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Europain consortium receives EU and industry funding and begins five year research into better treatments for chronic pain Europain, a public-private consortium funded by the Innovative Medicines Initiative (IMI), announced today the launch of a five-year research project to understand and improve treatment of chronic pain. The project will receive 6M€ from the IMI as well as 12.5M€ in kind contribution from the European Federation of Pharmaceutical Industries and Associations (EFPIA) over the coming five years.

One in five adults suffers from chronic pain. This constitutes a major cause of long-term sick leave and forced early retirement, placing a great financial burden on both individuals and healthcare systems. Despite extensive research programmes by biopharmaceutical companies and academia, there remains a need for treatments that are more effective and with fewer side-effects.

Europain has established an international team of leading researchers and clinicians from both academia and industry to undertake multidisciplinary translational research. This team aims to increase the understanding of chronic pain mechanisms, help to develop novel analgesics, and develop better biomarkers for pain. Their ultimate goal is to improve the lives of people suffering from chronic pain.

During the five-year project, Europain will undertake a large number of preclinical and clinical studies. The program will be delivered through collaboration between laboratories in the Europain network, sharing resources to improve the value derived from the budget. Results will be made public during and after the project, ensuring that the knowledge created can be widely applied to the development of better therapies for patients suffering from chronic pain.

King’s College London, the managing entity of Europain and the academic lead institution will contribute to both the pre-clinical and clinical aspects of the project. One role will be to study the expression of potential pain mediators in both animal models of pain and samples from patients suffering from chronic pain. The role of novel pain mediators will then be investigated using an array of techniques ranging from cell culture to quantitative sensory testing in humans.

Professor Steve McMahon, who along with Dr Dave Bennett will be running the project at King’s, comments: ‘There are some big questions facing the pain field at the moment and this consortium, drawing on the skills and expertise of both academia and industry, is in a unique position to address them’.

The consortium network involves scientists representing 12 renowned European Universities: King’s College London (Academic lead), University College London, Imperial College London, the University of Oxford, the Christian-Albrechts-University of Kiel, the Medical Faculty Mannheim/Heidelberg University, the Technische Universität München, the Goethe University of Frankfurt, the BG University Hospital Bergmannsheil/Ruhr University Bochum, the University Hospitals of Aarhus, Rigshospitalet Copenhagen, University of Southern Denmark, the SME Neuroscience Technologies from Barcelona, and the research resources and expertise of Europe’s most active pharmaceutical companies working in the field of analgesics, including AstraZeneca (co-ordinator), Boehringer-Ingelheim, Eli Lilly, Esteve, Pfizer, Sanofi-Aventis, UCB Pharma.

About the Innovative Medicines Initiative

IMI is a unique Public-Private Partnership (PPP) between the pharmaceutical industry represented by the European Federation of Pharmaceutical Industries and Associations (EFPIA) and the European Union represented by the European Commission.
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Current Research
Higher level processing of sensory messages in different pain states
In chronic pain states, pain can persist even after local recovery of damaged tissue and does not always reflect the degree of tissue damage. On the other hand, while nociceptive pain is elicited by stimulation of the sensory endings in the tissue, neuropathic pain (NP) results from injury or disease of neurons in the peripheral or central nervous system (Schaible and Richter, 2004). Despite the loss of input, peripheral nerve injury results in positive symptoms in a number of patients where central sensitization, related to channel and receptor changes within the spinal cord that increase the output of neurons within the nociceptive pathway and changes in top-down processing through descending pathways appear to be maladaptive compensations for the sensory loss. This type of pain usually occurs within days, weeks, or months after the injury and tends to occur in waves of frequency and intensity indicative of multiple processes of pain and modulation. The main signs of neuropathic pain (NP) are spontaneous pain, hyperalgesia and allodynia but other signs or symptoms that are usually present are mood disorders like depression and anxiety It is also known that pain is enhanced by unpleasant emotional states such as fear, anxiety, depression and insomnia and reduced by pleasant emotions The amygdala (AMY), as part of the limbic system, plays a key role in the affective and autonomic aspects of pain, the evaluation of the emotional significance of sensory stimuli, emotional learning and memory, fear, anxiety and depression.
Contrary to acute pain cases, analgesics can be inefficient in chronic pain conditions, and the use of drugs like antidepressants and anticonvulsants in pain control as become widespread Anticonvulsants have shown to be useful for chronic NP, and gabapentin and pregabalin are the two anticonvulsants that have the strongest evidence for the treatment of pain. They selectively bind to the alpha/2delta-subunit protein of calcium channels in various regions of the brain and the superficial dorsal horn of the spinal cord, inhibiting the release of excitatory neurotransmitters that are important in the first stages of pain processing. Their efficacy however is controlled by descending pathways from the brain.
Our first goal is to characterize the neurons of the AMY through extracellular in vivo electrophysiology, in the spinal nerve ligation (SNL) model, We also propose to analyze the effects of the systemic and spinal injection of pregabalin in the activity of AMY neurones. We then intend to link in with concurrent interests in the group and probe, using site ¡V specific neuronal ablation, the roles of defined spinal and brain stem populations of neurons, such as within the RVM to probe the input and modulating pathways to the AMY. Further studies would investigate other pain models to compare across different patterns of afferent and central activity.