Descripción del proyecto
La luz azul equivale a un STOP para las neuronas rebeldes que envían señales de dolor falsas
Cualquiera que viva con dolor crónico, aproximadamente una de cada cinco personas en todo el mundo, puede dar fe de sus efectos físicos debilitantes y sus complicaciones graves, incluidas la depresión, la ansiedad y la dificultad para conciliar el sueño. Todo esto puede tener consecuencias para las relaciones personales y profesionales, así como para la estabilidad económica. El dolor neuropático es un dolor crónico que se manifiesta cuando los nervios dañados envían señales incorrectas a los centros de dolor del encéfalo. La transmisión de señales nerviosas implica diversas señales eléctricas y químicas, entre las cuales se encuentra el efecto inhibidor de un influjo de iones de potasio. El proyecto financiado con fondos europeos BREAK se centra en el bloqueo de los canales del potasio de las neuronas mediante un novedoso analgésico inyectable. El bloqueo del envío de señales de dolor desde las neuronas locales al encéfalo podría aliviar el dolor neuropático de millones de personas en todo el mundo.
Objetivo
Chronic pain (CP) is a medical condition affecting around 20% of adults in Europe, characterised by an abnormal duration of pain (> 12 weeks) originally initiated by a trauma or illness. Despite significant progress, CP remains extremely hard to treat, with only one-third to two-thirds of patients reporting adequate some pain relief. This situation is even worse for neuropathic pain (NP), a specific class of CP affecting 8% of global population and whose origin mostly depend on peripheral or central nervous damage or disorder, which leads the brain to interpret as pain normally non painful stimuli. NP is difficult to treat due to the large number of entities involved (cells, genes and proteins working in synergy), which makes it hard to rapidly diagnose the exact cause of pain. Drugs targeting the central nervous system (e.g. antidepressants and opioids) provide only partial pain relief and are nonspecific, also causing side effects like addiction, and nausea, thus restraining their adoption for prolonged treatments.
BREAK is the first non-invasive inhibitory optogenetic tool specifically designed for NP treatment, with potential application to the whole spectrum of CP. BREAK is composed of a drug and an optical device. The protein BLINK2 is injected in the painful area using a genetically engineered virus, and respond to a specific blue light by silencing the addressed neuron. The lamp can be kept at some distance (cm) from the skin and no implant is required. Just some minutes of treatment results in hours of pain relief, making the invasiveness of BREAK far lower than actually existing solution.
A first version of BREAK has already demonstrated in in-vivo experiments on rats. During this project we plan to further develop the treatment and explore its commercial potential. In particular, leveraging from the experience of different partners, we will constitute a fruitful stakeholder network, including Academic centers, hospitals, pharma companies and investor
Ámbito científico
Palabras clave
Programa(s)
Régimen de financiación
ERC-POC - Proof of Concept GrantInstitución de acogida
20122 Milano
Italia