Project R-12129

Carnosine in neuroinflammation and demyelination: a versatile dipeptide to halt damage and boost repair in Multiple Sclerosis? (Research)

Multiple sclerosis (MS) is a chronic disorder of the central nervous system (CNS) that is characterised by demyelination, the destruction of the fatty layer (myelin) that insulates nerves to enhance signal transduction. Although some repair (remyelination) occurs spontaneously, it is usually insufficient/inadequate. To date, MS therapies successfully decrease disease severity in the initial phase, but do not affect long-term disease progression and do not directly stimulate myelin repair. The present project focusses on carnosine, a molecule that is abundantly present in the CNS, where it possesses several protective functions. Carnosine has never been investigated in relation to MS, but I have recently shown that carnosine treatment reduces disability in an animal model for MS. Based on my preliminary data I now hypothesize that such effects are explained by the ability of carnosine to (1) halt CNS damage (demyelination), and (2) boost CNS repair (remyelination). Secondly, I hypothesize that naturally occurring carnosine is actively involved in MS pathophysiology to preserve CNS health. I investigate this in blood and urine samples from MS patients. My project will clarify the role of carnosine in MS and investigate the underlying mechanisms of carnosine treatment for MS. This may help to introduce carnosine as a novel complementary treatment strategy for MS in the future.

01 November 2021 - 30 September 2023