Institute of Healthy Ageing - Dunhill Medical Trust PhD programme (IDP)
About the programme
Upon joining our programme, students will be integrated into the IHA community and will enjoy substantial personal support and access to world-class research and teaching facilities. Students will be encouraged to think creatively and ambitiously to develop cutting edge techniques and to solve the most important questions in the field of ageing and age-associated disease. Opportunities for cross group interaction and collaboration will be strongly encouraged, thereby facilitating cross-species studies and new links between subject areas. In addition, students will form broader academic connections by attending and presenting their work at departmental/institutional research seminars and the annual Graduate Symposium, by contributing to undergraduate teaching, and by participating in social events.
Apply for our programme
To apply, please email your CV and a one page cover letter to email@example.com. Your CV and cover letter should contain details of your academic achievements and relevant research experience, as well as an explanation of why you want to pursue a PhD within our programme and the names of at least two PIs that you would be interested in working with. Applications should be submitted as a single file.
The closing date for applications is 5 pm, Friday, April 29th
Enquiries regarding the programme or the application process should be directed to Dr John Labbadia (firstname.lastname@example.org), Dr Teresa Niccoli (email@example.com) and Dr. Kerri Kinghorn (firstname.lastname@example.org).
Please see below for descriptions of our projects.
About the Dunhill Medical Trust
The Dunhill Medical Trust was founded by a donation from Herbert E Dunhill in 1950. Today, it funds innovative research aimed at improving the quality of life, functional capacity and well-being of older people, and into creating the context for change in the future: preventing, delaying or reducing future health and social care requirements. The Dunhill Medical Trust currently supports a diverse portfolio of research projects across these areas, providing more than £18M of funding to the ageing research community. https://dunhillmedical.org.uk
About the IHA
Although ageing is the primary cause of morbidity in late life, its causes and mechanisms are not understood at a fundamental level. At the Institute of Healthy Ageing (IHA), we use various genetic model organisms to investigate basic mechanisms and universal principles of ageing, and their relationships to diseases of ageing.
The IHA is a cross-faculty entity that integrates research on fundamental ageing mechanisms and ageing-related diseases across UCL and beyond. Since its founding, the IHA has grown into a vibrant and thriving community of researchers that consists of eight core PIs, twelve associate PIs, 16 Postdoctoral Fellows and 18 PhD students, the success of which is reflected in our publication output, substantial research grant income, blossoming young researchers, popular taught courses, public engagement activities and successful alumni.
Our main strengths are: 1) the use of genetic model organisms (yeast, worms, flies, killifish, mice) to dissect universal principles of ageing with the prospect for cross-species studies; 2) a track record of innovation and disruptive thinking; 3) a collaborative, supportive research environment fostered by shared space; and 4) UCL’s wider excellence in biomedical research and diseases of ageing.
How does a reduction in ribosome biogenesis improve health and survival in older fruit flies? (PI: Nazif Alic)
Pol I transcribes a single gene to generate the precursor transcript for all bar one ribosomal RNA (rRNA); its activity is rate-limiting for ribosome biogenesis. Our recently published study showed that the activity of this fundamental eukaryotic enzyme limits health and survival in fruit flies. Together with previous studies showing ribosome biogenesis as an important driver of yeast and worm ageing, our findings affirm the evolutionarily conserved relevance of ribosome biogenesis to animal health and longevity. We now propose to capitalise on the power of Drosophila genetics, genomics and ageing physiology, to gain a detailed understanding of the mechanistic basis whereby ribosome biogenesis impacts ageing
Nutrient sensing and innate immune signalling in mammalian metabolic ageing (PI: Lazaros Foukas)
Exposure of cells to nutrient overload (excessive lipids and carbohydrates), as a result of dietary intake or age-related metabolic decline, causes cellular stress. Cellular metabolic stress underpins the development of age-related pathological conditions such as obesity and associated type-2 diabetes and cancer. The liver and the adipose tissue are key organs that regulate metabolism in coordination with immune cells that reside in these tissues. The lab has developed cellular models of nutrient overload and leukocyte activation. Through transcriptome, proteome and biochemical analyses, we aim to dissect the crosstalk between nutrient sensing and innate immunity pathways and identify targets for potential pharmacologic interventions to combat age-related metabolic deterioration.
Establishing new pathways that protect the ageing proteome (PI: John Labbadia)
Maintenance of the proteome is essential for normal cell and tissue function throughout life. As cells age, the integrity of the proteome deteriorates, as evidenced by the increased presence of misfolded, mislocalised and aggregated proteins in aged tissues. This “protein homeostasis collapse” compromises tissue function and can result in age-associated diseases. Therefore, finding ways to protect the ageing proteome could be a powerful way to suppress age-associated morbidities. Mitochondrial-to-cytosolic protein quality control pathways have emerged as powerful suppressors of protein homeostasis collapse and ageing. Among these, activation of the mitochondria-to-HSF1 stress response (MHSR) robustly safeguards the ageing proteome in C. elegans tissues and cultured human cells. However, the mechanisms by which cells activate the MHSR remain incompletely understood. This proposal aims to determine precisely how the MHSR is regulated and establish new factors that can be manipulated to safeguard the ageing proteome and promote healthy tissue function in humans.
Unravelling the roles of glial dysfunction and lipid droplet formation in the ageing brain (PI: Kerri Kinghorn)
Microglia accumulate lipid droplets and display defective phagocytosis in human and murine ageing brains. We have recently shown dysregulation of glial lipid droplet formation and the glial phagocytic receptor during brain ageing in flies. Glial lipid droplets play a neuroprotective role in response to reactive oxidative species production (ROS) in the brain, by sequestering oxidized lipids generated by neurones. Using the glial transcriptome of ageing flies, differentially expressed genes, including those linked to lipid droplet metabolism, will be genetically modulated in fly glia and neurones to investigate their effects on lifespan and age-related neuronal function. We will also test whether pharmacological or dietary interventions targeting lipid metabolism affect glial lipid droplet formation to promote healthy ageing.
Neuronal cell ageing and neurodegeneration (PI: Teresa Niccoli)
As brains age they become increasingly susceptible to neurodegenerative diseases. An analysis of single cells in an ageing Drosophila brain highlighted 6 genes as the most predictive of Drosophila age. Most of these genes are involved in translation and mitochondrial metabolism. Genes involved in these pathways have also been implicated in a number of neurogenerative disease. This project will modulate these genes to see whether they can affect brain ageing and offer protection to insults connected with common neurodegenerative diseases.