bind and regulate their RNA targets in the post-translation regulation of gene expression remains unanswered. Research aims and objectives. Elucidating the RNA-binding function of IDRs represents a major frontier in biology and our research proposal aims to tackle this challenge in a systematic manner. Our bottom-up investigations have enabled us to reveal new and diverse features by which IDRs contribute to the RNA-binding function of RBPs, that we propose to investigate towards a better understanding of IDR signatures and complexities. We aim to challenge tenets and some of the prevailing notions of IDRs by providing insights into the immense variety of interaction modes displayed by IDRs sequences and motifs, as well as the context-dependency of their structural disorder and functional behaviour. Through the investigation of evolutionarily linked model proteins, we propose to study these unorthodox interactions and expect to reveal new paradigms for protein-RNA biology. We will be integrating, adapting and/or developing methodologies and protocols to tackle our objectives and respond to the challenges posed by these systems. Potential applications and benefits. This research will contribute to a deeper understanding of the intrinsically disordered ‘dark’ portion of the human proteome and of fundamental molecular recognition processes that are critical for life. As RBPs interact with RNAs to carry out a myriad of essential functions of all cells and organisms, no area of biology is untouched by an understanding of the roles and modes of action of RBPs. Predicting RNA-binding preferences for RBPs based on computational analysis is not yet possible, and this is a considerably greater challenge for disordered and cryptic RNA-binding motifs. Our proposed study will therefore be highly relevant, timely and important for the wide and vibrant community of RNA biology scientists and beyond. Relevance to the BBSRC long-term research and innovation priorities. These aims align with the BBSRC long-term research and innovation priority of ‘Frontier bioscience: understanding the rules of life’.  

UKRI Gateway to Research · FY 2025 · 2025-09

Doctoral Training Partnerships: a range of postgraduate training is funded by the Research Councils. For information on current funding routes, see the common terminology at https://www.ukri.org/apply-for-funding/how-we-fund-studentships/. Training grants may be to one organisation or to a consortia of research organisations. This portal will show the lead organisation only.

UKRI Gateway to Research · FY 2025 · 2025-09

Internationalism is typically studied as an elite and institutional project; its history written from the viewpoint of either states or large multilateral organisations. What happens, however, when we re-orient our perspective and study internationalism from the vantage point of those at the interstate system’s margins? My interdisciplinary PhD thesis does precisely that by examining the international politics of the Naga Indigenous community in Northeast India. Nagas have campaigned for self-determination since 1947 when Naga leaders declared Naga independence from India. India has consistently forestalled these efforts by refusing to recognise Naga nationhood and asserting that the ‘Naga issue’ is a domestic Indian concern. In response, Naga actors have repeatedly made claims on and to ‘the international’ to legitimate demands for collective rights. My PhD investigated how Naga actors have conceived of alternative, internationally legible geopolitical projects for the protection of the Naga community from 1946 to 2022. I wrote a history of Naga intellectual thought during this period, exploring how Naga nationalist demands have been re-articulated at different points in response to shifting domestic and international conditions. I conducted archival research in Europe and India, analysis of Naga social media, and interviews with Naga human rights activists. I charted a shift in the nature of the Nagas' geopolitical claim, from mid-twentieth-century calls for Naga statehood, towards recent calls for Naga Indigenous self-determination outside the nation-state. The core of my argument is that internationalism has been integral to the construction of Naga national identities. I call for scholars to pay greater attention to the internationalist practices of Indigenous, minority, and stateless communities who are typically absent from histories of internationalism. My work shows how communities at the margins of the international order can tell us much about the so-called norms of inter-state politics, while offering important insights into the future of geopolitics. My work is extremely timely. In 2015, Naga leaders signed an historic accord with India establishing a framework for peace; amid conflicting proposals for the future Indo-Naga relationship, substantive negotiations have since stalled. Uncovering the historical lineage of Naga geopolitical ideas is vital to understanding these ongoing negotiations and, more broadly, for conceptualising the Nagas’ competing possible futures. The fellowship will maximise the impact of my PhD research for (1) Naga communities; (2) international human rights policy professionals; and (3) interdisciplinary social science scholars. I will: Conduct a research communication trip to Nagaland. Here, I will host a dissemination workshop with Naga human rights activists and present my findings to Naga publics via a lecture. Collaborate with the Unrepresented Nations and Peoples Organisation (UNPO) to write a policy brief on Naga self-determination to be submitted to the UN. The briefing will draw from my PhD findings and the workshop described above.  Submit two journal articles to leading geography and IR journals, and a proposal to LSE-press for an academic book based upon my thesis. These publications will establish my reputation as an expert on Indigenous, stateless, and minority communities’ international politics. I will also speak at two conferences. I will also engage in career development. I will: Write funding applications to the British Academy and Leverhulme Trust for future research comparing Naga international politics with those of other Southeast Asian Indigenous communities. I will also build interdisciplinary collaborations with other scholars studying Highland Asia at The Highland Institute (Kohima).

UKRI Gateway to Research · FY 2025 · 2025-09

Polyomaviruses infect a variety of animals and in humans they cause various illnesses in immunocompromised individuals. For example, Trichodysplasia spinulosa polyomavirus causes a skin condition, BK polyomavirus causes kidney disease and is a leading cause of kidney transplant failure and JC polyomavirus is associated with a fatal neurodegenerative disease. Furthermore, Merkel cell polyomavirus causes the aggressive and quickly spreading skin cancer, Merkel cell carcinoma. A viral initiator of cancer is of immense scientific interest and in this respect a tumorigenic mouse polyomavirus (MPyV) has become an important research model into cancer-causing biochemical pathways. Animal cells have an internal ‘cytoskeleton’ composed of filaments that can grow and shrink and are further organised into various macro-architectures, in order to mediate vital cellular processes such as changing shape, migration and cell division. Furthermore, cell components are moved along these filaments for delivery to cellular subregions. In the late stages of MPyV infection, the viral protein VP1 has been observed to coat a vital cytoskeletal filament type known as microtubules, preventing their growth and shrinkage. This coating causes issues with cell functions, cell division and causes increased cell death. This manipulation of the host cellular cytoskeleton by the virus may be a key strategy in its replicative cycle and/or be involved in causing illness including cancer. However, it is unknown how MPyV VP1 attaches to microtubules and why this prevents their growth and shrinkage. Furthermore, it is unknown whether evolutionarily equivalent VP1 proteins from human polyomaviruses associate with microtubules and regulate their dynamics in the same way. This project’s core goals are to decipher how polyomavirus VP1 proteins attach to microtubules to regulate their growth and shrinkage and how generalisable this is to human polyomaviruses linked to diseases including cancer. We aim to detail at the 3D nanoscale how MPyV VP1 associates with microtubules, both as purified components and in the cellular environment during infection, including, in order to understand VP1’s inhibition of dynamics, at the ends of microtubules where shrinkage and growth occurs. We will also determine if VP1 accessory proteins (VP2 and VP3) are involved in the interaction with microtubules. Finally, we will further investigate the crucial question of whether VP1 proteins of human disease-causing polyomaviruses have the same evolutionarily conserved properties. Towards these aims, we will chiefly use the recent Nobel prize-winning technique of cryo-electron microscopy (cryo-EM), alongside supporting cutting-edge biochemical and imaging methodologies. Cryo-EM allows the artefact-free visualisation of proteins (including viral and cytoskeletal proteins) at up to atomic level detail, when purified or even within their cellular context. Recently, rapid improvements in cryo-EM hardware and software, including artificial intelligence (AI)-based image processing approaches, have produced an incredibly effective and versatile technique suited to the objectives of this work. Uncovering how polyomaviruses manipulate their host cells’ cytoskeletons will better our grasp of the mechanisms behind polyomavirus-related medical conditions. Furthermore, given the tumour-causing nature of polyomavirus species, it will also bolster our understanding of biochemical pathways leading to cancer. Structural studies of protein interactions such as this give us vital information towards drug and vaccine design, conferring this project significant therapeutic potential.

UKRI Gateway to Research · FY 2025 · 2025-09

Random Matrix Theory (RMT) serves already for some time as a paradigmatic framework for successfully describing so-called "universal" properties of physical systems, both quantum and classical, identifying those features which are largely independent of particular detail of underlying structures. The universal characteristics then serve as fingerprints for particular classes of systems of very different microscopic nature. For long time the main effort in RMT was concentrated on studies of Hermitian matrices, one of the reasons being that the Hermiticity condition in Quantum Mechanics is necessary to ensure conservation of the number of particles. Similarly, in Classical Mechanics, and eventually in Statistical Mechanics based on it, a somewhat analogous property is known as "reciprocity of interactions" (at the lowest level encapsulated, in particular, in obeying Newton’s third law "action equals reaction"). In the last decade it however became clear that systems with non-Hermitian (respectively, non-reciprocal) interactions do appear in Nature, and show many properties which are not seen in their Hermitian counterparts.    In classical systems of many interacting degrees of freedom nonreciprocal interactions are operative under far-from-equilibrium conditions, in particular they play a crucial role in numerous biological (or "active matter") processes, including neural networks dynamics. In quantum systems, non-Hermiticity appears as a result of taking into account various gain and loss mechanisms due to ever-present environment, and is especially important in systems with many-body quantum chaos. All these developments increased interest in analysis of properties of non-Hermitian random matrices of various types. Among other characteristics,  properties of eigenvectors of such matrices are very different from their Hermitian counterparts and remain poorly studied, despite some progress achieved in recent years.  Bringing our understanding of eigenvectors  of non-Hermitian random matrices at higher level poses a serious challenge, as addressing their properties is highly nontrivial and requires new insights and techniques. The present project aims to study in a systematic way those and other related objects for several classes of non-Hermitian random matrices,  in particular arising in applications in physics, and beyond. This knowledge is important, among other things,  for understanding mechanisms controlling stability of non-Hermitian and  non-reciprocal systems, as well as for more detailed description of scattering of waves in disordered media.  Any progress in such studies is expected to provide solid mathematical basis for reliably identifying some universal characteristics of behaviour of systems with violated Hermiticity or/and presence of non-reciprocal interactions.

UKRI Gateway to Research · FY 2025 · 2025-09

Over the past decades, many collections of moving images have been digitised, catalogued and preserved in various formats, at different scales, and in different archives around the world. The BFI National Archive is one of the most important collections of film and television in the world. It holds a living and expanding record of the evolution of the moving image over the past 90 years, including digital-born content across major television channels in the UK. Since the 1980s, the BFI archive has been capturing and preserving off-air television from UK public service broadcasters, including all advertisements broadcast across all main commercial PSB channels since 2016. Advertisements are the “literature of economics”, in aggregate these TV adverts are likely to be the largest collection of its kind worldwide and one of the most significant records of consumer culture in the UK over the past decade. However, this collection is fragmented and scattered across thousands of hours of digital video, and despite its cultural significance it remains entirely undocumented and therefore inaccessible. This project aims to: Define this wealth of material into a usable collection. Develop a systematic understanding of the collection as a record of consumer culture in the UK. Create the kind of documentation that opens this resource as a public record for research across disciplines and to wider audiences.  The challenge to bring such collection to light is technical as much as a conceptual ? it requires the student to critically re-imagine and reshape advertisement records as computational objects. To tackle this challenge, this project adopts an interdisciplinary approach that combines interpretive frameworks in film, television and media scholarship with advanced methods in computational humanities to design a “computational lens” with which to machine-see the archive, not only to identify, extract, and catalogue the adverts, but to understand them in context, as an evolving record of social norms, values and relations, as they are expressed in UK screen culture. Opening this collection through such lens will make it possible for media studies to collaborate with other disciplines to explore the formation and impact of consumer culture in recent major socio-political events, potentially enabling new research about the wider social transformations that led to events like Brexit, the Black Lives Matter movement, the global COVID pandemic and evolving social attitudes towards climate change, for example. The student will have the opportunity to bring their own focus to identify suitable angles to explore this collection through appropriate sampling. At the same time, the new methods and tools developed for this project will impact the wider heritage sector, insofar as its institutions and preservation practices increasingly rely on large collections of highly fragmented peripheral visual records. Drawing out patterns that are useful to humanities inquiry from large collections of images will have wide applicability for cultural heritage beyond the specificity of consumer culture.

UKRI Gateway to Research · FY 2025 · 2025-09

Efficient control of light and interaction of light with materials is essential for advances in imaging, sensing, communications, and quantum technologies. However, a major challenge is the scale mismatch between nanoscale quantum emitters and micrometer-scale spatial confinement of light, which limits the interaction efficiency. This scale mismatch is one of the fundamental roadblocks in the development of future communications and quantum devices. In this program, an international team comprising Duke University, the University of Massachusetts Lowell, and King’s College London aims to utilize nano-structured composite media to design a fundamentally new generation of devices capable of manipulating complex light beams simultaneously at small spatial (nanometer) and fast temporal (sub-nanosecond) scales. The new class of developed devices will be applied to manipulate important quantum transitions in molecules, which are difficult to access otherwise (dipole-forbidden transitions). The program aims to advance computational modeling, machine learning, advanced nanofabrication and engineering, and novel characterization methods, while preparing a new workforce that is ready to address complex interdisciplinary challenges in photonics and quantum engineering.

UKRI Gateway to Research · FY 2025 · 2025-09

Vascular calcification (VC) is a serious and widespread clinical problem manifesting in atherosclerosis, chronic kidney disease (CKD), diabetes and ageing. It is an independent risk factor for cardiovascular mortality in all disease contexts. Currently, there are no treatments to prevent or regress VC. Therefore, there is a serious unmet clinical need to understand the molecular mechanisms driving the calcification process, and to identify novel treatment strategies. VC is a cell-mediated process, driven by vascular smooth muscle cells (VSMCs). Signalling pathways activated in response to stressors cause VSMCs to undergo phenotypic change and conversion to osteogenic-like cells capable of orchestrating the calcification process. The development of VC is also highly dependent on the extracellular matrix (ECM) environment surrounding the VSMCs. The ECM undergoes changes in ageing and disease that significantly modify the niche occupied by the cells and these modifications promote osteogenic change and mineralisation. Current mechanistic and preclinical research into VC relies predominantly on 2D in vitro models of rodent VSMCs grown in the absence of ECM. Calcification can only be induced by addition of supraphysiological levels of minerals such as calcium and/or phosphate leading to rapid mineralisation that does not mimic the in vivo situation where mineralisation is a slow process occurring in the context of a modified ECM.  Similarly, rodent models used in mechanistic studies and preclinical drug testing, rely on toxic mineral overload or diets often coupled with complex surgeries such as nephrectomy to induce calcification. This is because rodents are resistant to the induction of calcification and even when induced, the process does not follow the same course as in man, as it is rapid and cartilaginous rather than osteogenic and the ECM environment is healthy. Our aim is to replace animal use with human models of VC. To this end we have developed two novel human 3D in vitro models of VC; a spheroid model and a modified ECM model.  Here, VSMC osteogenic differentiation and mineralisation occurs without the need for additional stimuli and in the context of the native ECM.  We propose to characterise and refine these models to determine mechanisms of calcification and to optimise them for use in high throughput screening (HTS) to identify drugs that inhibit calcification processes. Importantly, these two models address different aspects of calcification and only require commercially available human VSMC cultures. Thus they will be widely accessible to the research community and easily established in any laboratory.  

UKRI Gateway to Research · FY 2025 · 2025-09

Focusing on the V&A East Storehouse, this CDP will explore innovative ways of managing stored collections, investigating the impact of a ‘dynamic’ and ‘flipped’ approach for collections management practices, and organisational identity.  In the context of calls to widen participation, museums are radically rethinking how they care for stored collections to demonstrate social value, relevance of resources, and to develop more transparent relationship with their publics. Yet little is known about what this “growing edge” (Bolton, 2010) of museum work means for these organisations, their audiences, and the collections themselves. Through a qualitative investigation, using mixed archival and desk-based and people-focused methods, the CDP will shed new light on this under-explored subject.

UKRI Gateway to Research · FY 2025 · 2025-09

Context: From the moment of conception to the time of our first breath, the human body undergoes numerous transformative processes. One of these pivotal shifts is the transition from fetal to adult haemoglobin in our bloodstream. This seemingly straightforward process, known as the 'globin switch,' is instrumental in developing strategies to combat one of the world's most challenging and prevalent blood disorders: sickle cell disease (SCD). The challenge the project addresses: SCD, a disorder with a global footprint, arises when blood cells deform into a distinct 'sickle' shape because of a haemoglobin abnormality due to a single amino acid change in the ß-globin change. These misshapen cells often cluster together, causing blockages in small blood vessels, with subsequent hypoxia resulting in chronic pain syndromes, tissue necrosis, severe bacterial infections and other complications. The persistence of fetal haemoglobin after birth is known to counteract the negative effects of sickle haemoglobin. Thus, the prospect of rekindling the production of this type of haemoglobin in adulthood could revolutionise treatment. Aims and Objectives: Central to the objective of reactivating fetal haemoglobin are two molecular protagonists: BCL11A and COUP-TFII. While the former acts as a suppressor of fetal haemoglobin, the latter appears to promote its production. With these molecules as our guideposts, we have charted the following objectives: Deep Dive into Development: We aim to meticulously study the patterns and influences of BCL11A and COUP-TFII during a critical developmental phase of erythropoiesis within the fetal liver. This phase in haematopoiesis provides a perfect window to understand the nuances of fetal haemoglobin production and switching. Isolation and Growth: employing state-of-the-art techniques, our goal is to single out cells influenced by COUP-TFII and cultivate them. This will allow us to characterise them in greater detail. Molecular Exploration: By understanding the intricacies of these cells, we hope to uncover previously unknown details about the regulation of fetal haemoglobin production. Manipulative Studies: By altering the levels of BCL11A and COUP-TFII, we aim to define their impact and potential interplay on fetal haemoglobin production and switching. This would provide insights into potential therapeutic strategies. Potential Applications and Benefits: Approximately 5% of the world’s population are thought to carry genetic traits for haemoglobinopathies, namely sickle cell disease or thalassemia, equating to 300,000 babies with severe forms being born per year. At present, therapeutic measures, such as blood transfusion, hydroxyurea treatment and haematopoietic stem cell transplantation, may improve quality of life for patients with SCD. However, strategies aimed at maintaining, or increasing, the production of fetal haemoglobin well into adulthood by manipulating the interplay of BCL11A and COUP-TFII as regulators of the haemoglobin switch, may offer novel therapeutic opportunities. This approach has far-reaching implications, whereby understanding the mechanisms behind the globin switch could allow a shift to proactive intervention, preventing the onset of SCD entirely and providing insight into other genetic disorders. Furthermore, it could guide future research into genetic interventions, offering a blueprint for addressing other genetic disorders.

UKRI Gateway to Research · FY 2025 · 2025-09

The theoretical understanding of human motor control and learning has a strong impact on the diagnosis and treatment of motor disorders, and vice versa. Recent progress has been made in the understanding of motor control and learning, particularly with respect to understanding the functional role of neuro-behavioural variability that is inherent to sensorimotor control. However, this progress has not yet been transferred appropriately into clinical therapy approaches. The goal of TReND is thus, to create a translational research network in motor disorder rehabilitation. The network will be highly interdisciplinary with doctoral and senior researchers from fundamental research areas (movement science, neuroscience, computer science), clinical practitioners (physical and occupational therapy, rehabilitation science, etc.) and partners from related industries. The overall aim is, to systematically translate recent theoretical and methodological advances in motor control and learning research into clinical practice to enhance clinical diagnosis and motor rehabilitation. More specific, we will investigate the functional role of variability in the sensorimotor coordination dynamics on behavioural and neurophysiological level in motor and mental disorders such as Stroke, Parkinson's or Alzheimer's disease. This will be addressed in three research objectives: 1. To investigate how different disorders affect the sensorimotor systems' capability to exploit functional variability for stable and adaptive motor control; 2. To investigate how novel therapy concepts can enhance the capacity to exploit functional variability and treat motor disorders across different patient populations; and 3. To develop novel approaches to translate the knowledge gain from our fundamental research into clinical practice.

UKRI Gateway to Research · FY 2025 · 2025-09

Context IRIS ( e-Infrastructure for Research and Innovation for STFC) is a community-driven project that coordinates computing infrastructure for STFC-supported research across the UK. It provides shared access to national computing, storage and related digital services, delivered through partners including GridPP, DiRAC and the Scientific Computing Department at STFC.  The IRIS Resource Allocation Panel (RSAP) reviews requests for use of these shared resources and submits recommendations to the IRIS Delivery Board. This ensures that allocations are handled independently and through a transparent and consistent process. Challenge Demand for IRIS computing resources continues to grow as research projects expand in scale and complexity. The RSAP must operate efficiently and consistently so that allocations are fair, clearly documented and that resources are used effectively across the community. Aims and objectives Lead the RSAP to deliver timely and well-justified recommendations to the Delivery Board. Work with the IRIS Secretary and Capacity Manager to ensure accurate reporting of resource usage and timely distribution of review materials. Maintain clear communication with applicants and panel members throughout the process. Ensure records, agendas and meeting outcomes are complete and accessible for future reference. Potential applications and benefits A clear and trusted allocation process allows IRIS resources to be used effectively across UK research. It helps projects plan their computing and storage use, supports efficient use of shared infrastructure and provides a stronger foundation for future investment decisions.  Consistent and transparent operation of the RSAP builds confidence among users, reduces administrative burden and contributes to a coordinated national approach to research computing.

UKRI Gateway to Research · FY 2025 · 2025-09

Cardiovascular disease remains the number one cause of death worldwide, of which coronary artery disease leading to heart attack and ultimately heart failure is the biggest contributor. There is no known cure for heart failure, other than organ transplantation which is compounded by limited donor hearts and a requirement for lifelong toxic drugs to prevent organ rejection. All current drug-based treatments only serve to assist the survived heart muscle and blood vessels after heart attack but do not reverse disease progression. Thus, there is an urgent unmet need for novel therapeutic approaches to regenerate the injured heart and to reverse established heart failure. Here we propose to establish a new MRC/BHF Centre of Research Excellence in Advanced Cardiac Therapies (REACT) to develop advanced therapies for heart attack and heart failure. We will bring together world leading scientists and clinicians from King's College London and the Universities of Oxford and Edinburgh, combined with other academic partners as well as biotech and pharmaceutical industry representatives to develop new medicines and to deliver them to the injured or failing heart. We will define patients for treatment based on current clinical guidelines. We will develop improved diagnostic measures to refine treatment groups across what is known to be a mixed population of heart attack and heart failure patients. The drugs will be made up of nucleic acids, such as modified RNA, as was used in COVID-19 vaccines. Together with delivery vehicles, we will ensure that they specifically target the heart in both models of disease and in patients, thereby maximising the impact of our therapies. Our approach will restore lost heart muscle, increase numbers of functioning blood vessels, reduce inflammation, and reduce tissue scarring to maintain or enhance heart function. By leveraging additional support, we will progress therapies to patient clinical trials within the lifetime of the Centre. We will develop delivery methods that are non-invasive, combined with cost-effective treatments to ensure that our therapies can be utilised in all primary health care systems, including those within developing countries. The Centre will widely disseminate its progress and key findings to the public and patients alike and is firmly committed to training, career development and the promotion of early career researchers. We will establish a fully inclusive and diverse research culture, all working towards the common goal of developing novel advanced therapies to treat heart attack and heart failure patients.

UKRI Gateway to Research · FY 2025 · 2025-09

Attention-deficit/hyperactivity disorder (ADHD) is characterised by difficulties with attention, impulsivity and motivation, stemming in part from unstable cognitive control. Cognitive control ensures the goal-directedness of behaviour, therefore its reliable operation is fundamental to everyday functioning. In the lab, control instability can be captured by increased variability in task performance (reaction time variability, RTV). Basic scientific studies, several from our lab, have shown that variability in the timing (phase) of frontal theta (4-8 Hz) oscillations in the brain correlates with RTV. Furthermore, foundational clinical work spearheaded by our group has found strong links between ADHD, and variability in both theta phases and behaviour (RTV). Advances in neurotechnology provide a powerful way to modulate brain oscillations, via rhythmic transcranial magnetic stimulation (rhTMS). We propose to integrate these interdisciplinary lines of research to investigate whether rhTMS can be used to normalise RTV in ADHD through regularising frontal theta (FT) phases, thus highlighting a novel non-pharmacological intervention target: FT phase variability (FT-PV). Non-pharmacological interventions in ADHD are hugely important: while psychostimulants can alleviate symptoms, they are ineffective for certain patients. Patients prefer non-pharmacological interventions, including neurostimulation, which represents a cost-efficient, personalisable, safe method, as of yet underresearched in ADHD. Our research has three specific objectives: Objective 1 (O1): Establish a causal relationship between RTV and the regulation of the timing of FT oscillations, as captured by inter-trial phase coherence (ITC, inverse of FT-PV) during a cognitive control task involving response conflict. To achieve this, we will administer theta rhTMS with simultaneous EEG to 60 neurotypical young adults. Hypotheses: FT rhTMS will significantly increase regulation of FT signalling (FT ITC) during the task compared to sham and beta rhTMS FT rhTMS will decrease RTV (standard deviation of RTs/SD-RT) during the task compared to sham and beta rhTMS. FT ITC will mediate the effect induced by theta rhTMS on SD-RT   Objective 2 (O2): Investigate the effects of rhTMS neuromodulation of FT ITC on behavioural and EEG measures (ERN, N2, Pe amplitude) in 40 individuals with ADHD and the same 60 neurotypical controls. Hypotheses: On the response conflict task at baseline (pre-rhTMS/EEG-only), compared to controls, individuals with ADHD will show lower theta ITC, ERN and Pe amplitudes, higher RTV, and a smaller conflict effect on N2 amplitude. RTV will improve following theta rhTMS compared to sham and beta stimulation in both groups with larger effects in the ADHD group. FT rhTMS will modulate theta ITC and ERPs in both groups, potentially bringing them to pre-TMS neurotypical levels in ADHD.   Objective 3 (O3): Investigate the longer lasting (~1 week) effects of neuromodulation on behavioural and EEG measures in young adults with ADHD and controls. Hypotheses: Observed changes in EEG measures will persist/show further improvement (increased ITC, increased amplitude of ERP components) one week after rhTMS stimulation with a significant difference to baseline (pre-rhTMS). Observed changes in behavioural performance will persist/show further improvement one week after rhTMS stimulation with a significant difference to baseline (pre-rhTMS EEG-only recording).   The application of rhTMS to influence FT oscillations could potentially correct the irregular cross-trial phase synchrony in ADHD and improve multiple measures associated with the condition. If this approach proves effective, rhTMS could be trialled as a way of improving cognitive control alterations in the condition, with highly reliable (.85) measures of FT-PV as candidate intervention targets.

UKRI Gateway to Research · FY 2025 · 2025-09

Our strategy addresses three of the STFC challenges: C1 (fundamental particles), C2 (fundamental laws and symmetries) and C8 (asymmetry between matter and antimatter). Our central involvement, and the one with which we founded our group at King’s in 2019, is in neutrino physics. The experiments we are involved in revolve around two high-level topics: understanding the matter-antimatter asymmetry measuring CP violation (T2K, Super-K, Hyper-K) and lepton flavour violation (SNO+, LEGEND), both are required by Sakharov’s conditions, and also astrophysics (IceCube, and also the above experiments can do astrophysics). It is a mix of currently running and future experiments, which can achieve higher potential. The direct detection of dark matter (DM) is a new research area for the group, established in 2022. The strategy is to pursue world-leading physics results using data from the now-running LUX-ZEPLIN (LZ) experiment, and taking a leading role in the construction of the proposed next-generation XLZD LXe-observatory at Boulby or elsewhere. King’s is actively engaged in technology R&D for current and future experiments, with a new initiative focusing on DRD-UK in liquid detectors Quantum Technologies for Fundamental Physics is an emerging area of importance for King’s, and activities are focused on the Atom Interferometric Observatory and Network (AION) project. AION is a proposed research infrastructure that will allow studies of DM and gravitational waves (GWs) from cosmological and astrophysical sources in the highly relevant but currently inaccessible mid-frequency band.

UKRI Gateway to Research · FY 2025 · 2025-09

Curiosity is a fundamental driver of learning, shaping how individuals seek information, sustain attention, and develop knowledge (Gottlieb & Oudeyer, 2018; Kidd & Hayden, 2015; Von Stumm et al., 2011). However, research suggests that curiosity manifests differently in individuals with attention-deficit/hyperactivity disorder (ADHD), presenting both opportunities and challenges in academic settings (Marvin et al., 2020; Whitecross & Smithson, 2023). While curiosity can enhance intrinsic motivation, engagement, and deep learning, it can also lead to distraction, impulsivity, and difficulty prioritizing tasks, particularly in structured learning environments that emphasize linear progression and rigid deadlines (Litman & Spielberger, 2003; Ashinoff & Abu-Akel, 2021; Stein et al., 2007). Despite growing recognition of curiosity’s role in learning (Gruber et al., 2014; Kang et al., 2009), little research has explored how students with ADHD perceive curiosity in their own learning experiences. Do they see it as an asset or a challenge? How do they manage curiosity to support their academic goals? What strategies could improve their learning outcomes? This fellowship will investigate the self-perceptions of curiosity in higher education students with ADHD, focusing on both the obstacles it presents and the strengths it offers. Building on my previous theoretical research exploring the evolutionary basis for the potentially high level of curiosity observed in ADHD (Le Cunff, 2024) and a quantitative survey (completion expected by September 2025), I will conduct qualitative interviews with university students with ADHD to explore their experiences with curiosity in academic contexts. This project will centre on student voices and lived experiences to explore curiosity as a potential strength in ADHD. The impact of this fellowship extends beyond research—it is about shaping real-world practices to support neurodivergent learners. Findings will be translated into practical applications, ensuring that students, educators, and policymakers can benefit from this knowledge. Key outcomes include: Peer-reviewed publications to advance knowledge in neuroeducation and ADHD research. Conference presentations to engage with experts in psychology, neuroscience, and education. Educational materials and training for universities to help educators design learning environments that accommodate curiosity-driven learning in ADHD students. Engagement with ADHD advocacy groups, student networks, and public audiences, through blog posts, podcasts, and social media outreach, ensuring that research findings are widely accessible. Policy recommendations for inclusive higher education, offering guidance on how institutions can better support curiosity-driven learning for neurodivergent students. By investigating how students with ADHD perceive their own curiosity and how it affects their academic experiences, this project will inform more inclusive teaching practices, challenge outdated models of ADHD in education, and promote strength-based approaches to neurodivergent learning. Through this fellowship, I will build the foundation for a long-term research career in neuroeducation and ADHD, while ensuring that my findings contribute to both academic knowledge and practical change in higher education.

UKRI Gateway to Research · FY 2025 · 2025-09

i) Background Manganese (Mn) is an essential trace metal in our diet that is required for normal brain function. However, exposure to high Mn concentrations causes brain damage and a debilitating movement disorder similar to Parkinson's disease. Mn toxicity, also known as manganism, occurs in children and adults upon environmental and occupational overexposure due to contaminated drinking water and drug formulations, industrial fumes or intravenous nutrition, and in patients with liver damage. The recent identification of inherited disorders of Mn transport due to abnormalities in the genes SLC30A10, SLC39A14 and SLC39A8 has further highlighted the important influence Mn has on brain physiology. These disorders lead to impaired control of the body's Mn load, resulting in Mn overload or deficiency, and are associated with detrimental neurodevelopmental disorders of childhood. There is increasing evidence that Mn imbalance is also a feature of common neurodegenerative disorders including Parkinson, Alzheimer and Huntington disease. Our understanding of how Mn imbalance leads to disease is poor and treatments to alleviate neurological symptoms for the above conditions remain unsatisfactory. Currently available therapies to lower Mn levels are extremely burdensome due to frequent intravenous administration requiring life-long, monthly hospital admissions, venous access related complications and medication side effects. Therefore, there is a great need for research in this field. ii) Aims of my research This fellowship intends to establish the role of Mn in normal brain function and to understand how Mn imbalance disturbs the physiological processes within nerve cells. Thereby, my work aims to identify novel therapeutic targets and improve treatments for Mn related disease. This will be accomplished through the study of established and validated genetically modified zebrafish as models for the human Mn transporter disorders. Zebrafish are ideally suited for the study of neurological processes as their nervous system is structurally and chemically similar to that of humans whilst also transparent allowing brain imaging while alive. First, I will determine which nerve cells are affected by Mn overload and deficiency through analysis of brain activity, anatomy and neuronal function. To better understand the effects of Mn imbalance I will generate cell culture models of the specific neuronal cells targeted by Mn. This will allow me to study the effect of Mn on energy metabolism, free radicals and cellular stress with a view to identifying the key events caused by Mn imbalance. My previous work has identified a novel Mn binding drug that effectively lowers Mn levels and normalises swimming activity in a zebrafish model of Mn toxicity. This and other compounds will be tested biochemically and in a mouse model of Mn overload in order to develop a suitable paediatric formulation for further preclinical studies beyond this fellowship. The project will be carried out by myself, a scientist with extensive expertise in Mn and zebrafish research, as well as a postdoctoral researcher with significant experience in mouse laboratory skills. A unique set of collaborators will share world-class expertise on zebrafish and mouse neuroscience, cell biology, paediatric drug development and chemistry ensuring translational relevance. iii) Expected benefit This fellowship will provide a better understanding of how Mn imbalance is involved in the disease processes underlying inherited and acquired disorders associated with Mn associated brain damage. This will allow the development of effective treatments to halt disease progression and reduce disability and mortality in children and adults suffering from these disorders. Identification of the role of Mn in neurodegenerative disease processes may also shed new light on the disease mechanisms underlying common neurodegenerative disorders such as Parkinson's disease.