Establishing Anti-Ageing Medicines

London, London
Wednesday, 26 February 2014

This is a Euroscicon Small Conference,  an outline of the day can be found at

This event will be held at The O2,  a large entertainment district on the Greenwich peninsula in South East London, England.

Establishing Anti-Ageing Medicines
Wednesday, 26 February 2014 09:30 - 17:00

Cineworld: The O2
Peninsula Square
SE10 0DX
United Kingdom

Map and Directions
The last three decades have shown us how plastic the ageing process can be. It is becoming apparent that, with increased knowledge, more and more of the negative consequences of ageing can now be tackled, postponed or avoided. This meeting aims to review the most up to date science about how we can positively modulate ageing and the implementation of such results to human ageing. This event is part of the 2014 Ageing Summit - This event  has CPD accreditation.

Abstracts for poster presentation only can be submitted up to two weeks before the event. You can download the instructions for authors at

Talks include

The effects and mechanisms of action of spermidine on ageing
Dr Nadège Minois, Biomedical Sciences Research Complex, University of St Andrews, Scotland, UK
Spermidine is a natural polyamine with important functions such as DNA stability, cell survival, growth and proliferation. Its level decreases with age and we have shown that supplementing spermidine in food or water increases life span in several model organisms and human cells in culture. It also increases stress resistance and delays age-related oxidative damage and locomotor activity decline. The main mechanisms of action of spermidine are general hypoacetylation and autophagy induction. The talk will review the findings on the role of spermidine on ageing and discuss the potential outcome for human ageing of spermidine supplementation.

Stem cell ageing and chemical intervention
Dr Ilaria Bellantuono, Reader in Stem Cell and Skeletal Ageing, The University of Sheffield, UK
Stem cells are responsible for tissue repair and maintenance and evidence suggest that changes in stem cells with age contribute to the decline in tissue function. The ability to intervene and increase even modestly the number of stem cells, delaying tissue dysfunction may have great impact in areas of degenerative diseases. Indeed limited rejuvenation of stem cells has been shown to rescue tissue function. Small molecules are attractive to amplify the endogenous stem cell pool, preserve it from ageing and direct its differentiation by targeting specific signaling pathways. Here we will present data showing how mesenchymal stem cell ageing can be delayed using chemical interventions.

Use of Kinetic Isotope Effect to Mitigate Age-related Oxidative Stress Diseases
Dr Mikhail Shchepinov, CSO, Retrotope, Inc, USA
Key oxidation prone positions within biomolecules can be reinforced with deuterium to make them more resistant to oxidative stress courtesy of the isotope effect. Use of this approach in mitigation of age-related diseases will be discussed.

Tenocyte metabolism in ageing and estrogen deficiency
Dr. Francesca Veronesi, Biotechnologist researcher, Laboratory of Preclinical and Surgical Studies, Rizzoli Orthopaedic Institute, Bologna, Italy
The study evaluated in vitro proliferation, metabolism and micro-wound healing of tenocytes isolated from the Achilles tendons of ovariectomised (OVX), middle-aged (OLD) and young (YOUNG) rats. OLD and OVX showed a lower proliferation, collagen I, aggrecan, elastin and nitric oxide production than YOUNG and fibronectin and elastin were lower in OVX than YOUNG and OLD. Vascular endothelial growth factor, collagen III and metalloproteinases-13 increased in OVX than in YOUNG and OLD. A lower healing rate was observed in OVX than OLD and YOUNG. Results highlighted how aging and more estrogen deficiency negatively affect tendon metabolism and healing.

Stress signalling pathways as targets for intervention in the premature ageing Werner Syndrome
Professor D Kipling, Cardiff University, School of Medicine, UK
Werner syndrome (WS, or adult progeria) is a rare human genetic disease associated with accelerated ageing.  Cells from WS individuals undergo premature senescence in culture, a phenomenon long suggested to underpin the clinical symptoms.  We have shown that small-molecule inhibition of the p38/MK2 stress signalling pathway can prevent the accelerated senescence of WS cells in culture.  We will discuss how such inhibitors, many of which are in advanced clinical trials for inflammatory disease, may provide a route to therapeutic intervention in WS.  They may also have potentially beneficial anti-ageing effects in normal individuals, via modulation of the senescence-associated secretory phenotype.


Experimental in vitro study on the behaviour of osteoclast in osteoporosis
Dr Francesca Salamanna, Biologist, Laboratory of Biocompatibility, Technological Innovations and Advanced Therapies, Rizzoli Research Innovation Technology, Rizzoli Orthopaedic Instistute,  Bologna, Italy.
The aim of the study was to set up an in vitro method for determining a pathology associated with an increased local and/or systemic bone resorption such as osteoporosis. We found a significant increase in ovariectomized osteoclast (OC) viability, differentiation, bone reabsorbing activity formation, Cathepsin-K and MMP-7 cells culture both with basal medium only (no differentiating factors toward the OC phenothype) and with differentiation medium (with diffrentiating factors toward OC phenothype) demonstrating an increased spontaneous osteoclastogenesis. Thus, the study could offer a methods for diagnosing increased local and/or systemic bone resorption that would prevent and/or limit the complications associated with osteoporosis conditions.

Gut microbes as drug targets to slow ageing
Dr David Weinkove, Lecturer, School of Biological and Biomedical Sciences, Durham University, UK We have coevolved with an amazing diversity of microbes. Evolution theories of ageing predict that gut microbes that aid nutrition might also increase ageing. Our research with the nematode Caenorhabditis elegans suggests that microbes limit lifespan through specific metabolic pathways. Targeting microbes with antibiotics disrupts microbiome diversity and increases susceptibility to harmful infection. However, we show the production of excess folate by the bacteria Escherichia coli can be inhibited without slowing the growth of either the microbe or animal. We propose that drugs that target specific pathways of microbial metabolism without killing cells are viable prospects for anti-ageing medicines.


Keywords:Spermidine, Longevity, Ageing, Model Organisms, Autophagy, Health; Stem cells, small molecules, ageing, DNA damage, microbes, ageing, folate, metabolic targets, isotope effect; ROS; age-related disease; essential polyunsaturated fatty acid; deuterium, Senescence, p38MAPK, Werner Syndrome, telomere, stress, Osteoporosis , Bone Resorption, Osteoclasts, Achilles tendons, Tenocytes,  Aging, Estrogen deficiency, Tendon healing


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