ライフサイエンスコーパス: amyotrophic lateral sclerosis

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

2 s in favor of the corticofugal hypothesis of amyotrophic lateral sclerosis.

3 A-binding prion-like protein associated with amyotrophic lateral sclerosis.

4 r FTD or a related neurodegenerative disease amyotrophic lateral sclerosis.

5 ported in neurodegenerative diseases such as amyotrophic lateral sclerosis.

6 's, Parkinson's, or Huntington's disease, or amyotrophic lateral sclerosis.

7 o form misfolded aggregates in patients with amyotrophic lateral sclerosis.

8 utations in TDP-43 are one cause of familial amyotrophic lateral sclerosis.

9 peutic approach to evaluate in patients with amyotrophic lateral sclerosis.

10 are crucial to the onset and progression of amyotrophic lateral sclerosis.

11 on the risk of Parkinson disease compared to amyotrophic lateral sclerosis.

12 ty of neurodegenerative disorders, including amyotrophic lateral sclerosis.

13 ion of RNA metabolism in the pathogenesis of amyotrophic lateral sclerosis.

14 rmal mouse tissues and a Drosophila model of amyotrophic lateral sclerosis.

15 overy in subjects with Alzheimer disease and amyotrophic lateral sclerosis.

16 es are implicated in human diseases, such as amyotrophic lateral sclerosis.

17 er, noted between the studied biomarkers and amyotrophic lateral sclerosis.

18 sed SOD1 silencing as a treatment option for amyotrophic lateral sclerosis.

19 expansion, the most common cause of familial amyotrophic lateral sclerosis.

20 nce the development of and predisposition to amyotrophic lateral sclerosis.

21 nerative diseases, including Parkinson's and amyotrophic lateral sclerosis.

22 milial form of the neurodegenerative disease amyotrophic lateral sclerosis.

23 pathogenesis of frontotemporal dementia and amyotrophic lateral sclerosis.

24 n disease, and TAR DNA-binding protein 43 in amyotrophic lateral sclerosis.

25 43 (TDP-43) have been identified in familial amyotrophic lateral sclerosis.

26 affected by pathological conditions such as amyotrophic lateral sclerosis.

27 al neuropathies, traumatic brain injury, and amyotrophic lateral sclerosis.

28 = 13), cerebrovascular diseases (1%; n = 2), amyotrophic lateral sclerosis (0.5%; n = 1) and cerebell

29 PS37A), transmembrane protein 251 (TMEM251), amyotrophic lateral sclerosis 2 (ALS2), and TMEM41B.

30 adjusted IRRs were 4.9 (95% CI, 3.5-6.9) for amyotrophic lateral sclerosis, 4.9 (95% CI, 3.1-7.7) for

31 een reported in the SOD1-G93A mouse model of amyotrophic lateral sclerosis, a disorder characterized

32 milial frontotemporal degeneration (FTD) and amyotrophic lateral sclerosis (ALS) (termed C9(+)).

33 er limb muscles of 4 patients with confirmed amyotrophic lateral sclerosis (ALS) and 6 healthy contro

34 d with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and Alzheimer's dise

35 e-onset neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS) and Alzheimer's, Hun

36 Neuroinflammation has been implicated in amyotrophic lateral sclerosis (ALS) and can be visualize

37 cortical thickness at the clinical onset of amyotrophic lateral sclerosis (ALS) and explore motor ma

38 The most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

39 e is the most common known genetic cause for amyotrophic lateral sclerosis (ALS) and frontotemporal d

40 ctor, are the most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

41 de repeat expansions (HREs) in C9orf72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal d

42 expansion (G4C2 HRE) in C9orf72 that causes amyotrophic lateral sclerosis (ALS) and frontotemporal d

43 C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

44 ORF72 is the most prevalent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

45 d GGGGCC (G(4)C(2)) repeats in C9ORF72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal d

46 brains tissues of Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and frontotemporal d

47 C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

48 ver of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal d

49 pansions account for almost half of familial amyotrophic lateral sclerosis (ALS) and frontotemporal d

50 prion-like domains (PrLDs) that aggregate in amyotrophic lateral sclerosis (ALS) and frontotemporal d

51 to fatal neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and frontotemporal d

52 In amyotrophic lateral sclerosis (ALS) and frontotemporal d

53 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

54 the overlapping neurodegenerative disorders amyotrophic lateral sclerosis (ALS) and frontotemporal d

55 de polymorphism in UNC13A is associated with amyotrophic lateral sclerosis (ALS) and frontotemporal d

56 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

57 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

58 mic aggregation is a pathogenic signature of amyotrophic lateral sclerosis (ALS) and frontotemporal d

59 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

60 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

61 The amyotrophic lateral sclerosis (ALS) and frontotemporal d

62 f72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

63 nclusions in neurodegenerative diseases like amyotrophic lateral sclerosis (ALS) and frontotemporal l

64 pathology in affected neurons of people with amyotrophic lateral sclerosis (ALS) and frontotemporal l

65 3) is found in the majority of patients with amyotrophic lateral sclerosis (ALS) and in approximately

66 Background Differential diagnosis between amyotrophic lateral sclerosis (ALS) and multifocal motor

67 disease (PD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and multiple scleros

68 Two patients with familial amyotrophic lateral sclerosis (ALS) and mutations in the

69 siological stress that is strongly linked to amyotrophic lateral sclerosis (ALS) and other neurologic

70 egation represents the defining pathology in amyotrophic lateral sclerosis (ALS) and related proteino

71 43) is a hallmark of degenerating neurons in amyotrophic lateral sclerosis (ALS) and subsets of front

72 A common pathological hallmark of amyotrophic lateral sclerosis (ALS) and the related neur

73 revalent neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) are limited, and opt

74 ination of the two compounds in persons with amyotrophic lateral sclerosis (ALS) are not known.

75 isms underlying motor neuron degeneration in amyotrophic lateral sclerosis (ALS) are yet unclear.

76 genesis of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) by analyzing whole-g

77 Patients with amyotrophic lateral sclerosis (ALS) can have abnormal TD

78 Amyotrophic lateral sclerosis (ALS) can overlap genetica

79 with frontotemporal dementia and those with amyotrophic lateral sclerosis (ALS) carrying FUS mutatio

80 Mutations causing amyotrophic lateral sclerosis (ALS) clearly implicate ub

81 Clinical trials in amyotrophic lateral sclerosis (ALS) continue to rely on

82 fersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD1 mutation

83 The most recent research concerning amyotrophic lateral sclerosis (ALS) emphasizes the role

84 Approximately 35% of patients with amyotrophic lateral sclerosis (ALS) exhibit mild cogniti

85 Large-scale sequencing efforts in amyotrophic lateral sclerosis (ALS) have implicated nove

86 Several features of amyotrophic lateral sclerosis (ALS) impact on sexuality

87 ELF-MF) and electric shocks with the risk of amyotrophic lateral sclerosis (ALS) in a pooled case-con

88 A recent neuroanatomical staging scheme of amyotrophic lateral sclerosis (ALS) indicates that a cor

89 Amyotrophic lateral sclerosis (ALS) is a complex disease

90 Amyotrophic lateral sclerosis (ALS) is a devastating neu

91 Amyotrophic lateral sclerosis (ALS) is a devastating neu

92 Amyotrophic lateral sclerosis (ALS) is a fatal and incur

93 Amyotrophic lateral sclerosis (ALS) is a fatal disease i

94 Amyotrophic lateral sclerosis (ALS) is a fatal disease,

95 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

96 Background Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

97 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

98 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

99 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

100 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

101 Amyotrophic lateral sclerosis (ALS) is a fatal neurologi

102 Amyotrophic lateral sclerosis (ALS) is a fatal neuromusc

103 Amyotrophic lateral sclerosis (ALS) is a late-onset fata

104 Amyotrophic lateral sclerosis (ALS) is a multifactorial,

105 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

106 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

107 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

108 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

109 Amyotrophic lateral sclerosis (ALS) is a progressive mot

110 Amyotrophic lateral sclerosis (ALS) is a progressive neu

111 Amyotrophic lateral sclerosis (ALS) is a progressive neu

112 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

113 Amyotrophic lateral sclerosis (ALS) is an incurable neur

114 Amyotrophic Lateral Sclerosis (ALS) is an inexorably pro

115 The neurodegenerative syndrome amyotrophic lateral sclerosis (ALS) is characterised by

116 ip between frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is incompletely unde

117 rf72 cause frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is not understood.

118 ndamental question regarding the etiology of amyotrophic lateral sclerosis (ALS) is whether the vario

119 Vs from nontransgenic (NTg) and a transgenic amyotrophic lateral sclerosis (ALS) mouse model, superox

120 gest a pathologic role of skeletal muscle in amyotrophic lateral sclerosis (ALS) onset and progressio

121 l dysfunction is postulated to be central to amyotrophic lateral sclerosis (ALS) pathophysiology.

122 lular processes are already disrupted in the amyotrophic lateral sclerosis (ALS) patient.

123 The findings that amyotrophic lateral sclerosis (ALS) patients almost univ

124 lation into phase 1 and 2 clinical trials in amyotrophic lateral sclerosis (ALS) patients.

125 to degenerating neurons in many subtypes of amyotrophic lateral sclerosis (ALS) patients; however, t

126 Amyotrophic lateral sclerosis (ALS) presents with focal

127 Although the aetiology of amyotrophic lateral sclerosis (ALS) remains poorly under

128 Paralysis occurring in amyotrophic lateral sclerosis (ALS) results from denerva

129 In amyotrophic lateral sclerosis (ALS) spinal motor neurons

130 Individuals who are diagnosed with amyotrophic lateral sclerosis (ALS) today face the same

131 ed the potential causal effect of smoking on amyotrophic lateral sclerosis (ALS) using the Project Mi

132 for cognitive and behavioural impairment in amyotrophic lateral sclerosis (ALS) with frontotemporal

133 Mutations in fused in sarcoma (FUS) lead to amyotrophic lateral sclerosis (ALS) with varying ages of

134 rogression of respiratory muscle weakness in amyotrophic lateral sclerosis (ALS) would identify disea

135 tations in the RNA-binding protein FUS cause amyotrophic lateral sclerosis (ALS), a devastating neuro

136 ne is mutated frequently in individuals with amyotrophic lateral sclerosis (ALS), a fatal neurodegene

137 Amyotrophic lateral sclerosis (ALS), a fatal neurodegene

138 ia have been implicated in playing a role in amyotrophic lateral sclerosis (ALS), a neurodegenerative

139 sociated neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), a relentlessly prog

140 patients with and without diagnoses of OAG, amyotrophic lateral sclerosis (ALS), Alzheimer's disease

141 f many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), and is characterise

142 s disease (AD), stroke, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), and other neuroinfl

143 e diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson's dis

144 ography of nutrient metabolism is altered in amyotrophic lateral sclerosis (ALS), as early as childho

145 zed to cause motoneuron (MN) degeneration in amyotrophic lateral sclerosis (ALS), but actual proof of

146 ant driver of neurological diseases, notably amyotrophic lateral sclerosis (ALS), but most likely als

147 als have been suggested as a risk factor for amyotrophic lateral sclerosis (ALS), but only retrospect

148 idely studied as a susceptibility factor for amyotrophic lateral sclerosis (ALS), but results are con

149 Mutations in UBQLN2 cause amyotrophic lateral sclerosis (ALS), frontotemporal deme

150 o contribute to the pathogenesis of familial amyotrophic lateral sclerosis (ALS), however the relativ

151 In amyotrophic lateral sclerosis (ALS), immune cells and gl

152 o test this approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes

153 Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodeg

154 t of the blood-spinal cord barrier (BSCB) in Amyotrophic Lateral Sclerosis (ALS), mainly by endotheli

155 chronic kidney disease (CKD), epilepsy, and amyotrophic lateral sclerosis (ALS), mantis-ml achieved

156 entral nervous system (CNS) diseases such as amyotrophic lateral sclerosis (ALS), multiple sclerosis,

157 ing use of non-invasive ventilation (NIV) in amyotrophic lateral sclerosis (ALS), the question of ent

158 use aberrant SG formation is associated with amyotrophic lateral sclerosis (ALS), understanding the c

159 To discover novel genes underlying amyotrophic lateral sclerosis (ALS), we aggregated exome

160 uronal NF-kappaB activity in pathogenesis of amyotrophic lateral sclerosis (ALS), we generated transg

161 Parallel proteomics with amyotrophic lateral sclerosis (ALS)-associated C9ORF72 d

162 RNA granule transport requires ANXA11, and amyotrophic lateral sclerosis (ALS)-associated mutations

163 ion into prognostic categories and targeting Amyotrophic Lateral Sclerosis (ALS)-associated pathways

164 In addition, expression of an amyotrophic lateral sclerosis (ALS)-associated superoxid

165 disease onset in mice expressing a familial amyotrophic lateral sclerosis (ALS)-causing mutant SOD1

166 treated cells expressing either wild-type or amyotrophic lateral sclerosis (ALS)-linked mutant FUS.

167 tion is a fundamental question to comprehend amyotrophic lateral sclerosis (ALS).

168 ein Fused in Sarcoma (FUS) cause early-onset amyotrophic lateral sclerosis (ALS).

169 inson's disease, polyglutamine diseases, and amyotrophic lateral sclerosis (ALS).

170 inal and bulbar muscular atrophy (SBMA), and amyotrophic lateral sclerosis (ALS).

171 r for fatal neurodegenerative disorders like amyotrophic lateral sclerosis (ALS).

172 nt role in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS).

173 to modulate the neurodegenerative cascade in amyotrophic lateral sclerosis (ALS).

174 systems as end points in clinical trials in amyotrophic lateral sclerosis (ALS).

175 rontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS).

176 ly naturally occurring large animal model of amyotrophic lateral sclerosis (ALS).

177 associate with or cause sporadic or familial amyotrophic lateral sclerosis (ALS).

178 Disease (PD), Huntington's Disease (HD) and Amyotrophic Lateral Sclerosis (ALS).

179 on progressively degenerate in patients with amyotrophic lateral sclerosis (ALS).

180 rgy metabolism has been repeatedly linked to amyotrophic lateral sclerosis (ALS).

181 e dismutase 1 (SOD1) cause familial forms of amyotrophic lateral sclerosis (ALS).

182 cortical atrophy are consistent features of amyotrophic lateral sclerosis (ALS).

183 n coding and non-coding regions of FUS cause amyotrophic lateral sclerosis (ALS).

184 aggregation in the neurodegenerative disease amyotrophic lateral sclerosis (ALS).

185 in disease-relevant regions in patients with amyotrophic lateral sclerosis (ALS).

186 ons in hANG have been found in patients with Amyotrophic lateral sclerosis (ALS).

187 ne associate with both sporadic and familial amyotrophic lateral sclerosis (ALS).

188 iruses play a role in the pathophysiology of amyotrophic lateral sclerosis (ALS).

189 on of motor neurons (MNs) is the hallmark of amyotrophic lateral sclerosis (ALS).

190 been reported in both familial and sporadic amyotrophic lateral sclerosis (ALS).

191 makes S1R a potential therapeutic target in amyotrophic lateral sclerosis (ALS).

192 n C9orf72 is the commonest cause of familial amyotrophic lateral sclerosis (ALS).

193 otor neuroplasticity may extend longevity in amyotrophic lateral sclerosis (ALS).

194 ) disruption is an early pathogenic event in amyotrophic lateral sclerosis (ALS).

195 licated in the initiation and progression of amyotrophic lateral sclerosis (ALS).

196 ic changes that accompany motoneuron loss in amyotrophic lateral sclerosis (ALS).

197 otein TDP43 are highly conserved features in amyotrophic lateral sclerosis (ALS).

198 pendent cohorts of individuals with sporadic amyotrophic lateral sclerosis (ALS).

199 frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).

200 Neuroinflammation is important in amyotrophic lateral sclerosis (ALS).

201 ning 1 (GLT8D1) are associated with familial amyotrophic lateral sclerosis (ALS).

202 ariations that may contribute to the risk of amyotrophic lateral sclerosis (ALS).

203 , and has been linked to the pathogenesis of amyotrophic lateral sclerosis (ALS).

204 ses of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS).

205 st sites to manifest pathological changes in amyotrophic lateral sclerosis (ALS).

206 UBQLN2 mutations result in familial amyotrophic lateral sclerosis (ALS)/frontotemporal demen

207 C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS)/frontotemporal demen

208 In a subgroup of patients with amyotrophic lateral sclerosis (ALS)/Frontotemporal demen

209 but did not differ between individuals with amyotrophic lateral sclerosis (ALS, n = 59) versus NC.

210 ve colitis and neurological diseases such as amyotrophic lateral sclerosis and Alzheimer's disease.

211 differences were noted between patients with amyotrophic lateral sclerosis and controls.

212 erative diseases, such as Alzheimer disease, amyotrophic lateral sclerosis and even schizophrenia.

213 is the most prevalent defect associated with amyotrophic lateral sclerosis and frontotemporal degener

214 tion of C9orf72 in normal physiology, and in amyotrophic lateral sclerosis and frontotemporal degener

215 )-repeats within C9orf72 are associated with amyotrophic lateral sclerosis and frontotemporal dementi

216 ted assemblies is implicated in the diseases amyotrophic lateral sclerosis and frontotemporal dementi

217 proteinopathy is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementi

218 on of C9ORF72 cause the most common familial amyotrophic lateral sclerosis and frontotemporal dementi

219 icated in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementi

220 tion of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementi

221 he C9orf72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementi

222 nderlie neurodegenerative diseases including amyotrophic lateral sclerosis and frontotemporal dementi

223 ntial therapeutic target for C9orf72-related amyotrophic lateral sclerosis and frontotemporal dementi

224 to generate a patient derived iPSC model of amyotrophic lateral sclerosis and frontotemporal dementi

225 eurodegenerative diseases, including C9orf72 Amyotrophic Lateral Sclerosis and Frontotemporal Dementi

226 t common genetic variant that contributes to amyotrophic lateral sclerosis and frontotemporal dementi

227 the C9orf72 gene is a main cause of familial amyotrophic lateral sclerosis and frontotemporal dementi

228 Amyotrophic lateral sclerosis and frontotemporal lobar d

229 e central nervous systems of mouse models of amyotrophic lateral sclerosis and human patients with am

230 s, or riluzole, an FDA-approved drug used in amyotrophic lateral sclerosis and known to block persist

231 t inheritance of frontotemporal dementia and amyotrophic lateral sclerosis and no mutation in known a

232 enic, irreversible TDP-43 aggregates form in amyotrophic lateral sclerosis and other neurodegenerativ

233 g constitutes a novel therapeutic target for amyotrophic lateral sclerosis and related disorders with

234 een identified as a mechanistic link between amyotrophic lateral sclerosis and spinal muscular atroph

235 se process affects the metabolic pathways in amyotrophic lateral sclerosis and whether these pathways

236 a-6 supplementation and IL-13 inhibition for amyotrophic lateral sclerosis) and influences on longevi

237 0.5-1% of ALS (Amyotrophic Lateral Sclerosis) and Parkinson's disease (

238 seases such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, and demyelinating disease

239 in Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease.

240 Frontotemporal dementia and amyotrophic lateral sclerosis are clinically and patholo

241 ve defects, such as muscle fasciculations in amyotrophic lateral sclerosis, as suggested by our compu

242 r example, HSPA1A reduced aggregation of the amyotrophic lateral sclerosis-associated protein variant

243 he use of cells from a patient with sporadic amyotrophic lateral sclerosis but can be applied more ge

244 dentified as a negative prognostic factor in amyotrophic lateral sclerosis, but there is no evidence

245 mmon cause of the neurodegenerative disorder amyotrophic lateral sclerosis (C9-ALS) and is linked to

246 induced astrocytes from C9orf72 and sporadic amyotrophic lateral sclerosis cases we measured the prod

247 temporal dementia, Huntington's disease, and amyotrophic lateral sclerosis-characteristic protein agg

248 neurological phenotypes (Alzheimer disease, amyotrophic lateral sclerosis, depression, insomnia, int

249 aimed to test the corticofugal hypothesis of amyotrophic lateral sclerosis experimentally.

250 ologic changes in transgenic mouse models of amyotrophic lateral sclerosis expressing mutant forms of

251 dismutase 1 (SOD1) cause 15-20% of familial amyotrophic lateral sclerosis (fALS) cases.

252 vant due to its occurrence within neurons in amyotrophic lateral sclerosis, frontotemporal dementia,

253 of neurodegenerative diseases, particularly amyotrophic lateral sclerosis, frontotemporal dementias

254 gates in neurodegenerative diseases, such as amyotrophic lateral sclerosis, frontotemporal lobar dege

255 ic lateral sclerosis and human patients with amyotrophic lateral sclerosis/frontotemporal dementia.

256 dentified as causing Parkinson's disease and amyotrophic lateral sclerosis/frontotemporal dementia/my

257 n's disease (PD) and frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS) are insidious an

258 Amyotrophic Lateral Sclerosis Functional Rating Scale-Re

259 he rate of decline in the total score on the Amyotrophic Lateral Sclerosis Functional Rating Scale-Re

260 ns encoded by frontotemporal dementia and/or amyotrophic lateral sclerosis genes (TBK1, OPTN and SQST

261 tions in several frontotemporal dementia and amyotrophic lateral sclerosis genes, including TBK1, OPT

262 ery that their conserved genes in humans are amyotrophic lateral sclerosis genetic risk factors.

263 umerous causative genes and risk factors for amyotrophic lateral sclerosis have been identified.

264 SegB A315E (residues 286-331 containing the amyotrophic lateral sclerosis hereditary mutation A315E)

265 system infections, meningitis, encephalitis, amyotrophic lateral sclerosis, Huntington disease, demen

266 urrently in development for the treatment of amyotrophic lateral sclerosis, Huntington's disease, and

267 opment of a number of human diseases such as amyotrophic lateral sclerosis, Huntington's disease, and

268 pproach identified that C9orf72 and sporadic amyotrophic lateral sclerosis induced astrocytes have di

269 Amyotrophic lateral sclerosis is a deleterious neurodege

270 Amyotrophic lateral sclerosis is a rapidly progressing a

271 of the disturbances in the kinome network in amyotrophic lateral sclerosis is needed to properly targ

272 Amyotrophic lateral sclerosis is the most common degener

273 common cause of frontotemporal dementia and amyotrophic lateral sclerosis, is translated through rep

274 rgy metabolism on the disease progression in amyotrophic lateral sclerosis, it is vital to understand

275 lfide-reduced mSOD1 might play a role in the amyotrophic lateral sclerosis-linked aggregation of SOD1

276 fic NogoA-overexpression of zebrafish and an Amyotrophic Lateral Sclerosis mouse model, SOD1 G93A.

277 ith substance abuse, temporal lobe epilepsy, amyotrophic lateral sclerosis, multiple system atrophy,

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

279 linical presentations, potentially mimicking amyotrophic lateral sclerosis or distal hereditary motor

280 trance in families with a high prevalence of amyotrophic lateral sclerosis or frontotemporal dementia

281 trategies to diminish the risk of developing amyotrophic lateral sclerosis or frontotemporal dementia

282 tive diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alz

283 and discuss the multiple roles of kinases in amyotrophic lateral sclerosis pathogenesis.

284 cell-derived motor neurons specifically from amyotrophic lateral sclerosis patients carrying C9orf72

285 erived human induced astrocytes from C9orf72 amyotrophic lateral sclerosis patients compared to norma

286 Recent studies carried out on amyotrophic lateral sclerosis patients suggest that the

287 life-prolonging effect of HCFD for the whole amyotrophic lateral sclerosis population.

288 from upper motor neuron-predominant forms of amyotrophic lateral sclerosis remains a significant chal

289 multiple sclerosis, Parkinson's disease and amyotrophic lateral sclerosis remains elusive despite de

290 [(18)F]3 detected CB2 upregulation in human amyotrophic lateral sclerosis spinal cord tissue and may

291 ss has been associated with diseases such as amyotrophic lateral sclerosis, stroke, and cancer.

292 revent Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis) study is a prospective, m

293 ance, the majority of patients with sporadic amyotrophic lateral sclerosis (up to 97%) and a substant

294 analyse the basis of the catabolic defect in amyotrophic lateral sclerosis we used a novel phenotypic

295 analyse the basis of the metabolic defect in amyotrophic lateral sclerosis we used a phenotypic metab

296 Using the South-East England Register for Amyotrophic Lateral Sclerosis, we performed a retrospect

297 In healthy individuals and in patients with amyotrophic lateral sclerosis, we show that the piezoele

298 s, the combined odds ratio (for AD, FTD, and amyotrophic lateral sclerosis, which shares clinicopatho

299 ould be a potential therapeutic strategy for amyotrophic lateral sclerosis with defective RNA metabol

300 of poly(GR), a dipeptide repeat derived from amyotrophic lateral sclerosis with frontotemporal dement