1 SPMS patients who attended the NHNN or the Royal Free Ho
2 inety-eight snap-frozen brain blocks from
13 SPMS cases together with complex IV/complex II histochem
3 inety-eight snap-frozen brain blocks from
13 SPMS cases together with complex IV/complex II histochem
4 his study: 30 controls, 21 CIS, 33 RR and
29 SPMS.
5 n an independent set of 50 RRMS patients,
51 SPMS patients, and 32 HCs.
6 physical disability in relapse-onset MS
and SPMS in particular.
7 NAs are differentially expressed in RRMS
and SPMS versus HCs and in RRMS versus SPMS.
8 ns were found in patients with both RRMS
and SPMS.
9 indicate that mechanisms differ in RRMS
and SPMS.
10 RMS subjects, but were not different
between SPMS and ALS, suggesting that similar processes may occu
11 For
comparison,
SPMS subjects from the intramuscular interferon beta-1a
12 The let-7 family of miRNAs
differentiated SPMS from HCs and RRMS from SPMS.
13 S subjects and may have efficacy in
disabled SPMS subjects.
14 ective therapy, but the processes that
drive SPMS are mostly unknown.
15 sms and potential therapeutic approaches
for SPMS.
16 hsa-miR-454 differentiated RRMS
from SPMS, and hsa-miR-145 differentiated RRMS from HCs and R
17 s differentiated SPMS from HCs and RRMS
from SPMS.
18 5 differentiated RRMS from HCs and RRMS
from SPMS.
19 columns were significantly more abnormal
in SPMS than in RRMS.
20 e no significant predictors of GM atrophy
in SPMS.
21 esion formation appears to be more common
in SPMS than RRMS.
22 MPF macromolecular proton fraction
in SPMS secondary progressive MS was reduced relative to RR
23 C lesions per person per year was greater
in SPMS (1.6 (1.9)) than RRMS (0.8 (1.9)) (Mann-Whitney p=0
24 PBR28 uptake across the brain was greater
in SPMS than in RRMS.
25 density of respiratory-deficient neurons
in SPMS was strikingly in excess of aged controls.
26 density of respiratory-deficient neurons
in SPMS was strikingly in excess of aged controls.
27 ents converting to RRMS to 14-fold normal
in SPMS.
28 ggesting that similar processes may occur
in SPMS and ALS.
29 loss and extension into other CA regions
in SPMS.
30 way is a potential new therapeutic target
in SPMS.
31 Lamotrigine trial
in SPMS was a randomised control trial to assess whether pa
32 sions arose from previously seen IC
lesions (
SPMS 1.4 (1.8) per person per year, and RRMS 1.1 (1.0)),
33 Among secondary progressive
MS (
SPMS) cases with attacks, all plaque types could be dist
34 ingle neurons from secondary progressive
MS (
SPMS) cases.
35 ingle neurons from secondary progressive
MS (
SPMS) cases.
36 ting MS (RRMS) and secondary progressive
MS (
SPMS) patients and controls.
37 Fifteen secondary-progressive
MS (
SPMS) patients, 12 relapsing-remitting MS (RRMS) patient
38 (RRMS) patients, 9 secondary progressive
MS (
SPMS) patients, and 9 healthy controls (HCs) using miRCU
39 om relapsing MS to secondary progressive
MS (
SPMS).
40 e to conversion to secondary-progressive
MS (
SPMS).
41 imited efficacy in secondary progressive
MS (
SPMS).
42 d 27 patients with secondary progressive
MS (
SPMS).
43 S patients (7 with secondary progressive
MS [
SPMS], 27 with relapsing remitting MS [RRMS]) and 30 hea
44 ting MS [RRMS], 17 secondary progressive
MS [
SPMS], and 40 primary progressive MS [PPMS]) from C1 to
45 om the phase 2 MS231 study, and
nonrelapsing SPMS subjects from the phase 1b DELIVER study.
46 ely) and in the thalamic ROIs (P = 0.027)
of SPMS patients, compared with the control group.
47 nal cell line, SK-N-SH, was seen with 70%
of SPMS sera compared with 25% of RRMS sera (P < 0.001).
48 ntal model that resembles several aspects
of SPMS, including neurodegeneration and disease progressio
49 ases of (11)C-PK11195 in the white matter
of SPMS patients, compared with healthy controls.
50 creased (11)C-PK11195 binding in the NAWM
of SPMS patients is in line with the neuropathologic demons
51 ivo, the central nervous system pathology
of SPMS.
52 k proteins that were not observed in PPMS
or SPMS.
53 RMS) and is followed by a progressive
phase (
SPMS).
54 nt difference between secondary
progressive (
SPMS) and relapsing-remitting (RRMS) subgroups.
55 t distinguished RRMS, secondary
progressive (
SPMS), and primary progressive (PPMS) MS from both healt
56 ation of the latter finding in a
prospective SPMS study is warranted.
57 hase 3 AFFIRM and SENTINEL trials,
relapsing SPMS subjects from the phase 2 MS231 study, and nonrelap
58 In addition,
RRMS,
SPMS, and PPMS were characterized by unique patterns of
59 econdary progressive MS multiple
sclerosis (
SPMS secondary progressive MS ) patients provided writte
60 th secondary progressive multiple
sclerosis (
SPMS) are lacking efficient medication to slow down the
61 th secondary progressive multiple
sclerosis (
SPMS).
62 or secondary progressive multiple
sclerosis (
SPMS).
63 Ten SPMS patients with a mean expanded disability status sca
64 INTERPRETATION: To our knowledge,
this SPMS cohort is the largest studied to date with comprehe
65 hed including active plaques, in contrast
to SPMS without attacks, in which inactive plaques predomin
66 gnosis accelerated the time to conversion
to SPMS by 4.7% (acceleration factor, 1.047; 95% CI, 1.023-
67 ents with EDSS progression and conversion
to SPMS, and longer time on treatment with lower risk of fi
68 ously each year after diagnosis converted
to SPMS faster than those who quit smoking, reaching SP dis
69 Rates of worsening and evolution
to SPMS were substantially lower when compared to earlier n
70 s associated with an acceleration in time
to SPMS and that those who quit fare better.
71 Time
to SPMS, measured using an accelerated failure time model,
72 were differentially expressed in RRMS
versus SPMS also differentiated amyotrophic lateral sclerosis (
73 It was different in RRMS
versus SPMS, and RRMS versus HCs, and showed an association wit
74 RRMS and SPMS versus HCs and in RRMS
versus SPMS.
75 27 people with RRMS, and 22
with SPMS were included in this study.
76 on of lesions were inactive in patients
with SPMS (35%) than RRMS (23%), but active lesions were foun
77 a-hydroxicholestene (15-HC) in patients
with SPMS and in mice with secondary progressive experimental
78 ble-blind, controlled trial of patients
with SPMS done at three neuroscience centres in the UK betwee
79 ity was higher in monocytes of patients
with SPMS, and PARP-1 inhibition suppressed the progression o
80 matter (NAWM) in the brains of patients
with SPMS.