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• Chronic pain
• Autophagy
• Psychedelic drugs
• Botulinum toxin
• Long Covid
• Neuroinflammation

My research focusses on pain mechanisms and the generation of new tools and drugs that could ameliorate persistent pain states. In particular, the aims of my research are:

1. To uncover new signalling pathways involved in chemotherapy-induced peripheral neuropathy (CIPN) and provide new targets for its treatment. My hypothesis is that dysfunction of autophagic mechanisms in peripheral and central nervous system leads to CIPN. Autophagy is a physiological process essential for a correct cellular homeostasis. Under normal conditions, autophagy is maintained at a basal level. However, following stress exposure such as in disease state, the autophagic pathway is rapidly activated. A dysfunction of autophagic process is thought to be deleterious affecting cell survival and indeed an increasing number of pathologies are linked to autophagy dysregulation. The key to successful autophagy-targeted therapeutic interventions is a thorough biological understanding of the relationship between autophagy and CIPN.
2. To investigate the long-term consequence of silencing pain-pathways using novel Botulinum constructs. Despite important progress in our understanding of pain mechanism, chronic pain has remained an area of unmet medical need. Our approach involves the use of new Botulinum constructs that target specific pain signalling neurons within the spinal cord. This research has the potential to lead to new treatments for neuropathic pain, but potentially it could also improve other forms of chronic pain, such as inflammatory pain or chemotherapy-induced pain.
3. To investigate the analgesic effect of psychedelic drugs in preclinical models of pain. Psychedelic drugs, such as lysergic acid diethylamide (LSD) and psilocybin, act on receptors for serotonin, primarily the 5-hydroxytryptamine (5-HT) 2A receptors, to stimulate a profound alteration of perception and mood. Growing evidence demonstrates beneficial effects of psychedelic drugs in patients with major depressive disorders, which are frequently comorbid with chronic pain states. Psychedelic drugs may work by boosting deficient serotoninergic pathways and efficacy in alleviating depression may be due to the reorganisation of neuronal networks within the cerebral cortex. Recently, the use of psychedelic drugs within a medical context has started to be more widely advocated. Using behavioural and molecular techniques, we will investigate whether psychedelic drug can be used to reduce the sensory and affective components of chronic pain.

External Role

• Scientific Advisor Board Member, Neuresta, USA
• Scientific Consultant, Lovelace Biomedical, USA
• Academic Editor