ライフサイエンスコーパス: sclerosis

1 (p = 1.76 x 10(-08) with amyotrophic lateral sclerosis).

2 y in the diagnosis and follow-up of multiple sclerosis.

3 's disease, Alzheimer's disease and multiple sclerosis.

4 c conditions, including progressive multiple sclerosis.

5 on, and 71.5% (2108 of 2948) for hippocampal sclerosis.

6 pathology in EAE and, potentially, multiple sclerosis.

7 ncluding Parkinson's and amyotrophic lateral sclerosis.

8 3 trials of patients with relapsing multiple sclerosis.

9 t include DMF, for the treatment of multiple sclerosis.

10 fy candidate therapeutic targets in multiple sclerosis.

11 itial lung disease in patients with systemic sclerosis.

12 luding active secondary progressive multiple sclerosis.

13 of systemic lupus erythematosus and systemic sclerosis.

14 eurodegenerative disease amyotrophic lateral sclerosis.

15 timal cortical lesion assessment in multiple sclerosis.

16 lomyelitis (EAE), a murine model of multiple sclerosis.

17 risk factor for the development of multiple sclerosis.

18 se as a new therapeutic strategy in multiple sclerosis.

19 months in patients with progressive multiple sclerosis.

20 omyelitis (EAE), an animal model of multiple sclerosis.

21 ntotemporal dementia and amyotrophic lateral sclerosis.

22 ations in them underlie the disease tuberous sclerosis.

23 e of demyelinating diseases such as multiple sclerosis.

24 ecomes inefficient in the course of multiple sclerosis.

25 ly advantageous in the treatment of multiple sclerosis.

26 NA-binding protein 43 in amyotrophic lateral sclerosis.

27 n identified in familial amyotrophic lateral sclerosis.

28 dent for all lesions, except for hippocampal sclerosis.

29 sease, autism spectrum disorder and multiple sclerosis.

30 g will probably not be continued in multiple sclerosis.

31 t always affected to some degree in multiple sclerosis.

32 gical conditions such as amyotrophic lateral sclerosis.

33 cial in autoimmune diseases such as multiple sclerosis.

34 ate for the treatment of fatigue in multiple sclerosis.

35 isease activity in a mouse model of multiple sclerosis.

36 und in Mexican patients with NMO or multiple sclerosis.

37 umatic brain injury, and amyotrophic lateral sclerosis.

38 metry and proton density mapping in multiple sclerosis.

39 rked than those in patients with hippocampal sclerosis.

40 3 trial of patients with relapsing multiple sclerosis.

41 ameliorate ambulatory disability in multiple sclerosis.

42 amage mouse model and in humans for multiple sclerosis.

43 nderway, in patients with relapsing multiple sclerosis.

44 onset and progression of amyotrophic lateral sclerosis.

45 e treatment for relapsing-remitting multiple sclerosis.

46 c targets for disability accrual in multiple sclerosis.

47 ogically isolated syndrome (RIS) to multiple sclerosis.

48 e tested in patients with relapsing multiple sclerosis.

49 toimmune rheumatic diseases such as systemic sclerosis.

50 e with RPE-specific deletion of the tuberous sclerosis 1 (Tsc1) gene which encodes an upstream suppre

51 disease, 2.2 (95% CI, 1.9-2.6) for multiple sclerosis, 1.7 (95% CI, 1.6-1.7) for head injury, 1.3 (9

52 s contribute to the pathogenesis of multiple sclerosis(2), but little is known about the heterogeneit

53 .9 (95% CI, 3.5-6.9) for amyotrophic lateral sclerosis, 4.9 (95% CI, 3.1-7.7) for Huntington disease,

54 SOD1-G93A mouse model of amyotrophic lateral sclerosis, a disorder characterized by progressive moton

55 this glial barrier system in human multiple sclerosis active lesions.

56 tive diseases, including amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD).

57 (HREs) in C9orf72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and le

58 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are ne

59 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are ov

60 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are tw

61 lzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) as wel

62 common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is a h

63 NC13A is associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) suscep

64 known genetic cause for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

65 pathogenic signature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

66 ajority of patients with amyotrophic lateral sclerosis (ALS) and in approximately 50% of patients dyi

67 o patients with familial amyotrophic lateral sclerosis (ALS) and mutations in the gene encoding super

68 ompounds in persons with amyotrophic lateral sclerosis (ALS) are not known.

69 Amyotrophic lateral sclerosis (ALS) can overlap genetically, pathologically

70 ely 35% of patients with amyotrophic lateral sclerosis (ALS) exhibit mild cognitive deficits in execu

71 Amyotrophic lateral sclerosis (ALS) is a fatal disease involving motor neuro

72 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease aff

73 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder ca

74 Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease charact

75 Amyotrophic lateral sclerosis (ALS) is a multifactorial, multisystem pro-inf

76 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease character

77 poral dementia (FTD) and amyotrophic lateral sclerosis (ALS) is incompletely understood.

78 s who are diagnosed with amyotrophic lateral sclerosis (ALS) today face the same historically intrans

79 inding protein FUS cause amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease

80 ted in playing a role in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characteriz

81 ke, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), and other neuroinflammatory conditions,

82 metabolism is altered in amyotrophic lateral sclerosis (ALS), as early as childhood, suggesting these

83 ron (MN) degeneration in amyotrophic lateral sclerosis (ALS), but actual proof of hyperexcitation in

84 usceptibility factor for amyotrophic lateral sclerosis (ALS), but results are conflicting and at risk

85 In amyotrophic lateral sclerosis (ALS), immune cells and glia contribute to mot

86 , we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant s

87 ase (CKD), epilepsy, and amyotrophic lateral sclerosis (ALS), mantis-ml achieved an average area unde

88 m (CNS) diseases such as amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Parkinson's dis

89 ive ventilation (NIV) in amyotrophic lateral sclerosis (ALS), the question of enteral nutrition is in

90 ivity in pathogenesis of amyotrophic lateral sclerosis (ALS), we generated transgenic mice with neuro

91 dition, expression of an amyotrophic lateral sclerosis (ALS)-associated superoxide dismutase 1 (SOD1)

92 al therapeutic target in amyotrophic lateral sclerosis (ALS).

93 monest cause of familial amyotrophic lateral sclerosis (ALS).

94 ly conserved features in amyotrophic lateral sclerosis (ALS).

95 ndividuals with sporadic amyotrophic lateral sclerosis (ALS).

96 degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).

97 ammation is important in amyotrophic lateral sclerosis (ALS).

98 associated with familial amyotrophic lateral sclerosis (ALS).

99 ontribute to the risk of amyotrophic lateral sclerosis (ALS).

100 tive diseases, including amyotrophic lateral sclerosis (ALS).

101 ubgroup of patients with amyotrophic lateral sclerosis (ALS)/Frontotemporal dementia (FTD), the (G4C2

102 common genetic cause of amyotrophic lateral sclerosis (ALS)/frontotemporal dementia (FTD).

103 = 54.2 +/- 9.6) with long-standing multiple sclerosis and 48 healthy controls (age = 50.8 +/- 7.0) w

104 cal lesions represent a hallmark of multiple sclerosis and are proposed as a predictor of disease sev

105 implications for disorders, such as multiple sclerosis and CNS injury.SIGNIFICANCE STATEMENT Cuprizon

106 Multiple sclerosis and experimental autoimmune encephalomyelitis

107 ormal physiology, and in amyotrophic lateral sclerosis and frontotemporal degeneration.

108 eases, including C9orf72 Amyotrophic Lateral Sclerosis and Frontotemporal Dementia (ALS/FTD).

109 a main cause of familial amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD).

110 iant that contributes to amyotrophic lateral sclerosis and frontotemporal dementia(1,2).

111 eatment of rheumatoid arthritis and multiple sclerosis and is re-emerging as an attractive target for

112 conditions within the CNS, such as multiple sclerosis and its animal model, experimental autoimmune

113 itional skin score in patients with systemic sclerosis and may additionally aid in the monitoring of

114 ntotemporal dementia and amyotrophic lateral sclerosis and no mutation in known amyotrophic lateral s

115 a sudden death (primary cause) with multiple sclerosis and obesity listed as secondary causes.

116 eral neurological diseases, such as multiple sclerosis and Parkinson's disease.

117 evelopment or in adulthood, such as multiple sclerosis and peripheral neuropathies, lead to severe pa

118 mechanistic link between amyotrophic lateral sclerosis and spinal muscular atrophy (SMA), and 3 mutat

119 Subchondral sclerosis and subchondral cysts were graded as present o

120 le of human patients diagnosed with systemic sclerosis and to an experiment that examined multiple lo

121 develop therapeutic modalities for multiple sclerosis and, indeed, has provided insight in modern dr

122 and IL-13 inhibition for amyotrophic lateral sclerosis) and influences on longevity (leukemia inhibit

123 hetic CT (sCT) in the depiction of erosions, sclerosis, and ankylosis of the SI joints compared with

124 in injury, Alzheimer's disease, and multiple sclerosis, and evaluated for their diagnostic performanc

125 se, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease.

126 myotrophic lateral sclerosis (ALS), multiple sclerosis, and Parkinson's disease, peripheral nervous s

127 the profound burden of progressive multiple sclerosis, and the recent development of effective treat

128 ntotemporal dementia and amyotrophic lateral sclerosis are clinically and pathologically overlapping

129 urbances in episodic memory, and hippocampal sclerosis are common in temporal lobe epilepsy (TLE), bu

130 HC-clinically isolated syndrome for multiple sclerosis BAC = 56.7%).

131 n accessibility of genes involved in lateral sclerosis, basal transcription factors, and folate metab

132 apies will be ready for people with multiple sclerosis, but there is a real sense of hope that resear

133 ive prognostic factor in amyotrophic lateral sclerosis, but there is no evidence regarding whether a

134 Relapses in multiple sclerosis can result in irreversible nervous system tiss

135 , CNS infection (viral and fungal), multiple sclerosis, cerebral ischemia, and cerebral malaria.

136 dities have a deleterious impact on multiple sclerosis clinical outcomes but it is unclear whether th

137 From the Amsterdam multiple sclerosis cohort, 133 patients (age = 54.2 +/- 9.6) with

138 elops in 70 to 90% of children with tuberous sclerosis complex (TSC) and is often resistant to medica

139 ient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) and other genetic disorders.

140 Tuberous Sclerosis Complex (TSC) is a complex and heterogeneous g

141 Tuberous sclerosis complex (TSC) is a potent inhibitor of TORC1.

142 Tuberous sclerosis complex (TSC) is a rare autosomal dominant neu

143 Tuberous sclerosis complex (TSC) is an autosomal dominant disease

144 The Tuberous Sclerosis Complex (TSC) protein complex (TSCC), comprisi

145 seizure reduction in patients with tuberous sclerosis complex (TSC), a disease with overactivated me

146 ive Rheb activation through loss of tuberous sclerosis complex subunit 2 (TSC2) exploit the PLD-PA pa

147 e matter lesions from patients with multiple sclerosis corroborate the function of this pathway durin

148 ypes (Alzheimer disease, amyotrophic lateral sclerosis, depression, insomnia, intelligence, neurotici

149 Effective biomarkers for multiple sclerosis diagnosis, assessment of prognosis, and treatm

150 ces of 23 patients with progressive multiple sclerosis directly after autopsy, at 3 T, using T1 and p

151 capable of identifying progressive multiple sclerosis early in the disease course.

152 itis while taking amantadine, and a multiple sclerosis exacerbation requiring hospital admission whil

153 rticofugal hypothesis of amyotrophic lateral sclerosis experimentally.

154 other and placebo in patients with multiple sclerosis fatigue.

155 MRI identified enhanced lesions in multiple sclerosis from images from unenhanced multiparametric MR

156 progressive, 31 primary progressive multiple sclerosis) from eight sites.

157 rrence within neurons in amyotrophic lateral sclerosis, frontotemporal dementia, and other neurodegen

158 rative diseases, such as amyotrophic lateral sclerosis, frontotemporal lobar degeneration, and Alzhei

159 Parkinson's disease and amyotrophic lateral sclerosis/frontotemporal dementia/myopathy, respectively

160 n the total score on the Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R; ran

161 Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised item scores fr

162 temporal dementia and/or amyotrophic lateral sclerosis genes (TBK1, OPTN and SQSTM1) suggests that it

163 ntotemporal dementia and amyotrophic lateral sclerosis genes, including TBK1, OPTN and SQSTM1, result

164 y statistics from the International Multiple Sclerosis Genetics Consortium (IMSGC) meta-analysis, inc

165 l vessel disease scores and, in the multiple sclerosis group, the relationship between multiple scler

166 EAT), vascular malformation, and hippocampal sclerosis had the best seizure outcome at 2 years after

167 In late disease stages, subchondral bone sclerosis has been linked to heightened osteogenic commi

168 The treatment of multiple sclerosis has been transformed by the successful develop

169 ent years, new imaging findings for multiple sclerosis have been described, and new evidence about th

170 nes and risk factors for amyotrophic lateral sclerosis have been identified.

171 ease-modifying therapy in relapsing multiple sclerosis have substantially increased over the past dec

172 ications for alleviating fatigue in multiple sclerosis; however, the evidence supporting their effica

173 Hippocampal sclerosis (HS) is a common histopathological abnormality

174 an exome-wide association study of systemic sclerosis in a Han Chinese population.

175 y of MD1003 in progressive forms of multiple sclerosis in a larger, more representative patient cohor

176 IL-4) suppresses the development of multiple sclerosis in a murine model of experimental autoimmune e

177 ECM differences suggest that glomerular sclerosis in cFSGS differs from that in other FSGS varia

178 ealed three signals associated with systemic sclerosis in Han Chinese and suggested the importance of

179 subset and implicates it in subchondral bone sclerosis in hip OA.

180 Minocycline reduced conversion to multiple sclerosis in patients with a clinically isolated syndrom

181 most pronounced in patients with hippocampal sclerosis in the ipsilateral parahippocampal cingulum an

182 tion for the treatment of relapsing multiple sclerosis including active secondary progressive multipl

183 Multiple sclerosis is a chronic inflammatory disease characterize

184 Multiple sclerosis is a chronic, demyelinating disease of the CNS

185 autoimmunity.SIGNIFICANCE STATEMENT Multiple sclerosis is an autoimmune neuroinflammatory disorder, b

186 , studying mitochondrial changes in multiple sclerosis is hampered by a paucity of non-invasive techn

187 Chronic disability in multiple sclerosis is linked to neuroaxonal degeneration.

188 Amyotrophic lateral sclerosis is the most common degenerative disorder of mo

189 he identification of progression in multiple sclerosis is typically retrospective.

190 immunomodulatory drug for treating multiple sclerosis, is an agonist of sphingosine-1-phosphate rece

191 f patients with primary progressive multiple sclerosis, laquinimod also did not reach the primary end

192 might play a role in the amyotrophic lateral sclerosis-linked aggregation of SOD1.

193 in schizophrenia, bipolar disorder, multiple sclerosis, mild cognitive impairment, dementia, and Park

194 Patients diagnosed with multiple sclerosis, minimum 1-year exposure to treatment, minimum

195 one of the four types of classic HL (nodular sclerosis, mixed cellularity, lymphocyte-depleted or lym

196 ve with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neur

197 is activated in oligodendrocytes in multiple sclerosis (MS) and its animal model experimental autoimm

198 system (CNS) in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoim

199 t of brain inflammation, notably in multiple sclerosis (MS) and its experimental autoimmune encephalo

200 epletion in patients with relapsing multiple sclerosis (MS) and primary progressive MS has led to a c

201 n changes detected in patients with multiple sclerosis (MS) and the degree of thalamic atrophy is a s

202 Clinical outcomes in multiple sclerosis (MS) are highly variable.

203 cines that promote remyelination in multiple sclerosis (MS) are making the transition from laboratory

204 s with regulatory approval to treat multiple sclerosis (MS) are unable to prevent inflammatory tissue

205 plexiform layer (GCIPL) thinning in multiple sclerosis (MS) attributable to normal aging increased fr

206 Recent advances in multiple sclerosis (MS) diagnostic criteria have expanded the num

207 Epidemiological research in multiple sclerosis (MS) has mainly been performed in socioeconomi

208 modifying therapies for people with multiple sclerosis (MS) have recently gained marketing approval.

209 Multiple sclerosis (MS) is a chronic autoimmune disease of the ce

210 Multiple sclerosis (MS) is a chronic autoimmune disease of the CN

211 Multiple sclerosis (MS) is a chronic demyelinating disease of the

212 Multiple sclerosis (MS) is a heterogeneous inflammatory demyelina

213 Multiple sclerosis (MS) is a neurological disease with a substant

214 Multiple sclerosis (MS) is an inflammatory demyelinating disorder

215 Disability in multiple sclerosis (MS) is considered primarily a result of axona

216 ly used method for the diagnosis of multiple sclerosis (MS) that is essential for the detection and f

217 hy volunteers and participants with multiple sclerosis (MS) underwent MRI between November 2018 and O

218 e strongest genetic risk factor for multiple sclerosis (MS), but our understanding of how it contribu

219 er damage since the early stages of multiple sclerosis (MS), but whether the cerebrospinal fluid (CSF

220 emyelination is a high priority for multiple sclerosis (MS), due to their potential for neuroprotecti

221 ases, including relapsing-remitting multiple sclerosis (MS), in which increased IFN responses result

222 ), traumatic brain injuries (TBIs), multiple sclerosis (MS), intracerebral hemorrhage (ICH), and neur

223 Background In multiple sclerosis (MS), knowledge about how spinal cord abnormal

224 ne encephalomyelitis (EAE) model of multiple sclerosis (MS), no one has yet examined the important cl

225 During the natural course of multiple sclerosis (MS), the brain is exposed to aging as well as

226 which are pathological features of multiple sclerosis (MS), the most common disabling neurological d

227 and in demyelinating diseases like multiple sclerosis (MS), where failure of remyelination promotes

228 rsening disability in patients with multiple sclerosis (MS).

229 evealing topological alterations in multiple sclerosis (MS).

230 omyelitis (EAE), an animal model of multiple sclerosis (MS).

231 key players in the pathogenesis of multiple sclerosis (MS).

232 t of autoimmune diseases, including multiple sclerosis (MS).

233 during autoimmune diseases such as Multiple Sclerosis (MS).

234 althy volunteers, and patients with multiple sclerosis (MS).

235 nated as a susceptibility locus for multiple sclerosis (MS).

236 ne encephalomyelitis (EAE) model of multiple sclerosis (MS).

237 ptomatic treatment of patients with multiple sclerosis (MS).

238 l-mediated autoimmunity that mimics multiple sclerosis (MS).

239 is a highly effective treatment for multiple sclerosis (MS).

240 al role in explaining disability in multiple sclerosis (MS): Lesion-induced damage in the lateral fun

241 lls have several potential roles in multiple sclerosis (MS): secretors of proinflammatory cytokines a

242 spective study of 560 patients with multiple sclerosis (MS, n = 147), rheumatoid arthritis (RA, n = 2

243 dy included patients (n = 212) with multiple sclerosis (MS; n = 418 eyes), 59 healthy controls (HCs;

244 brain material from a subset of the multiple sclerosis (n = 42; age range 39-84 years, median 61.5 ye

245 nts: temporal lobe epilepsy with hippocampal sclerosis (n = 599), temporal lobe epilepsy with normal

246 in patients more than 3 years from multiple sclerosis onset.

247 and no mutation in known amyotrophic lateral sclerosis or dementia genes.

248 s, potentially mimicking amyotrophic lateral sclerosis or distal hereditary motor neuropathy (56%), m

249 h the risk of developing amyotrophic lateral sclerosis or frontotemporal dementia, or to slow progres

250 etiology of CNS diseases including multiple sclerosis, Parkinson's disease and amyotrophic lateral s

251 remitting, 15 secondary progressive multiple sclerosis participants and 11 age-matched healthy contro

252 iple roles of kinases in amyotrophic lateral sclerosis pathogenesis.

253 ggested the importance of LRP2BP in systemic sclerosis pathogenesis.

254 ebral small vessel disease or worse multiple sclerosis pathology.

255 oth the acute and chronic phases of multiple sclerosis pathophysiology.

256 ts on two datasets corresponding to multiple sclerosis patients treated with interferon are included

257 by microperimetry was decreased in multiple sclerosis patients with normal visual acuity and no hist

258 elination.SIGNIFICANCE STATEMENT In multiple sclerosis patients, demyelination progresses with aging

259 sticity in stroke, brain injury and multiple sclerosis patients, who are often undergoing concurrent

260 s to explain physical disability in multiple sclerosis patients, with a predominant impact of intrame

261 natalizumab in relapsing-remitting multiple sclerosis patients.

262 Primary lateral sclerosis (PLS) is a neurodegenerative disorder of the a

263 a (IFN beta-1a) in paediatric-onset multiple sclerosis (PoMS).

264 ct of HCFD for the whole amyotrophic lateral sclerosis population.

265 ed diagnosis of primary progressive multiple sclerosis (PPMS) is uncertain.

266 immune diseases (such as arthritis, multiple sclerosis, psoriasis, inflammatory bowel disease, among

267 Data from two multiple sclerosis registries, MSBase (multinational) and OFSEP (

268 sis group, the relationship between multiple sclerosis-related pathology and both vascular scores.

269 try in the detection of subclinical multiple sclerosis-related retinal damage and visual dysfunction.

270 reduced efficiency and integrity in multiple sclerosis relative to healthy controls (both P < 0.05).

271 Parkinson's disease and amyotrophic lateral sclerosis remains elusive despite decades of research re

272 hysical disability in patients with multiple sclerosis remains modest.

273 nic conditions in humans, including multiple sclerosis, rheumatoid arthritis, type-I diabetes, and ca

274 ent response in relapsing-remitting multiple sclerosis (RRMS) are lacking.

275 transition from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive MS (SPMS) repr

276 tinguished from relapsing-remitting multiple sclerosis (RRMS).

277 Subjects with relapsing-remitting multiple sclerosis showed a greater predominance of spinal cord l

278 me, an MRC and NIHR partnership, UK Multiple Sclerosis Society, and US National Multiple Sclerosis So

279 Sclerosis Society, and US National Multiple Sclerosis Society.

280 tions are more severely affected by multiple sclerosis-specific damage than short-range connections.

281 f genetic risk loci associated with systemic sclerosis (SSc) and Crohn's disease (CD), some of which

282 curs in virtually all patients with systemic sclerosis (SSc) and is often the earliest clinical manif

283 The autoimmune disease systemic sclerosis (SSc) causes microvascular changes that can be

284 Systemic sclerosis (SSc) is a complex, multiorgan, autoimmune dis

285 the fibrotic process is limited in systemic sclerosis (SSc).

286 rey and white matter from the early multiple sclerosis stages and occur mostly independent from brain

287 ed with diseases such as amyotrophic lateral sclerosis, stroke, and cancer.

288 toimmune encephalomyelitis model of multiple sclerosis, TAGAP deficient mice develop significantly at

289 We identified astrocytes in EAE and multiple sclerosis that were characterized by decreased expressio

290 discovered, using a mouse model of multiple sclerosis, that the transfusion of autologous regulatory

291 tion introduced to the treatment of multiple sclerosis, the question of how to select and sequence di

292 ly assigned patients with relapsing multiple sclerosis to receive subcutaneous ofatumumab (20 mg ever

293 is already licensed for symptomatic multiple sclerosis treatment, we performed a retrospective, multi

294 Multiple sclerosis treatments (n = 4) had the greatest increases

295 f patients with sporadic amyotrophic lateral sclerosis (up to 97%) and a substantial proportion of pa

296 evalence of cognitive impairment in multiple sclerosis varies across the lifespan and might be diffic

297 combined CSF and plasma markers for multiple sclerosis were 85.7% and 73.5%, respectively.

298 ed with autoimmune diseases such as multiple sclerosis, which has no curative treatment.

299 ation in normal-appearing tissue in multiple sclerosis, which is associated with both cognitive and c

300 5 years) with secondary progressive multiple sclerosis who were not on disease-modifying treatment an