An increased or decreased ability to perceive pain has drastic and costly effects on the European population in terms of their performance at work and daily quality of life. Specifically, moderate to severe chronic pain in both musculoskeletal conditions and neuropathic pain states occurs in 19% of adult Europeans and in 50% of these cases, patients receive inadequate treatment for their chronic pain. Novel, more effective treatments are therefore required. Furthermore, pain is a major comorbidity in age-related neurodegenerative diseases and with the predicted near doubling of the EU population aged >65 reaching 151 million in 2060, the management of pain is a significant public health concern.
An emerging concept in the pain research area is that the inflammatory response associated with damage in the central nervous system (CNS) and peripheral nervous system (PNS), namely neuroinflammation, may contribute to a variety of pain states, encompassing those that have either a peripheral or CNS origin.
TOBeATPAIN does propose an innovative approach that will examine the neuroinflammation associated with pain in peripheral and central diseases and will identify the critical non–neuronal cellular players and mediators involved in pathological pain signalling. The following two hypothesis will be tested. The first is that neuroinflammation represents an underlying mechanism of pathological pain that occurs as a result of diseases within the brain as well as in the peripheral nervous system. The second is that the precise mechanisms of neuroinflammation in peripheral and brain diseases share some features but also vary and possess individual characteristics.