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Fingolimod downregulates brain sphingosine-1-phosphate receptor 1 levels but does not promote remyelination or neuroprotection in the cuprizone model
| Content Provider | Semantic Scholar |
|---|---|
| Author | Nystad, Agnes E. Lereim, Ragnhild Reehorst Wergeland, Stig Oveland, Eystein Torkildsen, Øivind |
| Copyright Year | 2020 |
| Abstract | Fingolimod is used to treat patients with relapsing-remitting multiple sclerosis; it crosses the blood-brain barrier and modulates sphingosine-1-phosphate receptors (S1PRs). Oligodendrocytes, astrocytes, microglia, and neuronal cells express S1PRs, and fingolimod could potentially improve remyelination and be neuroprotective. We used the cuprizone animal model, histo-, immunohistochemistry, and quantitative proteomics to study the effect of fingolimod on remyelination and axonal damage. Fingolimod was functionally active during remyelination by downregulating S1PR1 brain levels, and fingolimod-treated mice had more oligodendrocytes in the secondary motor cortex after three weeks of remyelination. However, there were no differences in remyelination or axonal damage compared to placebo. Thus, fingolimod does not seem to directly promote remyelination or protect against axonal injury or loss when given after cuprizone-induced demyelination. |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/j.jneuroim.2019.577091 |
| PubMed reference number | 31739156 |
| Journal | Medline |
| Volume Number | 339 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0165572819304126 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0165572819304126?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/j.jneuroim.2019.577091 |
| Journal | Journal of Neuroimmunology |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
