Axonal Damage in Relapsing Multiple Sclerosis is Markedly Reduced by Natalizumab
2011 (English)In: ANNALS OF NEUROLOGY, ISSN 0364-5134, Vol. 69, no 1, 83-89 p.Article in journal (Refereed) Published
Objective: The impact of present disease-modifying treatments (DMTs) in multiple sclerosis (MS) on nerve injury and reactive astrogliosis is still unclear. Therefore, we studied the effect of natalizumab treatment on the release of 2 brain-specific tissue damage markers into cerebrospinal fluid (CSF) in MS patients. Methods: CSF samples from 92 patients with relapsing forms of MS were collected in a prospective manner prior to natalizumab treatment and after 6 or 12 months. In 86 cases, natalizumab was used as second-line DMT due to breakthrough of disease activity. The levels of neurofilament light (NFL) and glial fibrillary acidic protein (GFAP) were determined using highly sensitive in-house developed enzyme-linked immunosorbent assays. Results: Natalizumab treatment led to a 3-fold reduction of NFL levels, from a mean value of 1,300 (standard deviation [SD], 2,200) to 400 (SD, 270) ng/l (p andlt; 0.001). The later value was not significantly different from that found in healthy control subjects (350ng/l; SD, 170; n = 28). Subgroup analysis revealed a consistent effect on NFL release, regardless of previous DMT or whether patients had relapses or were in remission within 3 months prior to natalizumab treatment. No differences between pre- and post-treatment levels of GFAP were detected. Interpretation: Our data demonstrate that natalizumab treatment reduces the accumulation of nerve injury in relapsing forms of MS. It is anticipated that highly effective anti-inflammatory treatment can reduce axonal loss, thereby preventing development of permanent neurological disability.
Place, publisher, year, edition, pages
John Wiley and Sons, Ltd , 2011. Vol. 69, no 1, 83-89 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-65960DOI: 10.1002/ana.22247ISI: 000286850800014OAI: oai:DiVA.org:liu-65960DiVA: diva2:400659