Search Results for “stefano pluchino”

Source: Stefano Pluchino

Stefano Pluchino (born May 31, 1971) is Professor of Regenerative Neuroimmunology, within the Department of Clinical Neurosciences, at the University of Cambridge.
His research studies whether the accumulation of neurological disability observed in patients with chronic inflammatory neurological conditions can be slowed down using next generation molecular therapies.

The overarching aim is to understand the basic mechanisms that allow exogenously delivered stem cells, gene therapy vectors and/or exosomes to create an environment that preserves damaged axons or prevents neurons from dying. Such mechanisms are being harnessed and used to modulate disease states to repair and/or regenerate critical components of the nervous system.
He is best known for having provided compelling evidence in support of the feasibility and efficacy of advanced stem cell therapies in rodent and non-human primate models of inflammatory neurological diseases, including multiple sclerosis. His work has contributed to reshape the classical view that advanced cell therapeutics (ACTs), including cellular grafts, may exert their therapeutic effects not only through structural cell replacement, but also through modulation of mitochondrial function and neuroinflammatory pathways, and has inspired the first-in-kind clinical trials of allogeneic somatic neural stem cells in patients with progressive MS.
His most recent research has also elucidated the role of mitochondrial complex I activity in microglia, showcasing its pivotal role in sustaining neuroinflammation. This finding, as reported in a study published in Nature, unveils a novel avenue for understanding the mechanisms underlying progressive multiple sclerosis (MS). The implications of this discovery are profound, as it suggests a new target for disease-modifying therapies. By targeting mitochondrial complex I activity in microglia, researchers may be able to intervene in the neuroinflammatory processes that contribute to disease progression in MS. This not only enhances our understanding of the pathophysiology of progressive MS but also opens avenues for the development of innovative treatments that could potentially halt or slow down disease progression.
His combined efforts towards the identification of new druggable targets, as well as the development of advanced regenerative therapies, underscore the importance of continued research into the intricate mechanisms underlying neurological diseases and the development of targeted therapies that can address these mechanisms.