For the first time, researchers have identified that inflammation – long associated with multiple sclerosis (MS) – appears to cause increased mutations that damage neurons linked to MS progression. Researchers at the Florey Institute and the University of Melbourne studied MS brain lesions, which are areas of past or ongoing brain inflammation that are visible as spots on MRI scans.

Tyrosine kinase 2 (TYK2), expressed in astrocytes and microglia, is involved in the activation of pathways triggered by proinflammatory cytokines, such as IL-23, IL-12 and type I interferons (IFNs), within the central nervous system (CNS). Dysregulated activation of astrocytes and microglia may contribute to the neuroinflammation associated with progressive forms of multiple sclerosis (MS).

Epstein-Barr virus (EBV) infection is a recognized risk factor that is now regarded as a prerequisite for the development of multiple sclerosis (MS). Recently, significant advances have been made in clarifying the precise mechanism by which EBV leads to the pathogenic features of MS. Now, a new study may have tied up more loose ends. Researchers from the University of Helsinki have mapped the immune landscape of deep cervical lymph nodes (dCLN) in patients recently diagnosed with MS.

Pheno Therapeutics Ltd. has received clinical trial authorization (CTA) from the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) for its lead candidate, PTD-802. The program will progress to a first-in-human phase I trial.

Ophthalmic diseases specialist Oculis Holding AG announced positive phase II data showing its serum-glucose corticoid kinase-2 activator OCS-05 protected nerve cells and improved vision in patients with acute optic neuritis. The placebo-controlled, randomized trial assessed the neuroprotective effect of OCS-05 in combination with standard-of-care steroid injections, against steroids alone, with a benefit seen in preserving both ganglions and retinal cell nerve fibers.