The neuropeptide galanin is widely distributed in the nervous system and levels are known to increase dramatically in response to injury. Galanin and galanin receptors have recently been shown to be overexpressed in some brain areas of people with Alzheimer’s disease and researchers at the University of Bristol have now shown that galanin is also upregulated in microglia from lesions and shadow plaques in multiple sclerosis sufferers as well as in oligodendrocytes from mice with EAE, an experimental form of the disease. To investigate whether the increased levels of galanin were modulating disease activity, the team monitored the development of EAE in wild type (WT) mice, galanin knockout (Gal-KO) mice, mice over-expressing galanin (Gal-OE) and mice expressing a mutated form of the galanin receptor-2 (GalR2-Mut). It was found that Gal-OE mice were completely resistant to the development of clinical symptoms whilst Gal-KO mice developed clinical disease earlier than WT mice and GalR2-Mut mice developed more severe disease than WT mice and at an earlier time point. The study clearly shows the importance of galanin in limiting disease severity in mice with EAE and suggests that GalR2 agonists, if these could be identified, may be of benefit to MS patients. The study is published in the August 26th online edition of PNAS.