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 Twenty-seven patients developed RRMS,
15 SPMS and 21 experienced no further neurological events;
4 Thirty-five patients (20 RRMS,
15 SPMS) completed AHSCT, with a median follow-up of 36 mon
5 articipants remained CIS while 60 had MS (
26 SPMS and 16 MS-related death).
6 Blood from 31 RRMS and
28 SPMS patients was subjected to different sample-handling
7 his study: 30 controls, 21 CIS, 33 RR and
29 SPMS.
8 n an independent set of 50 RRMS patients,
51 SPMS patients, and 32 HCs.
9 physical disability in relapse-onset MS
and SPMS in particular.
10 d be considered before amalgamating PPMS
and SPMS in clinical trials.
11 neuroimaging features differentiate PPMS
and SPMS; both are characterized by imaging findings reflect
12 we examined the differences between RRMS
and SPMS and the relationship between MRI measures and clini
13 col remained discriminatory between RRMS
and SPMS despite these sample-handling variations.
14 test remained able to discriminate RRMS
and SPMS samples that had experienced additional freeze-thaw
15 NAs are differentially expressed in RRMS
and SPMS versus HCs and in RRMS versus SPMS.
16 ns were found in patients with both RRMS
and SPMS.
17 indicate that mechanisms differ in RRMS
and SPMS.
18 RMS subjects, but were not different
between SPMS and ALS, suggesting that similar processes may occu
19 greatest differences in MRI measures
between SPMS and RRMS were the number of cortical lesions, which
20 Results were mainly driven
by SPMS participants (n=613, aHR 1.242 (1.073 to 1.438), p=
21 For
comparison,
SPMS subjects from the intramuscular interferon beta-1a
22 accrual in PPMS and operationally
diagnosed SPMS in the international, clinic-based MSBase cohort.
23 ses were replicated with physician-
diagnosed SPMS.
24 The let-7 family of miRNAs
differentiated SPMS from HCs and RRMS from SPMS.
25 S subjects and may have efficacy in
disabled SPMS subjects.
26 tify potential biomarkers for
distinguishing SPMS by analyzing gene expression differences between no
27 ective therapy, but the processes that
drive SPMS are mostly unknown.
28 phate receptors has proven beneficial
during SPMS, the underlying mechanisms are poorly understood.
29 0.73 for benign MS, and 0.76 versus 0.75
for SPMS, respectively.
30 ressive MS, 0.81 for benign MS, and 0.81
for SPMS.
31 sms and potential therapeutic approaches
for SPMS.
32 study provides a novel set of biomarkers
for SPMS from lesioned grey matter of SPMS cases, offering p
33 CCR1) were identified as key biomarkers
for SPMS, supported by LASSO regression and RF analyses.
34 agement and variable diagnostic criteria
for SPMS.
35 trating significant predictive potential
for SPMS.
36 rum metabolomics could distinguish RRMS
from SPMS with high diagnostic accuracy.
37 hsa-miR-454 differentiated RRMS
from SPMS, and hsa-miR-145 differentiated RRMS from HCs and R
38 s differentiated SPMS from HCs and RRMS
from SPMS.
39 5 differentiated RRMS from HCs and RRMS
from SPMS.
40 columns were significantly more abnormal
in SPMS than in RRMS.
41 ssive phase and slower disability accrual
in SPMS versus PPMS.
42 report later onset and/or faster accrual
in SPMS.
43 e no significant predictors of GM atrophy
in SPMS.
44 + cells among CD4+ memory T cells (%CCR9)
in SPMS did not correlate with age, disease duration or exp
45 esion formation appears to be more common
in SPMS than RRMS.
46 s may balance greater baseline disability
in SPMS, yielding convergent disability trajectories across
47 in slowing the progression of disability
in SPMS.
48 s impaired in unaffected eyes, especially
in SPMS.
49 MPF macromolecular proton fraction
in SPMS secondary progressive MS was reduced relative to RR
50 C lesions per person per year was greater
in SPMS (1.6 (1.9)) than RRMS (0.8 (1.9)) (Mann-Whitney p=0
51 PBR28 uptake across the brain was greater
in SPMS than in RRMS.
52 er of cortical lesions, which were higher
in SPMS (the presence of cortical lesions had 100% sensitiv
53 , and grey matter volume, which was lower
in SPMS.
54 density of respiratory-deficient neurons
in SPMS was strikingly in excess of aged controls.
55 ents converting to RRMS to 14-fold normal
in SPMS.
56 ggesting that similar processes may occur
in SPMS and ALS.
57 cells acquire a more inflammatory profile
in SPMS, reporting similar aspects to CCR9+ memory T cells
58 astatin in slowing disability progression
in SPMS.
59 ed the highest amount of altered proteins
in SPMS.
60 loss and extension into other CA regions
in SPMS.
61 way is a potential new therapeutic target
in SPMS.
62 MS but did not include the right thalamus
in SPMS.
63 Lamotrigine trial
in SPMS was a randomised control trial to assess whether pa
64 did not include the right putamen whilst
in SPMS the right thalamus was also not included.
65 sions arose from previously seen IC
lesions (
SPMS 1.4 (1.8) per person per year, and RRMS 1.1 (1.0)),
66 Among secondary progressive
MS (
SPMS) cases with attacks, all plaque types could be dist
67 ingle neurons from secondary progressive
MS (
SPMS) cases.
68 tting MS (RRMS) to Secondary Progressive
MS (
SPMS) in many cases.
69 ting MS (RRMS) and secondary progressive
MS (
SPMS) patients and controls.
70 Fifteen secondary-progressive
MS (
SPMS) patients, 12 relapsing-remitting MS (RRMS) patient
71 (RRMS) patients, 9 secondary progressive
MS (
SPMS) patients, and 9 healthy controls (HCs) using miRCU
72 clerosis (RRMS) to secondary progressive
MS (
SPMS) represents a huge clinical challenge.
73 g-remitting MS and secondary progressive
MS (
SPMS) than clinically isolated syndrome, while no simila
74 ssive MS (PPMS) or secondary progressive
MS (
SPMS) with at least one GFAP value and at least three fo
75 mitting MS (RRMS), secondary-progressive
MS (
SPMS), and primary-progressive MS (PPMS).
76 imited efficacy in secondary progressive
MS (
SPMS).
77 mitting (RRMS) and secondary progressive
MS (
SPMS).
78 isease severity in secondary progressive
MS (
SPMS).
79 ture disability in secondary progressive
MS (
SPMS).
80 ng-remitting MS or secondary progressive
MS (
SPMS).
81 and conversion to secondary progressive
MS (
SPMS).
82 imited efficacy in secondary progressive
MS (
SPMS).
83 om relapsing MS to secondary progressive
MS (
SPMS).
84 e to conversion to secondary-progressive
MS (
SPMS).
85 d 27 patients with secondary progressive
MS (
SPMS).
86 S patients (7 with secondary progressive
MS [
SPMS], 27 with relapsing remitting MS [RRMS]) and 30 hea
87 ting MS [RRMS], 17 secondary progressive
MS [
SPMS], and 40 primary progressive MS [PPMS]) from C1 to
88 om the phase 2 MS231 study, and
nonrelapsing SPMS subjects from the phase 1b DELIVER study.
89 ely) and in the thalamic ROIs (P = 0.027)
of SPMS patients, compared with the control group.
90 nal cell line, SK-N-SH, was seen with 70%
of SPMS sera compared with 25% of RRMS sera (P < 0.001).
91 ntal model that resembles several aspects
of SPMS, including neurodegeneration and disease progressio
92 es or ageing, may lead to the development
of SPMS.
93 cipants aged 18-65 years with a diagnosis
of SPMS and an Expanded Disability Status Scale (EDSS) of b
94 arkers for SPMS from lesioned grey matter
of SPMS cases, offering potential for diagnosis and targete
95 ases of (11)C-PK11195 in the white matter
of SPMS patients, compared with healthy controls.
96 creased (11)C-PK11195 binding in the NAWM
of SPMS patients is in line with the neuropathologic demons
97 rse (95% CI: 0.04 to 0.40; p=0.015), odds
of SPMS 1.33 times higher (95% CI: 1.08 to 1.64; p=0.008),
98 contribute to understand the pathogenesis
of SPMS.
99 ivo, the central nervous system pathology
of SPMS.
100 seases and MS subtypes and the uniqueness
of SPMS.
101 Inclusion required PPMS
or SPMS with onset at age >=18 years since 1995.
102 k proteins that were not observed in PPMS
or SPMS.
103 RMS) and is followed by a progressive
phase (
SPMS).
104 ondary progressive multiple sclerosis (
PPMS,
SPMS) report similar ages at onset of the progressive ph
105 Relative to
PPMS,
SPMS had older age at onset of the progressive phase (me
106 n number (beta=0.87) independently
predicted SPMS conversion (C-index=0.91).
107 ressive MS (PPMS), 36 secondary
progressive (
SPMS) and 51 healthy controls (HCs).
108 nt difference between secondary
progressive (
SPMS) and relapsing-remitting (RRMS) subgroups.
109 independent cohort of secondary
progressive (
SPMS) patients, but not in a third cohorts of relapsing-
110 t distinguished RRMS, secondary
progressive (
SPMS), and primary progressive (PPMS) MS from both healt
111 remission) patients, secondary
progressive (
SPMS, n = 6) MS patients, and noninflammatory and inflam
112 ation of the latter finding in a
prospective SPMS study is warranted.
113 hase 3 AFFIRM and SENTINEL trials,
relapsing SPMS subjects from the phase 2 MS231 study, and nonrelap
114 In addition,
RRMS,
SPMS, and PPMS were characterized by unique patterns of
115 econdary progressive MS multiple
sclerosis (
SPMS secondary progressive MS ) patients provided writte
116 th secondary progressive multiple
sclerosis (
SPMS) are lacking efficient medication to slow down the
117 in secondary progressive multiple
sclerosis (
SPMS) are mediated by reducing cholesterol or are indepe
118 of secondary-progressive multiple
sclerosis (
SPMS), brain T2-lesion volume (T2LV) and brain parenchym
119 to secondary progressive multiple
sclerosis (
SPMS), characterized by accumulating fixed disability, i
120 in secondary progressive multiple
sclerosis (
SPMS), the adjusted difference in brain atrophy rate bet
121 nd secondary progressive multiple
sclerosis (
SPMS), which in part is reflective of inclusion of subje
122 th secondary progressive multiple
sclerosis (
SPMS).
123 or secondary progressive multiple
sclerosis (
SPMS).
124 Ten SPMS patients with a mean expanded disability status sca
125 INTERPRETATION: To our knowledge,
this SPMS cohort is the largest studied to date with comprehe
126 hed including active plaques, in contrast
to SPMS without attacks, in which inactive plaques predomin
127 ard ratio, 1.23; P < .001) and conversion
to SPMS (hazard ratio, 1.16; P = .008).
128 gnosis accelerated the time to conversion
to SPMS by 4.7% (acceleration factor, 1.047; 95% CI, 1.023-
129 ents with EDSS progression and conversion
to SPMS, and longer time on treatment with lower risk of fi
130 ously each year after diagnosis converted
to SPMS faster than those who quit smoking, reaching SP dis
131 Rates of worsening and evolution
to SPMS were substantially lower when compared to earlier n
132 patients with relapsing-remitting evolved
to SPMS.
133 sociated with conversion from CIS or RRMS
to SPMS (+26.4 mm(3); 95% CI: 4.2 mm(3), 56.9 mm(3); d = 0.
134 RRMS and predicting the evolution of RRMS
to SPMS.
135 me (CIS) or relapsing-remitting MS (RRMS)
to SPMS.
136 s associated with an acceleration in time
to SPMS and that those who quit fare better.
137 Time
to SPMS, measured using an accelerated failure time model,
138 were differentially expressed in RRMS
versus SPMS also differentiated amyotrophic lateral sclerosis (
139 It was different in RRMS
versus SPMS, and RRMS versus HCs, and showed an association wit
140 RRMS and SPMS versus HCs and in RRMS
versus SPMS.
141 sts, the results confirmed that the RRMS
vs.
SPMS test is resistant to sample-handling variations and
142 While SPMS progression is associated with brain atrophy, in pr
143 27 people with RRMS, and 22
with SPMS were included in this study.
144 S (47% men; 50% with activity) and 2575
with SPMS (32% men; 40% with activity).
145 The identified biomarkers link closely
with SPMS pathology, especially regarding immune system modul
146 on of lesions were inactive in patients
with SPMS (35%) than RRMS (23%), but active lesions were foun
147 a-hydroxicholestene (15-HC) in patients
with SPMS and in mice with secondary progressive experimental
148 ble-blind, controlled trial of patients
with SPMS done at three neuroscience centres in the UK betwee
149 lls in the peripheral blood of patients
with SPMS relative to healthy controls.
150 the MS-STAT trial in which 140 patients
with SPMS were randomized to receive placebo or simvastatin.
151 ity was higher in monocytes of patients
with SPMS, and PARP-1 inhibition suppressed the progression o
152 L-17A and IFNgamma was high in patients
with SPMS, indicating a loss of regulatory function.
153 IS, with differences driven by patients
with SPMS.
154 matter (NAWM) in the brains of patients
with SPMS.
155 In our cohort of people
with SPMS and long disease duration, OCT measures correlated
156 We investigated people
with SPMS from the Multiple Sclerosis-Secondary Progressive M
157 T), from a clinical trial in 988 people
with SPMS.