b"Medicine & Researchshrinkage and cognitive changes associated that improve mitochondrial function inwith MS. These new ndings provide a platform patients with progressive MS.forspecicnewMStherapiesthattarget The paper was published in the journaldamaged brain cells to be developed. The Brain.research was published in the journal Nature.Dr. Thrower: Understanding the pathology Dr. Thrower: Oneofthebiggestmysteriesand immunology of MS has been compared surrounding MS is that of progression ofto peeling a never-ending onion. With each disability. Relapses and new lesions on MRIlayer, we understand more and more. This is are clearly linked to active inflammation.both daunting and promising. The discovery Explaining progression of disability in a personof a specic cell that is being targeted by an with no new MRI lesions and no clinicalimmune system gone awry in MS may lead relapses is tougher. Progression of disability hastonewerandmorefocusedtherapies. been thought to be the result of inammation,Understandinghowandwhyprojection both current and past, loss of neural reserves,neurons are attacked will hopefully bring us deconditioning and normal human aging.one step closer to the cure. This study sheds new light on CSF factorsthat may be contributing to the mystery ofCerebrospinal uid (CSF) dierence disability progression. Hopefully, this discoverykey to progression-halting drugs will lead to new treatments such that we canResearchers at the Advanced Science consistently stop MS in its tracks.Research Center at The Graduate Center, Schwann cells show potentialCUNY, and Friedman Brain Institute at the to generate myelinIcahn School of Medicine at Mount Sinai took Researchers at Oregon Health and ScienceCSF samples from 15 patients with relapsing- University discovered that Schwann cells areremitting MS and 29 with progressive MS. much more prolic in generating a protectiveResearchers detected a characteristic elongation sheath covering nerve bers than previouslyof mitochondria exposed to CSF samples from believed. The revelation raises the possibilityprogressive MS patients. This characteristic of new avenues to treat nerve injuries andresponse was not present in mitochondria various forms of neuropathy. Further researchexposed to CSF from patients with a relapsing- could prove useful in promoting myelinremitting MS. Biochemical characterization repair in central nervous system disordersof mitochondrial activity further revealed that such as multiple sclerosis, where damage toelongated mitochondria were less functional myelin slows or blocks electric signals fromand therefore less capable of producing energy, the brain. Researchers made the discoverywhich eventually resulted in neuronal demise. after conducting a genetic screen in zebrashThe researchers were able to prevent the in the laboratory. They discovered some shneurotoxic eect of CSF on cultured neurons had more myelin than expected, and thoseby supplementing glucose. Supplementation sh carried a mutation in a gene called fbxw7.isn't a sustainable approach in the diseased When they knocked out the gene in geneticallybrain, however, so a dierent approach will modied mice, they discovered an unexpectedultimately be needed for developing therapies characteristic: individual Schwann cells beganmsfocusmagazine.org 58"