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1 n appealing candidate drug for patients with secondary progressive multiple sclerosis.
2 as a potential neuroprotective treatment for secondary progressive multiple sclerosis.
3 ferent pathogenetic mechanisms compared with secondary progressive multiple sclerosis.
4 ine is also neuroprotective in patients with secondary progressive multiple sclerosis.
5 cal spinal cord in patients with primary and secondary progressive multiple sclerosis.
6 tic neuritis, and chronically in primary and secondary progressive multiple sclerosis.
7 EAE) and in brain samples from patients with secondary progressive multiple sclerosis.
8 ications for the axonal loss associated with secondary progressive multiple sclerosis.
9 ng tissue loss in both arms of this study of secondary progressive multiple sclerosis.
10 ing-remitting multiple sclerosis and 20 with secondary progressive multiple sclerosis.
11 -beta-1b was also shown to be efficacious in secondary progressive multiple sclerosis.
12 carried out in 20 patients with primary and secondary progressive multiple sclerosis.
13 um concentrations were higher in primary and secondary-progressive multiple sclerosis.
14 se, and 2.89 cm3/year in those who developed secondary progressive multiple sclerosis, a difference o
15 from 23 patients with relapsing-remitting or secondary progressive multiple sclerosis, all of whom we
17 nges has been identified as a key feature of secondary progressive multiple sclerosis and may contrib
18 clerosis, with higher concentrations seen in secondary-progressive multiple sclerosis and in patients
19 atients with relapsing remitting and 28 with secondary progressive multiple sclerosis, and 38 healthy
20 4 years disease duration), 13 subjects with secondary progressive multiple sclerosis, and in 17 age-
21 esion development in relapsing-remitting and secondary progressive multiple, sclerosis, and this usua
23 cid levels (i) are abnormal in patients with secondary progressive multiple sclerosis compared with h
24 etization transfer ratio were greater in the secondary progressive multiple sclerosis compared with r
25 ) stimulation was lower in the patients with secondary progressive multiple sclerosis, compared with
26 otrigine on cerebral volume of patients with secondary progressive multiple sclerosis did not differ
27 amma was found in the meninges of cases with secondary progressive multiple sclerosis exhibiting tert
29 ed patients aged 18-65 years with primary or secondary progressive multiple sclerosis from 27 UK neur
30 s was equally low in primary progressive and secondary progressive multiple sclerosis groups versus c
33 xonal damage between primary progressive and secondary progressive multiple sclerosis have not been r
34 tem cells were safely given to patients with secondary progressive multiple sclerosis in our study.
38 ients with primary progressive compared with secondary progressive multiple sclerosis raise the quest
39 ase duration 11 years), and 27 patients with secondary progressive multiple sclerosis (secondary prog
40 rferon beta-1b (IFNbeta-1b) in patients with secondary progressive multiple sclerosis (SP multiple sc
41 te that grossly unaffected white matter from secondary progressive multiple sclerosis (SP-MS) patient
46 We conclude that for relapsing-remitting and secondary progressive multiple sclerosis, the combinatio
47 tients with relapsing-remitting or relapsing secondary progressive multiple sclerosis to receive 3 mg
52 We report the findings in 60 patients with secondary progressive multiple sclerosis who had monthly
53 e disability in both primary progressive and secondary progressive multiple sclerosis with a common p
54 res in an extensive collection of cases with secondary progressive multiple sclerosis with a wide age
55 on-beta1b was performed on 718 patients with secondary progressive multiple sclerosis with follow-up
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