Repair of myelin disease: strategies and progress in animal models
被引:71
作者:
Duncan, ID
论文数: 0引用数: 0
h-index: 0
机构:
Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USAUniv Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA
Duncan, ID
[1
]
Grever, WE
论文数: 0引用数: 0
h-index: 0
机构:
Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USAUniv Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA
Grever, WE
[1
]
Zhang, SC
论文数: 0引用数: 0
h-index: 0
机构:
Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USAUniv Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA
Zhang, SC
[1
]
机构:
[1] Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA
来源:
MOLECULAR MEDICINE TODAY
|
1997年
/
3卷
/
12期
关键词:
D O I:
10.1016/S1357-4310(97)01162-3
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Myelin disorders form an important group of human neurological diseases that are as yet incurable. Recent studies on experimental remyelination have suggested that it might be feasible to repair the CNS, either by transplanting normal myelinating cells or by enhancing endogenous repair. Progress in animal models, particularly in transplanting cells of the oligodendrocyte lineage, has resulted in significant focal remyelination acid physiological evidence of restoration of function. These data suggest that focal lesions in multiple sclerosis could be repaired by the transplantation of myelin-forming cells. Future therapies could involve both transplantation acid promotion of endogenous repair, and the two approaches could be combined with ex vivo manipulation of the donor tissue.