2015 grant awards
In 2015 the Foundation awarded the following grants.
Open-call grant awards
Principal Investigator: Dr Thomas Gobbetti, Centre for Biochemical Pharmacology, WHRI
Study title: Novel n-3 DPA-derived bioactive mediators control intestinal inflammation
- Award: £20,100
Crohn’s Disease and Ulcerative Colitis are life-long conditions with recurring episodes of intestinal inflammation that severely affect those suffering these chronic diseases. With few treatments and no cures available, there is an urgent need to discover new ways to curb intestinal inflammation.
Our studies focus on understanding the natural ways inflammation subsides and resolves to restore healthy tissue function, as well as how inflammatory processes are regulated to avoid overshooting and inflicting tissue injury. Our aim is to develop a new approach to managing inflammation by promoting natural protective mechanisms. This project will investigate the role of omega-3 fatty acids and their bioactive derivatives as novel protective factors. We hypothesise that molecules derived from omega-3 fatty acids can form the basis for innovative therapeutic strategies for intestinal inflammation. Insights from this research may have applications in other diseases where inflammation is an important symptom, and may ultimately lead to novel anti-inflammatory medicines.
Principal Investigator: Dr Sian Henson, Centre for Microvascular Research, WHRI
Study title: Removing inflammation from senescent human T cells by targeting TAB1-beta, a novel driver of senescence
- Award: £24,740
Senescent (old) cells accumulate in ageing tissues. However, their presence is not benign as they secrete molecules that trigger inflammation. Because chronic inflammation underlies many age-related diseases, including cardiovascular and autoimmune diseases, identification of novel ways to reduce cellular senescence is a fundamental goal for research leading to anti-ageing therapies.
Cells of the immune system, T lymphocytes (a type of white blood cell) are particularly affected by ageing. My research on T lymphocytes has linked exaggerated inflammatory responses to the appearance of a unique protein in senescent cells. Hence, the aim of this project is to test whether inactivation of this ‘only-in-senescence’ protein could be a suitable target for new medicines aimed at turning off excessive inflammation in senescent human T lymphocytes.
Principal Investigator: Dr Giovanna Nalesso, Centre for Experimental Medicine and Rheumatology, WHRI
Study title: Modulation of the calcium calmodulin kinase II (CaMKII) pathway as a new therapeutic strategy for the treatment of osteoarthritis
- Award: £24,769
Osteoarthritis (OA) is a disease mainly characterised by cartilage breakdown in joints, leading to impaired mobility and chronic pain. The lack of medicines to reverse these changes makes OA a heavy social and economic burden for our society since it affects 50% of people over the age of 65.
We discovered in experimental studies of OA that inhibition of an enzyme called calcium calmodulin kinase II (CaMKII) led to a greater loss of cartilage. This suggests that activating CaMKII may halt cartilage destruction in OA. To confirm the role of CaMKII in regulating cartilage this project will genetically block or artificially activate CaMKII. We aim to generate two genetically modified mice that allow suppression or artificial activation of CaMKII specifically in cartilage. This will verify the role of CaMKII in cartilage loss and may enable the identification of new medicines to treat OA.
Principal Investigator: Dr Muriel Nobles, William Harvey Heart Centre, WHRI
Study title: Changes in the electrophysiology of human atrial myocyte in atrial fibrillation, study of the right and left atria
- Award: £9,848 (for equipment)
Atrial fibrillation (AF) is the most common cardiac arrhythmia - an irregular heart beat that starts in the top chambers of the heart (atria). AF affects at least 10% of people over the age of 80. As well as causing debilitating symptoms, AF is a major cause of stroke and heart failure. Current treatments are often ineffective.
This project funding will support the purchase of equipment that will enable the investigation of single heart cells isolated from human atrial tissue. To investigate cellular mechanisms that can lead to AF, measurements of electrical signals (like a single cell ECG) will be compared with changes in calcium concentrations in theses cells measured by imaging techniques. These studies will help elucidate the cellular events that trigger AF in human atria. This understanding can help define targets for developing new medicines to treat AF.
Principal Investigator: Dr James Whiteford, Centre for Microvascular Research, WHRI
Study title: Novel syndecan-4 derived anti-angiogenic therapeutics for the treatment of West Age Related Macular Degeneration
- Award: £26,261
Wet age-related macular degeneration (AMD) is caused by the growth of abnormal blood vessels at the back of the eye, which leads to retinal detachment and loss of central vision. It is the leading cause of blindness amongst ageing individuals. Current therapies have limited benefit and are not suitable for everybody. Hence, there is a critical need to identify novel targets for developing better medicines.
We have identified the critical role of a protein called Syndecan-4 in abnormal blood vessel growth. The objective of this study is to test the therapeutic potential of blocking the function of Syndecan-4 in a pre-clinical experimental model of wet AMD using gene-therapy.
This project will confirm the suitability of Syndecan-4 as a therapeutic target for new medicine development. This promises to be an important step in the search for new treatments of wet AMD, which could benefit a large proportion of the ageing population globally.
Principal Investigator: Professor Roger Corder, Centre for Translational Medicine and Therapeutics, WHRI
Study title: Investigations into the actions of dietary polyphenols - new treatments for endothelial dysfunction and the prevention of vascular ageing
- Award £99,000 (funded by the Masonic Samaritan Fund)
Changes in the function of the endothelium (the single layer of cells that lines every blood vessel) underlie many aspects of vascular ageing. These changes increase the risk of heart disease, and also vascular dementia, stroke, and the age-related decline in kidney function. Currently, there is no medical treatment for this condition, which is referred to as endothelial dysfunction. This project will investigate, using human endothelial cells in culture, how dietary polyphenols (the natural molecules found in red wine and chocolate) prevent and reverse endothelial dysfunction, and slow vascular ageing. This will provide fundamental new insights that can help lead to new medicines, and also to diagnostic tests that can detect endothelial dysfunction and guide prevention to those at most risk.
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