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1 ew strategies for promoting myelin repair in demyelinating disorders.
2 promising new approach for the treatment of demyelinating disorders.
3 new therapeutic avenue for the treatment of demyelinating disorders.
4 a primary goal for regenerative medicine in demyelinating disorders.
5 at promote functional myelin regeneration in demyelinating disorders.
6 of benefit for multiple sclerosis and other demyelinating disorders.
7 us system injuries and neurodegenerative and demyelinating disorders.
8 enues for treatment of neurodegenerative and demyelinating disorders.
9 tuberculosis, other serious infections, and demyelinating disorders.
10 XCR2 as a promising drug target for clinical demyelinating disorders.
11 ons, but also provide potential insight into demyelinating disorders.
12 sis and specific gene defects leads to fatal demyelinating disorders.
13 ive Abs in autoimmune central nervous system demyelinating disorders.
14 tion contributes to remyelination failure in demyelinating disorders.
15 tractive candidate for therapy of autoimmune demyelinating disorders.
16 or investigating the MAG to dMAG reaction in demyelinating disorders.
17 s may be beneficial in neuroinflammatory and demyelinating disorders.
19 of these central nervous system inflammatory demyelinating disorders and discuss neuropathological st
20 effective remyelination in the treatment of demyelinating disorders and in identifying pathways invo
22 r accidents, brain trauma, brain tumors, and demyelinating disorders), and 60 normal controls were ex
23 y develop concurrent or separate episodes of demyelinating disorders, and conversely patients with NM
24 bolic diseases, and traumatic brain injury), demyelinating disorders, and infectious brain lesions.
25 etaR-Ig as a candidate biological therapy in demyelinating disorders, because it is beneficial during
26 w strategies for therapeutic intervention in demyelinating disorders by promoting oligodendrocyte reg
27 is believed to contribute to immune-mediated demyelinating disorders by targeting the myelin-producin
28 multifocal leukoencephalopathy (PML), a rare demyelinating disorder caused by oligodendrocyte destruc
31 Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure co
35 e disseminated encephalomyelitis (ADEM) is a demyelinating disorder most common in childhood and adol
36 ic oligodendrocyte loss, which occurs in the demyelinating disorder multiple sclerosis (MS), contribu
39 utes significantly to the development of the demyelinating disorder multiple sclerosis and its animal
42 ase or globoid cell leukodystrophy is a rare demyelinating disorder of the central and peripheral ner
44 e sclerosis (MS), an inflammatory autoimmune demyelinating disorder of the central nervous system, is
45 ral form of X-linked adrenoleukodystrophy, a demyelinating disorder of the central nervous system, le
46 tis is considered a monophasic, inflammatory demyelinating disorder of the central nervous system.
47 tis (EAE) is a CD4 Th1-mediated inflammatory demyelinating disorder of the CNS and a well-established
51 ve multifocal leukoencephalopathy (PML) is a demyelinating disorder of the human brain caused by infe
53 , optic neuritis presents as an inflammatory demyelinating disorder of the optic nerve, which can be
54 s include both the vascular and inflammatory demyelinating disorders of adulthood, as well as the chi
57 unty population-based cohort of inflammatory demyelinating disorders of the central nervous system we
58 lay a key regulatory role in immune-mediated demyelinating disorders of the central nervous system, i
60 ng central nervous system (CNS) inflammatory demyelinating disorders related to NMO from multiple scl
62 disseminated encephalomyelitis) and from non-demyelinating disorders such as chronic small vessel dis
63 okine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and v
64 nation.SIGNIFICANCE STATEMENT Myelin loss in demyelinating disorders such as multiple sclerosis resul
65 slowing of conduction velocities in acquired demyelinating disorders, such as chronic inflammatory de
66 /- mice to IFN-gamma implicates ER stress in demyelinating disorders that are induced by CNS inflamma
68 imply that the development of therapies for demyelinating disorders will require defining which OPC
69 sorders, and conversely patients with NMO or demyelinating disorders with atypical symptoms (eg, dysk
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