ライフサイエンスコーパス: sclerosis

1 he treatment of relapsing-remitting multiple sclerosis.

2 temporal lobe epilepsy with mesial temporal sclerosis.

3 elapse rates in relapsing-remitting multiple sclerosis.

4 pathology or therapeutic effects in multiple sclerosis.

5 that is associated with amyotrophic lateral sclerosis.

6 is the most-studied animal model of multiple sclerosis.

7 pathology of FUS-related amyotrophic lateral sclerosis.

8 eurodegenerative diseases including multiple sclerosis.

9 the treatment of relapsing forms of multiple sclerosis.

10 tive and viable immunotherapies for multiple sclerosis.

11 s found with Parkinson's disease or multiple sclerosis.

12 ificant predictors of conversion to multiple sclerosis.

13 icates vitamin D in the etiology of multiple sclerosis.

14 in primary T cells of patients with systemic sclerosis.

15 t an environmental consideration in multiple sclerosis.

16 g function implicated in amyotrophic lateral sclerosis.

17 kinson's disease, and 9247 cases of multiple sclerosis.

18 ties approved for use in amyotrophic lateral sclerosis.

19 acute graft-versus-host disease and multiple sclerosis.

20 utic targets for mitigating pain in multiple sclerosis.

21 tis, celiac disease, psoriasis, and multiple sclerosis.

22 ibility in an inflammatory model of multiple sclerosis.

23 e in demyelinating diseases such as multiple sclerosis.

24 rs are implicated in dysimmunity in multiple sclerosis.

25 hort of patients in early stages of multiple sclerosis.

26 lasia, Mohr-syndrome and amyotrophic lateral sclerosis.

27 ome, inflammatory bowel disease and multiple sclerosis.

28 nduction akin to muscle weakness in multiple sclerosis.

29 olved in several diseases including multiple sclerosis.

30 flammation and neurodegeneration in multiple sclerosis.

31 dementia, Parkinson's disease, and multiple sclerosis.

32 , and genetic causes that can mimic multiple sclerosis.

33 d-like fibrils linked to amyotrophic lateral sclerosis.

34 eloid cells and in a mouse model of multiple sclerosis.

35 a clinically isolated syndrome) to multiple sclerosis.

36 Huntington disease, and amyotrophic lateral sclerosis.

37 te as a treatment for patients with multiple sclerosis.

38 of chronic demyelinating injury in multiple sclerosis.

39 cells influence the pathogenesis of multiple sclerosis.

40 Administration to treat refractory multiple sclerosis.

41 f genes involved in pathogenesis of systemic sclerosis.

42 omyelitis (EAE) and, ostensibly, in multiple sclerosis.

43 muscular dystrophy, and amyotrophic lateral sclerosis.

44 ients developed clinically definite multiple sclerosis.

45 critical impediment to recovery in multiple sclerosis.

46 ater stages can resemble amyotrophic lateral sclerosis.

47 of the motor function in amyotrophic lateral sclerosis.

48 but not with Parkinson's disease or multiple sclerosis.

49 testinal-related illness (5 cases), multiple sclerosis (3 cases), sepsis (3 cases), and Lyme disease

50 had cancer, 79 (8%) had amyotrophic lateral sclerosis, 44 (4.5%) had lung disease, 26 (2.6%) had hea

51 and typical of relapsing-remitting multiple sclerosis, a complete neurological examination, a baseli

52 and tested their effect on risk of multiple sclerosis, a disease influenced by low vitamin D concent

53 were related to ADHD in offspring: multiple sclerosis (adjusted odds ratio [OR] = 1.8; 95% confidenc

54 uorescence, including in amyotrophic lateral sclerosis-affected cranial nerve motor nuclei but not in

55 he exception of microinfarcts and arteriolar sclerosis, all neuropathologies were associated with the

56 mutated in patients with amyotrophic lateral sclerosis (ALS) [5, 6].

57 symptom in patients with amyotrophic lateral sclerosis (ALS) although it is reported by most of these

58 y found in patients with amyotrophic lateral sclerosis (ALS) and developmental delay, intellectual di

59 such as those that cause amyotrophic lateral sclerosis (ALS) and fragile X syndrome, is challenging f

60 Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) share

61 ue of most cases of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

62 common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the

63 tive diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

64 d to the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

65 d in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Lobar Dementia (FTLD)

66 inflammatory reaction in amyotrophic lateral sclerosis (ALS) and is toxic for motor neurons.

67 corticospinal neurons in amyotrophic lateral sclerosis (ALS) and to neocortical hyperexcitability, a

68 logical underpinnings of amyotrophic lateral sclerosis (ALS) are complex and incompletely understood,

69 In trying to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-

70 Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is chara

71 Amyotrophic lateral sclerosis (ALS) is a devastating and incurable neurodege

72 Amyotrophic lateral sclerosis (ALS) is a heterogeneous degenerative motor ne

73 Amyotrophic lateral sclerosis (ALS) is a multifactorial lethal motor neuron

74 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative condi

75 Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerativ

76 Amyotrophic lateral sclerosis (ALS) is debilitating neurodegenerative diseas

77 Amyotrophic lateral sclerosis (ALS) may be associated with low body mass ind

78 cause familial forms of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characteriz

79 y reliable biomarkers of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease

80 ury, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease.

81 common cause of familial amyotrophic lateral sclerosis (ALS), but the mechanisms underlying repeat-in

82 ct (PBA) is prevalent in amyotrophic lateral sclerosis (ALS), but there is limited information on its

83 cular disorders, such as amyotrophic lateral sclerosis (ALS), end life via respiratory failure, the a

84 temporal dementia (FTD), amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), progress

85 eimer disease (LOAD) and amyotrophic lateral sclerosis (ALS), two major neurodegenerative diseases, i

86 n is a major hallmark of amyotrophic lateral sclerosis (ALS), which is currently untreatable.

87 mitochondrial defects in Amytrophic Lateral Sclerosis (ALS)- and Alzheimer's disease (AD)-linked neu

88 nclusions is promoted by amyotrophic lateral sclerosis (ALS)-linked mutations, but the cellular funct

89 suffering from advanced amyotrophic lateral sclerosis (ALS)-two of them in permanent CLIS and two en

90 opathological feature of amyotrophic lateral sclerosis (ALS).

91 eurodegenerative disease amyotrophic lateral sclerosis (ALS).

92 mice, a mouse model for amyotrophic lateral sclerosis (ALS).

93 encoding SOD1 all cause amyotrophic lateral sclerosis (ALS).

94 physiological markers of amyotrophic lateral sclerosis (ALS).

95 n the pathophysiology of amyotrophic lateral sclerosis (ALS).

96 predictor of survival in amyotrophic lateral sclerosis (ALS).

97 cyte and mouse models of amyotrophic lateral sclerosis (ALS).

98 d (CSF) of patients with amyotrophic lateral sclerosis (ALS).

99 set degenerative disease amyotrophic lateral sclerosis (ALS).

100 such as stroke, spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and Alzh

101 are key players in the pathology of multiple sclerosis and can assume beneficial and detrimental role

102 mer's disease, Parkinson's disease, multiple sclerosis and cardiovascular disease.

103 ces between the eyes of people with multiple sclerosis and control eyes were found in the peripapilla

104 we review the clinical features of systemic sclerosis and describe the best practice approaches for

105 t conversion to clinically definite multiple sclerosis and disability.

106 In conclusion, we identified segmental sclerosis and extracapillary hypercellularity as novel,

107 common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD).

108 t known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia.

109 of patients with diffuse cutaneous systemic sclerosis and identified differentially expressed protei

110 In the autoimmune disease multiple sclerosis and its animal model, experimental autoimmune

111 e in autoimmune diseases, including multiple sclerosis and its animal model, experimental autoimmune

112 us of cell-based therapies to treat multiple sclerosis and make consensus recommendations for future

113 inical targets for the treatment of multiple sclerosis and other autoimmune disorders.

114 t status of therapy for progressive multiple sclerosis and outline prospects for the future.

115 or C. elegans models for amyotrophic lateral sclerosis and Parkinson's disease, and show a partial re

116 a-synuclein, involved in amyotrophic lateral sclerosis and Parkinson's disease, respectively, using t

117 plications for vitamin D biology in multiple sclerosis and perhaps other autoimmune diseases as well.

118 rus translate to the severity of hippocampal sclerosis and seizure burden in chronic epilepsy.

119 age degradation, less subchondral bone plate sclerosis and smaller osteophytes.

120 ce along with increased segmental and global sclerosis and/or collapse of juxtamedullary glomeruli, m

121 n in human diseases such as cancer, multiple sclerosis, and fibromyalgia.

122 effects of exercise in people with multiple sclerosis, and the absence of a conceptual framework and

123 une diseases such as Crohn disease, multiple sclerosis, and ulcerative colitis and hereby elucidate t

124 factor (BAFF), was associated with multiple sclerosis as well as SLE.

125 ether spread of a mutant amyotrophic lateral sclerosis-associated cytosolic superoxide dismutase 1 (S

126 50K and M98K, but not an amyotrophic lateral sclerosis-associated mutant, E478G, induced cell death s

127 data on eyes into healthy controls, multiple-sclerosis-associated optic neuritis (MSON), and multiple

128 otor unit dismantling in amyotrophic lateral sclerosis at late disease stage.

129 nsive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital.

130 linical attack (clinically definite multiple sclerosis) at months 36 and 60.

131 nation and neurodegeneration in the multiple sclerosis brain and are thought to play a central role i

132 tem imaging and histopathology in 9 multiple sclerosis brain donors.

133 isease spontaneously separated from multiple sclerosis but overlapped with AQP4 antibody disease.

134 erwent randomization at 12 Canadian multiple sclerosis clinics; 72 participants were assigned to the

135 ged 20-50 years (about 4.4 million; multiple sclerosis cohort) and all adults aged 55-85 years (about

136 elds were highest for children with tuberous sclerosis complex (9 of 11 [81.8%]), metabolic diseases

137 harbor mTOR-activating mutations in tuberous sclerosis complex (TSC) genes, and recruit abundant stro

138 Tuberous sclerosis complex (TSC) is a pediatric disorder of dysre

139 Tuberous sclerosis complex (TSC) is an autosomal dominant tumor-s

140 ion abnormalities are a hallmark of tuberous sclerosis complex (TSC) manifestations; however, the gen

141 Loss of the tuberous sclerosis complex (TSC) tumor suppressors results in act

142 suppressors Tsc1 and Tsc2 form the tuberous sclerosis complex (TSC), a regulator of mTOR activity.

143 w interactions between R2TP and the tuberous sclerosis complex (TSC), pointing to a potential link be

144 rodevelopmental disorders including tuberous sclerosis complex (TSC).

145 spectrum disorders (ASD), including tuberous sclerosis complex (TSC).

146 To test this, we used cells lacking tuberous sclerosis complex 2 (TSC2(-/-) cells), which show consti

147 ctivation of mTORC1 by depletion of tuberous sclerosis complex 2 (TSC2) inhibits lipophagy induction

148 /Cas9-mediated genetic knock-out of tuberous sclerosis complex-2 (Tsc2) blocked the IL-4-dependent ex

149 nk and extremities of patients with tuberous sclerosis complex.

150 onald and 2016 MAGNIMS criteria for multiple sclerosis diagnosis in a large multicentre cohort of pat

151 vide evidence to guide revisions of multiple sclerosis diagnostic criteria.

152 mune encephalomyelitis, a model for multiple sclerosis, even in myelin regions that appear morphologi

153 sis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemt

154 e causative for familial amyotrophic lateral sclerosis (fALS).

155 tions linked to familial amyotrophic lateral sclerosis (fALS/SOD1).

156 The most common categories were hippocampal sclerosis, found in 36.4% of the patients (88.7% of case

157 However, in participants with multiple sclerosis, fractional anisotropy decreased and mean diff

158 on, which degenerates in amyotrophic lateral sclerosis from the early disease stage.

159 d patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts.

160 ncreased accuracy in distinguishing multiple sclerosis from these disorders, but misdiagnosis can occ

161 tive diseases, including amyotrophic lateral sclerosis, frontotemporal lobar dementia, and Alzheimer'

162 r histocompatibility complex-linked systemic sclerosis genetics, we performed genotyping of major his

163 thin the HLA region are observed for nodular sclerosis Hodgkin lymphoma (rs9269081, HLA-DPB1*03:01, V

164 rom the earliest clinical stages of multiple sclerosis; (ii) they occur independent of white matter l

165 2 patients with primary progressive multiple sclerosis in a 2:1 ratio to receive intravenous ocrelizu

166 uctural MRI biomarkers reflect the extent of sclerosis in human hippocampi.

167 and time (DIT) for the diagnosis of multiple sclerosis in patients with clinically isolated syndrome

168 l-being in patients with amyotrophic lateral sclerosis-induced locked-in state and their next of kin

169 Multiple sclerosis is a degenerative inflammatory disease of the

170 Multiple sclerosis is a major cause of neurological disability, w

171 Amyotrophic lateral sclerosis is a progressive neurodegenerative disease of

172 Systemic sclerosis is an autoimmune disease characterized by fibr

173 Systemic sclerosis is an autoimmune disease characterized by T-ce

174 Systemic sclerosis is an orphan, systemic autoimmune disease with

175 The diagnosis of multiple sclerosis is based on neurological symptoms and signs, a

176 ethal complications associated with systemic sclerosis is substantial and is likely to become more of

177 One major challenge in multiple sclerosis is to understand the cellular and molecular me

178 sfer ratio gradient occurs early in multiple sclerosis, is clinically relevant, and may arise from on

179 0/fingolimod, used for treatment of multiple sclerosis, is phosphorylated by nuclear sphingosine kina

180 We examined multiple sclerosis lesions and other central nervous system patho

181 d HTB1M) of two familial amyotrophic lateral sclerosis-linked SOD1 mutants, SOD1(G93A) and SOD1(G85R)

182 , the Magnetic Resonance Imaging in Multiple Sclerosis (MAGNIMS) network proposed modifications to th

183 ng of lesions and immune cells in a multiple sclerosis mouse model.

184 tinal architecture in patients with multiple sclerosis (MS) and corresponding alterations in the mela

185 yer (RNFL) changes in patients with multiple sclerosis (MS) and healthy controls with a 5-year follow

186 inically isolated syndrome (CIS) to multiple sclerosis (MS) and MS activity and disability.

187 crucial role in the progression of multiple sclerosis (MS) and other neurodegenerative diseases.

188 long-term outcomes in patients with multiple sclerosis (MS) and to assign patients to individual trea

189 MicroRNAs (miRNAs) are promising multiple sclerosis (MS) biomarkers.

190 uantify peripheral nerve lesions in multiple sclerosis (MS) by magnetic resonance neurography (MRN).

191 ical trials testing the efficacy of multiple sclerosis (MS) disease-modifying drugs) at a genome-wide

192 ncurrent or subsequent diagnosis of multiple sclerosis (MS) from a population-based cohort (n=30).

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

194 Multiple sclerosis (MS) is a common autoimmune disease that targe

195 Multiple sclerosis (MS) is a disease that is characterized by imm

196 Multiple sclerosis (MS) is an autoimmune disease of the central n

197 Multiple sclerosis (MS) is an autoimmune inflammatory demyelinati

198 n MS and EAE.SIGNIFICANCE STATEMENT Multiple sclerosis (MS) is an inflammatory demyelinating disease

199 Multiple Sclerosis (MS) is an inflammatory demyelinating disorder

200 Multiple sclerosis (MS) is caused by immune-mediated damage of my

201 t Id2 are increased in demyelinated multiple sclerosis (MS) lesions.

202 al-appearing white matter (NAWM) of multiple sclerosis (MS) patients using PET.

203 lated syndrome (pCIS) suggestive of multiple sclerosis (MS) patients.

204 he high female-to-male sex ratio of multiple sclerosis (MS) prevalence has continuously confounded re

205 Despite continuous interest in multiple sclerosis (MS) research, there is still a lack of neurop

206 studies have shown that people with multiple sclerosis (MS) suffer from increased morbidity and morta

207 ed (IPS) impairment associated with multiple sclerosis (MS) that might result from functional disconn

208 ional connectivity abnormalities in multiple sclerosis (MS) to explore their impact on balance impair

209 In multiple sclerosis (MS), a chronic inflammatory and degenerative

210 n is a common and severe symptom in multiple sclerosis (MS), a chronic inflammatory and demyelinating

211 ished environmental risk factor for Multiple Sclerosis (MS), a chronic inflammatory and neurodegenera

212 rive the development of progressive multiple sclerosis (MS), although inflammatory factors, such as m

213 bacteria impact the pathogenesis of multiple sclerosis (MS), an autoimmune disorder of the CNS and th

214 ciation between age at menarche and multiple sclerosis (MS), and results are conflicting.

215 h very similar clinical features to multiple sclerosis (MS), but the international diagnostic imaging

216 ccurs in the demyelinating disorder multiple sclerosis (MS), contributes to axonal dysfunction and ne

217 ccur frequently in individuals with multiple sclerosis (MS), either as the initial presenting complai

218 trate of irreversible disability in multiple sclerosis (MS), is a recognized feature of MS cortical p

219 In the chronic inflammatory disease multiple sclerosis (MS), reports on lipoprotein level alterations

220 act neurological diseases including multiple sclerosis (MS), stroke, and Alzheimer's disease.

221 on of CLEC12A in an animal model of multiple sclerosis (MS), we administered blocking antibody to CLE

222 tis (EAE), an animal model of human multiple sclerosis (MS).

223 filtration in an EAE mouse model of multiple sclerosis (MS).

224 y (Simoa) serum NfL (sNfL) assay in multiple sclerosis (MS).

225 ation, in the demyelinating disease multiple sclerosis (MS).

226 eral autoimmune diseases, including multiple sclerosis (MS).

227 y of neurological diseases, such as multiple sclerosis (MS).

228 rototypic neuroinflammatory disease multiple sclerosis (MS).

229 r disease activity in patients with multiple sclerosis (MS).

230 l spastic paraparesis (HAM/TSP) and multiple sclerosis (MS).

231 t of demyelinating diseases such as multiple sclerosis (MS).SIGNIFICANCE STATEMENT Myelin loss and su

232 ere identified as a risk factor for Multiple Sclerosis (MS); however, the potential biological releva

233 onditions affecting humans, such as multiple sclerosis, neuromyelitis optica spectrum disorders, Park

234 ases, including ataxias, amyotrophic lateral sclerosis, nucleotide expansion disorders (Friedreich at

235 tions can be clearly separated from multiple sclerosis on conventional brain imaging, both in adults

236 tic diagnosis, and FSGS or diffuse mesangial sclerosis on initial biopsy as well as age, serum albumi

237 One patient was diagnosed with multiple sclerosis, one with cortical dysplasia, one with pineal

238 as Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease

239 ing Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and the prototypic neuro

240 sociated genes might be critical in systemic sclerosis pathogenesis.

241 radigm by grafting healthy donor or multiple sclerosis patient lymphocytes in the demyelinated lesion

242 n biopsy-derived RNAs from 14 early systemic sclerosis patients and six healthy individuals were sequ

243 ment of relapse/remission cycles in multiple sclerosis patients by providing information currently in

244 e cerebrospinal fluid of amyotrophic lateral sclerosis patients in early disease stage.

245 s are deregulated in skin tissue of systemic sclerosis patients suggesting a novel class of genes inv

246 nctional at the epigenetic level in systemic sclerosis patients, indicating that hypomethylation and

247 f subsequent disease progression in multiple sclerosis patients.

248 in the diagnosis and monitoring of multiple sclerosis patients.

249 (SBP), urinary albumin excretion, segmental sclerosis, podocyte injury, and apoptosis.

250 of life (QOL; based on the 54-item Multiple Sclerosis Quality of Life Scale score).

251 fective in vivo in a mouse model of multiple sclerosis, reducing clinical severity and weight loss.

252 In multiple sclerosis, remyelination can fail despite abundant oligo

253 in demyelinating disorders such as multiple sclerosis results in disability due to loss of axon cond

254 diseases, Alzheimer's disease, and multiple sclerosis revealed that autophagy and inflammasomes inte

255 ole in the onset and progression of multiple sclerosis, rheumatoid arthritis, and breast cancer.

256 f patients with relapsing remitting multiple sclerosis (RRMS) have higher replacement mutation freque

257 y be useful in classifying atypical multiple sclerosis, seronegative neuromyelitis optica spectrum di

258 t in demyelinating diseases such as multiple sclerosis.SIGNIFICANCE STATEMENT In the present study, w

259 assess changes in diffuse cutaneous systemic sclerosis skin disease over time.

260 luding a murine model of amyotrophic lateral sclerosis (SOD1G93A), middle cerebral artery occlusion,

261 patients with secondary progressive multiple sclerosis (SPMS).

262 Systemic sclerosis (SSc) is a multi-organ fibrotic disease with f

263 Systemic sclerosis (SSc) is a multisystem inflammatory and vascul

264 Systemic sclerosis (SSc) is a spreading fibrotic disease affectin

265 Skin fibrosis in systemic sclerosis (SSc) is accompanied by attrition of dermal wh

266 vasculature of <2 mm in diameter in Systemic Sclerosis (SSc) patients with (n = 17) and without (n =

267 id not differ significantly between multiple sclerosis subjects and controls.

268 anding of the immunopathogenesis of multiple sclerosis suggests that depleting B cells could be usefu

269 patients receiving natalizumab for multiple sclerosis, supporting yearly benefit-risk re-evaluation

270 more than 10 years since the first multiple sclerosis symptom.

271 Effective therapies for progressive multiple sclerosis that prevent worsening, reverse damage, and re

272 eins not previously associated with systemic sclerosis that provide insight into pathogenesis and pot

273 eposition in a progressive model of multiple sclerosis, the Theiler's murine encephalomyelitis virus-

274 tex and white matter in early stage multiple sclerosis, their distribution in lesional and normal-app

275 In established multiple sclerosis, tissue abnormality-as assessed using magnetiz

276 821 and 835 patients with relapsing multiple sclerosis to receive intravenous ocrelizumab at a dose o

277 n patients with relapsing-remitting multiple sclerosis treated for up to 5 years.

278 from skin biopsies of patients with systemic sclerosis treated with five therapies: mycophenolate mof

279 and quality of life in progressive multiple sclerosis treatment trials.

280 [the VO lead]) for the treatment of multiple sclerosis tremor.

281 on for improving severe, refractory multiple sclerosis tremor.

282 omorbid with autism - fragile X and tuberous sclerosis types 1 and 2 syndromes.

283 ropic EBV is a major risk factor in multiple sclerosis, via as yet unclear mechanisms.

284 e encephalomyelitis animal model of multiple sclerosis was assessed.

285 Multiple sclerosis was discriminated from MOG antibody disease an

286 m a clinically isolated syndrome to multiple sclerosis was significantly lower with minocycline than

287 ocal epilepsy requiring surgery, hippocampal sclerosis was the most common histopathological diagnosi

288 in advanced clinical development in multiple sclerosis, was equipotent in both assays (EC50 1.5 and 1

289 ve signature genes in patients with multiple sclerosis, we find that TH1/17 cells have elevated expre

290 dementia, Parkinson's disease, and multiple sclerosis were ascertained from provincial health admini

291 ssociated with neurodegeneration in multiple sclerosis when measured with SD-OCT.

292 henomenon seems to occur in vivo in multiple sclerosis, where it reflects the remission/relapse alter

293 eptic seizures cause progressive hippocampal sclerosis, which is associated with caspase-3 activation

294 s disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related p

295 ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neuropathy on

296 conditions were differentiated from multiple sclerosis with high accuracy.

297 hose developing clinically definite multiple sclerosis within 2 years compared to those who did not (

298 ary outcomes included conversion to multiple sclerosis within 24 months after randomization and chang

299 sociated optic neuritis (MSON), and multiple sclerosis without optic neuritis (MSNON).

300 T cells infiltrate the CNS in multiple sclerosis, yet little is known about T cell functions in