References
- Papers of special note have been highlighted as:
- • of interest
- •• of considerable interest
- Patrikios P, Stadelmann C, Kutzelnigg A, et al. Remyelination is extensive in a subset of multiple sclerosis patients. Brain. 2006;129(Pt 12):3165–3172.
••This study illustrates that endogenous potential for remyelination is different in different multiple sclerosis patients.
- Frischer JM, Weigand SD, Guo Y, et al. Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque. Ann Neurol. 2015;78(5):710–721.
- Xing YL, Roth PT, Stratton JA, et al. Adult neural precursor cells from the subventricular zone contribute significantly to oligodendrocyte regeneration and remyelination. J Neuroscience Off J Soc Neurosci. 2014;34(42):14128–14146.
- Honmou O, Felts PA, Waxman SG, et al. Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells. J Neuroscience Off J Soc Neurosci. 1996;16(10):3199–3208.
- Slowik A, Schmidt T, Beyer C, et al. The sphingosine 1-phosphate receptor agonist FTY720 is neuroprotective after cuprizone-induced CNS demyelination. Br J Pharmacol. 2015;172(1):80–92.
•It provides clear evidence that axonal degeneration continues despite ongoing remyelination.
- Nave KA. Myelination and the trophic support of long axons. Nat Rev Neurosci. 2010;11(4):275–283.
- Blakemore WF, Franklin RJ. Remyelination in experimental models of toxin-induced demyelination. Curr Top Microbiol Immunol. 2008;318:193–212.
- Kipp M, Clarner T, Dang J, et al. The cuprizone animal model: new insights into an old story. Acta Neuropathol. 2009;118(6):723–736.
- Skripuletz T, Manzel A, Gropengiesser K, et al. Pivotal role of choline metabolites in remyelination. Brain. 2015;138(Pt 2):398–413.
- Huang JK, Jarjour AA, Nait Oumesmar B, et al. Retinoid X receptor gamma signaling accelerates CNS remyelination. Nat Neurosci. 2011;14(1):45–53.
- Deshmukh VA, Tardif V, Lyssiotis CA, et al. A regenerative approach to the treatment of multiple sclerosis. Nature. 2013;502(7471):327–332.
- Chang A, Tourtellotte WW, Rudick R, et al. Premyelinating oligodendrocytes in chronic lesions of multiple sclerosis. N Engl J Med. 2002;346(3):165–173.
- Baxi EG, DeBruin J, Tosi DM, et al. Transfer of myelin-reactive th17 cells impairs endogenous remyelination in the central nervous system of cuprizone-fed mice. J Neuroscience Off J Soc Neurosci. 2015;35(22):8626–8639.
•It elegantly shows that encephalogenic T-cells cannot just initiate lesion development but as well interfere with reparative pathways.
- Lindner M, Fokuhl J, Linsmeier F, et al. Chronic toxic demyelination in the central nervous system leads to axonal damage despite remyelination. Neurosci Lett. 2009;453(2):120–125.
- Kipp M, Gingele S, Pott F, et al. BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions. Brain Behav Immun. 2011;25(8):1554–1568.
- Shields SA, Gilson JM, Blakemore WF, et al. Remyelination occurs as extensively but more slowly in old rats compared to young rats following gliotoxin-induced CNS demyelination. Glia. 1999;28(1):77–83.
••It provides clear evidence that capacity of remyelination decreases with age.
- Chari DM, Crang AJ, Blakemore WF. Decline in rate of colonization of oligodendrocyte progenitor cell (OPC)-depleted tissue by adult OPCs with age. J Neuropathol Exp Neurol. 2003;62(9):908–916.
- Gilson J, Blakemore WF. Failure of remyelination in areas of demyelination produced in the spinal cord of old rats. Neuropathol Appl Neurobiol. 1993;19(2):173–181.
- Manrique-Hoyos N, Jurgens T, Gronborg M, et al. Late motor decline after accomplished remyelination: impact for progressive multiple sclerosis. Ann Neurol. 2012;71(2):227–244.
••It provides clear evidence that axonal degeneration continues after remyelination has been completed.
- Mei F, Fancy SP, Shen YA, et al. Micropillar arrays as a high-throughput screening platform for therapeutics in multiple sclerosis. Nat Med. 2014;20(8):954–960.