Neuroregeneration in multiple sclerosis

There is currently no treatment that causes tissue regeneration and functional recovery in the adult central nervous system (CNS), i.e. brain and spinal cord, after injury or disease. Regeneration in the CNS is a rare event and is severely limited to the replacement of so-called oligodendroglial cells and their electrically insulating elements of axons called myelin sheaths. This is also true for Multiple Sclerosis (MS), a disease that affects millions of people worldwide and leads to lifelong and progressive impairment of patients. The research team of Prof. Patrick Küry at the Department of Neurology at the University Hospital Düsseldorf now describes in the journal Lancet EBioMedicine that the corticosteroid Medrysone is highly effective in promoting the replacement of lost oligodendroglial cells and and also improves the restoration of myelin sheaths hence the electrical isolation of axons. In their latest research article led by first author Markley Silva Oliveira-Junior, a talented PhD student from Brazil working with the Düsseldorf group, the observation in the mouse model that the regeneration effect by Medrysone was is mediated via a completely unexpected cell type - astrocytes - was surprising.

In their study, the scientists were able to show for the first time that astrocytes react specifically in situations where myelin structures are damaged and appear in many different subtypes. Some of these phenotypes attempt to support local tissue repair activities, while others are more oriented toward more severe tissue destruction and even contribute additionally to lesion formation. Highly complex and dynamic behavior was observed, but this in fact be directed by the Medrysone drug toward protective and regenerative cells and toward "taming" neurotoxic astrocyte populations. These findings are unexpected and novel in the field of neuroregeneration in MS.

Küry and team have been studying regenerative processes for many years with the goal of identifying new aspects, cell responses, and pharmacological agents to improve regeneration efficiency.