Can we reverse aging?

Last month we had the opportunity to speak to Professor Lorna Harries about her work on RNA and gene expression in the regulation of cellular aging. Professor Harries is the CSO and co-founder of Senisca, a University of Exeter spin out company, who are working on a technology with the potential to repair and rejuvenate aging cells.

If we all age, what's the problem?

The NHS spends an estimated 40% of it’s total expenditure to combat illness associated with aging in patients over 65. As over 65s are the fastest growing demographic, these costs will only continue to increase unless alternative solutions are found to our current medical interventions. "If we could cure aging we could save the NHS £4 trillion by 2050" states Professor Harries. This is one of the motivations behind her work at Senisca to develop a new generation of therapeutic interventions to target the diseases caused by aging.

What causes aging?

The pathology of a large number of age related illnesses is linked back to an accumulation of senescent cells within the body. Senescence is triggered when cells are exposed to various extrinsic or intrinsic stressors such as oxidative and genotoxic stress, radiation or structural changes. Rather than allow damaged cells to proliferate, which may lead to potential malignant cell transformations and tumours, cells become senescent, undergoing cellular arrest where they then cease to replicate.

Professor Harries explains "as we age, we lose the ability to regulate the expression of genes. This decision is made by a group of proteins, called splicing factors, which get turned off as we age and that means your cells cannot adapt to their environment, they can't deal with challenge and may increase the probability of cellular senescence”.

Although senescence is designed to protect us, the accumulation of senescent cells can induce inflammation in the surrounding tissues, which can interfere with cell signalling processes and slow the rate of cellular regeneration. Our immune system is responsible for removing these senescent cells but as we age, the rate of senescent accumulation accelerates and so the senescent cells remain, making us more susceptible to age related morbidities such as osteoporosis, cardiovascular disease, osteoarthritis, pulmonary fibrosis, renal disease, neurodegenerative diseases, and metabolic dysfunction.

Senisca’s discovery unlocks new potential for reducing age-related disease…

Until recently, the mechanism of senescence was thought to be an irreversible process which naturally occurs as we age, but Professor Harries' discovered a new cellular mechanism, which can be used to turn the splicing factors in senescent cells back on and even rejuvenate cells. Senisca was spun out in early 2021 to develop oligonucleotide therapies, based on chemically synthesised sequences of RNA strands, to be used in restoring cellular gene expression to a pre-senescent state, returning the level of cell function to that of a new cell.

Professor Harries and her team were "not thinking about commercialisation at all" but soon realised that being able to reverse cellular ageing had exciting potential within a variety of different sectors. This mechanism can be used in anything driven by senescence, making it an attractive option to turn back the ageing clock in old cells and is particularly appealing for reducing the severity of age-related disease. Senisca are currently focusing on applications in skin ageing and pharmaceuticals, with plans to eventually expand into the systemic treatment of diseases.

We are excited to see Senisca’s progress so far and look forward to seeing how their journey unfolds. You can hear the full conversation with Prof. Harries on our podcast.