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

1 "DNAJC6 variants in Parkinson's disease and amyotrophic lateral sclerosis".

2 f superoxide dismutase 1 (linked to familial amyotrophic lateral sclerosis).

3 , Alzheimer disease, Huntington disease, and amyotrophic lateral sclerosis.

4 presentation of motoneuron disorders such as amyotrophic lateral sclerosis.

5 ration in SOD1(G93A) mice, a mouse model for amyotrophic lateral sclerosis.

6 , but it also forms aggregates implicated in amyotrophic lateral sclerosis.

7 Huntington disease, muscular dystrophy, and amyotrophic lateral sclerosis.

8 s protective in cellular and mouse models of amyotrophic lateral sclerosis.

9 ative diseases such as Parkinson disease and amyotrophic lateral sclerosis.

10 ed to a variety of human diseases, including amyotrophic lateral sclerosis.

11 ), are associated with sporadic and familial amyotrophic lateral sclerosis.

12 rkinsonism and the later stages can resemble amyotrophic lateral sclerosis.

13 detrimental outcome of the motor function in amyotrophic lateral sclerosis.

14 treatment of neurodegenerative diseases like amyotrophic lateral sclerosis.

15 r's disease, but not Huntington's disease or amyotrophic lateral sclerosis.

16 gy of primary open angle glaucoma (POAG) and amyotrophic lateral sclerosis.

17 eat shock response pathway is compromised in amyotrophic lateral sclerosis.

18 at sequences expanded in the C9orf72 form of amyotrophic lateral sclerosis.

19 lateral sclerosis and patients with sporadic amyotrophic lateral sclerosis.

20 ximately 40% of autosomal recessive juvenile amyotrophic lateral sclerosis.

21 rf72 leads to frontotemporal dementia and/or amyotrophic lateral sclerosis.

22 rotein domain (MSPd) that is associated with amyotrophic lateral sclerosis.

23 lization of FUS and pathology of FUS-related amyotrophic lateral sclerosis.

24 tracellular signaling function implicated in amyotrophic lateral sclerosis.

25 uroprotective properties approved for use in amyotrophic lateral sclerosis.

26 rt-rib thoracic dysplasia, Mohr-syndrome and amyotrophic lateral sclerosis.

27 ongation into amyloid-like fibrils linked to amyotrophic lateral sclerosis.

28 enuating the disease progression of familial amyotrophic lateral sclerosis.

29 tion is linked to various diseases including amyotrophic lateral sclerosis.

30 .001) consistent with an oligogenic basis of amyotrophic lateral sclerosis.

31 o contribute to motor neuron degeneration in amyotrophic lateral sclerosis.

32 762 (77%) recipients had cancer, 79 (8%) had amyotrophic lateral sclerosis, 44 (4.5%) had lung diseas

33 een reported in motor neuron degeneration of amyotrophic lateral sclerosis, abnormalities of RNA/RNA-

34 extensive double fluorescence, including in amyotrophic lateral sclerosis-affected cranial nerve mot

35 , abnormal aggregation of which is linked to amyotrophic lateral sclerosis (ALS) - a fatal neurodegen

36 ofilin-1 (PFN1) are mutated in patients with amyotrophic lateral sclerosis (ALS) [5, 6].

37 a largely neglected symptom in patients with amyotrophic lateral sclerosis (ALS) although it is repor

38 have been previously found in patients with amyotrophic lateral sclerosis (ALS) and developmental de

39 To elucidate the genetic architecture of amyotrophic lateral sclerosis (ALS) and find associated

40 dem repeats (STRs), such as those that cause amyotrophic lateral sclerosis (ALS) and fragile X syndro

41 or cause of two neurodegenerative syndromes, amyotrophic lateral sclerosis (ALS) and frontotemporal d

42 s represent the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

43 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

44 asing complexity of the genetic landscape in amyotrophic lateral sclerosis (ALS) and frontotemporal d

45 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

46 ions in C9orf72 are the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

47 G4C2) in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

48 epeat in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

49 and might contribute to neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal d

50 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

51 anges in eating behaviours and metabolism in amyotrophic lateral sclerosis (ALS) and frontotemporal d

52 ecent report on TDP-43, an RBP implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal d

53 FUS is an RNA-binding protein involved in amyotrophic lateral sclerosis (ALS) and frontotemporal d

54 sent in nervous tissue of most cases of both amyotrophic lateral sclerosis (ALS) and frontotemporal d

55 s and has been linked to the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal d

56 F72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

57 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

58 72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal d

59 everal neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal d

60 Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal D

61 orders, with particularly high prevalence in amyotrophic lateral sclerosis (ALS) and frontotemporal d

62 ated protein involved in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal l

63 in 43 kDa) is a hallmark of certain forms of amyotrophic lateral sclerosis (ALS) and frontotemporal l

64 ding protein involved in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal L

65 Amyotrophic lateral sclerosis (ALS) and frontotemporal l

66 ediator of the neuroinflammatory reaction in amyotrophic lateral sclerosis (ALS) and is toxic for mot

67 atients with chronic low back pain (cLBP) or amyotrophic lateral sclerosis (ALS) and matching healthy

68 The study of amyotrophic lateral sclerosis (ALS) and potential interv

69 3) is genetically and functionally linked to amyotrophic lateral sclerosis (ALS) and regulates transc

70 TFs) extend the survival of motor neurons in amyotrophic lateral sclerosis (ALS) and that the combine

71 ive degeneration of corticospinal neurons in amyotrophic lateral sclerosis (ALS) and to neocortical h

72 The etiological underpinnings of amyotrophic lateral sclerosis (ALS) are complex and inco

73 Astrocytes isolated from individuals with amyotrophic lateral sclerosis (ALS) are toxic to motor n

74 eports the long-term epidemiologic trends of amyotrophic lateral sclerosis (ALS) based on a prospecti

75 t expansion in the C9orf72 form of heritable amyotrophic lateral sclerosis (ALS) binds to the central

76 A proportion of Amyotrophic lateral sclerosis (ALS) cases result from im

77 nderstanding the natural history of familial amyotrophic lateral sclerosis (ALS) caused by SOD1 mutat

78 ients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) caused by this mutat

79 Amyotrophic lateral sclerosis (ALS) has an immune compon

80 Prospective population based-registers of amyotrophic lateral sclerosis (ALS) have operated in Eur

81 he Cu,Zn superoxide dismutase gene (sod1) to amyotrophic lateral sclerosis (ALS) in 1993, researchers

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

83 Amyotrophic Lateral Sclerosis (ALS) is a complex neurode

84 Amyotrophic lateral sclerosis (ALS) is a degenerative di

85 Amyotrophic lateral sclerosis (ALS) is a degenerative mo

86 Amyotrophic lateral sclerosis (ALS) is a devastating adu

87 Amyotrophic lateral sclerosis (ALS) is a devastating and

88 Amyotrophic lateral sclerosis (ALS) is a devastating neu

89 Amyotrophic lateral sclerosis (ALS) is a fatal motor neu

90 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

91 Amyotrophic lateral sclerosis (ALS) is a fatal, adult-on

92 Amyotrophic lateral sclerosis (ALS) is a heterogeneous d

93 Amyotrophic lateral sclerosis (ALS) is a heterogeneous d

94 Amyotrophic lateral sclerosis (ALS) is a lethal neurodeg

95 Amyotrophic lateral sclerosis (ALS) is a multifactorial

96 isease in ALS rodents.SIGNIFICANCE STATEMENT Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

97 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

98 Amyotrophic lateral sclerosis (ALS) is a progressive and

99 Amyotrophic lateral sclerosis (ALS) is a progressive and

100 Amyotrophic lateral sclerosis (ALS) is a progressive mot

101 Amyotrophic lateral sclerosis (ALS) is a progressive neu

102 Amyotrophic lateral sclerosis (ALS) is a progressive neu

103 Amyotrophic lateral sclerosis (ALS) is a progressive neu

104 Amyotrophic lateral sclerosis (ALS) is a progressive, ad

105 Amyotrophic lateral sclerosis (ALS) is a progressive, fa

106 Amyotrophic lateral sclerosis (ALS) is a progressive, fa

107 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

108 ur understanding of genetic aetiology of ALS.Amyotrophic lateral sclerosis (ALS) is a rapidly progres

109 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

110 Amyotrophic lateral sclerosis (ALS) is an adult-onset de

111 Amyotrophic lateral sclerosis (ALS) is an idiopathic and

112 Amyotrophic lateral sclerosis (ALS) is caused by the pro

113 Amyotrophic lateral sclerosis (ALS) is characterized by

114 Amyotrophic lateral sclerosis (ALS) is debilitating neur

115 ation and accurate differential diagnosis of amyotrophic lateral sclerosis (ALS) is lacking.

116 filament light chain (NFL) as a biomarker in amyotrophic lateral sclerosis (ALS) is needed.

117 selective motor neuron (MN) vulnerability in amyotrophic lateral sclerosis (ALS) is not known.

118 The disease course of amyotrophic lateral sclerosis (ALS) is rapid and, becaus

119 Although amyotrophic lateral sclerosis (ALS) is relatively rare,

120 Amyotrophic lateral sclerosis (ALS) is the most common a

121 nal transport defects in patient-derived MNs.Amyotrophic lateral sclerosis (ALS) leads to selective l

122 Amyotrophic lateral sclerosis (ALS) may be associated wi

123 TI) findings and functional rating scales in amyotrophic lateral sclerosis (ALS) may be due to sympto

124 s S-acylated (palmitoylated) in vitro and in amyotrophic lateral sclerosis (ALS) mouse models, and th

125 ration, is a recently recognized hallmark of Amyotrophic Lateral Sclerosis (ALS) pathogenesis.

126 sychiatric conditions are overrepresented in amyotrophic lateral sclerosis (ALS) patient kindreds and

127 n the cerebrospinal fluid (CSF) and serum of amyotrophic lateral sclerosis (ALS) patients.

128 The method was submitted to the DREAM Amyotrophic Lateral Sclerosis (ALS) Stratification Chall

129 Neurochemical markers of amyotrophic lateral sclerosis (ALS) that reflect underly

130 ed protein B (VAPB) gene have been linked to amyotrophic lateral sclerosis (ALS) type 8.

131 trostomy (PEG) tube for patients living with amyotrophic lateral sclerosis (ALS) using data from a cl

132 Modeling amyotrophic lateral sclerosis (ALS) with human induced p

133 RATIONALE: Biomarkers for survival in amyotrophic lateral sclerosis (ALS) would facilitate the

134 irectly linked to both familial and sporadic amyotrophic lateral sclerosis (ALS), a devastating, late

135 We show using a mouse model of amyotrophic lateral sclerosis (ALS), a disease in which

136 tations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegene

137 utations in the profilin 1 (PFN1) gene cause amyotrophic lateral sclerosis (ALS), a neurodegenerative

138 in Liposarcoma (FUS) cause familial forms of amyotrophic lateral sclerosis (ALS), a neurodegenerative

139 nisms and to identify reliable biomarkers of amyotrophic lateral sclerosis (ALS), a progressive neuro

140 we use cross-ethnic genetic data in sporadic amyotrophic lateral sclerosis (ALS), an adult-onset, rap

141 oke, spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and Alzheimer's dis

142 ctice, with an emphasis on fasciculations in amyotrophic lateral sclerosis (ALS), and in benign fasci

143 uronal class that is principally affected in amyotrophic lateral sclerosis (ALS), but it is widely kn

144 Apathy is a prominent symptom of amyotrophic lateral sclerosis (ALS), but measurement is

145 3 (TDP-43) and RNA-binding protein FUS cause amyotrophic lateral sclerosis (ALS), but the biophysical

146 represent the most common cause of familial amyotrophic lateral sclerosis (ALS), but the mechanisms

147 Pseudobulbar affect (PBA) is prevalent in amyotrophic lateral sclerosis (ALS), but there is limite

148 EMENT Since neuromuscular disorders, such as amyotrophic lateral sclerosis (ALS), end life via respir

149 ps extensively with the motor neuron disease amyotrophic lateral sclerosis (ALS), especially at the g

150 s are detected in the brain of patients with amyotrophic lateral sclerosis (ALS), including carriers

151 Mutations in FUS cause amyotrophic lateral sclerosis (ALS), including some of t

152 r communication in a patient with late-stage amyotrophic lateral sclerosis (ALS), involving a fully i

153 tase 1 (SOD1), and its mutant form linked to amyotrophic lateral sclerosis (ALS), is also secreted by

154 ecular signature in microglia from models of amyotrophic lateral sclerosis (ALS), multiple sclerosis

155 disease (HD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), multiple system atr

156 rotein misfolding and aggregation, including amyotrophic lateral sclerosis (ALS), Parkinson's disease

157 de dismutase 1 (SOD1), which causes familial amyotrophic lateral sclerosis (ALS), self-propagation of

158 schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetio

159 ogliosis is a hallmark of advanced stages of amyotrophic lateral sclerosis (ALS), the role of microgl

160 ween late-onset Alzheimer disease (LOAD) and amyotrophic lateral sclerosis (ALS), two major neurodege

161 To identify genetic factors contributing to amyotrophic lateral sclerosis (ALS), we conducted whole-

162 TDP-43 is the major pathological hallmark of amyotrophic lateral sclerosis (ALS), we generated mice i

163 ssue structural connectivity associated with amyotrophic lateral sclerosis (ALS), which extends beyon

164 Neuroinflammation is a major hallmark of amyotrophic lateral sclerosis (ALS), which is currently

165 The early motor manifestations of sporadic amyotrophic lateral sclerosis (ALS), while rarely docume

166 icing (AS), including skipping of an exon in amyotrophic lateral sclerosis (ALS)-associated D-amino a

167 Subsequent network analyses focusing on amyotrophic lateral sclerosis (ALS)-associated genes, su

168 ition or depletion of TBK1, or expression of amyotrophic lateral sclerosis (ALS)-associated OPTN or T

169 Formation of FUS inclusions is promoted by amyotrophic lateral sclerosis (ALS)-linked mutations, bu

170 Four patients suffering from advanced amyotrophic lateral sclerosis (ALS)-two of them in perma

171 reported as a negative prognostic factor in amyotrophic lateral sclerosis (ALS).

172 precedes the loss of motor neurons (MNs) in amyotrophic lateral sclerosis (ALS).

173 ients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).

174 iant frontotemporal dementia (bvFTD) develop amyotrophic lateral sclerosis (ALS).

175 m cell derived astrocyte and mouse models of amyotrophic lateral sclerosis (ALS).

176 is mutated in a form of distal myopathy and amyotrophic lateral sclerosis (ALS).

177 n cerebrospinal fluid (CSF) of patients with amyotrophic lateral sclerosis (ALS).

178 uclease that is compromised in patients with amyotrophic lateral sclerosis (ALS).

179 oprotein metabolisms with the future risk of amyotrophic lateral sclerosis (ALS).

180 or neurons leads to progressive paralysis in amyotrophic lateral sclerosis (ALS).

181 ophagy genes can cause familial and sporadic amyotrophic lateral sclerosis (ALS).

182 asticity after spinal cord injury and during amyotrophic lateral sclerosis (ALS).

183 turnover may be associated with the risk of amyotrophic lateral sclerosis (ALS).

184 TDP-43) is a product of a causative gene for amyotrophic lateral sclerosis (ALS).

185 trocyte dysfunction and neurodegeneration in amyotrophic lateral sclerosis (ALS).

186 of its fragments TDP-25 and TDP-35 occurs in amyotrophic lateral sclerosis (ALS).

187 lum (ER) proteostasis is a common feature of amyotrophic lateral sclerosis (ALS).

188 lowed investigators to develop new models of amyotrophic lateral sclerosis (ALS).

189 herapeutic solutions for pathologies such as amyotrophic lateral sclerosis (ALS).

190 causing the adult-onset degenerative disease amyotrophic lateral sclerosis (ALS).

191 n diseases spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS).

192 d in the gene-time-environment hypothesis in amyotrophic lateral sclerosis (ALS).

193 ly been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS).

194 ition in the pathogenesis and progression of amyotrophic lateral sclerosis (ALS).

195 to the remarkable variations in mortality in amyotrophic lateral sclerosis (ALS).

196 e disease with similarities to some forms of amyotrophic lateral sclerosis (ALS).

197 reported as a negative prognostic factor in amyotrophic lateral sclerosis (ALS).

198 vation in a mutant SOD1(G93A) mouse model of amyotrophic lateral sclerosis (ALS).

199 es are implicated in human diseases, such as amyotrophic lateral sclerosis (ALS).

200 in several neurological disorders, including amyotrophic lateral sclerosis (ALS).

201 might be associated with the development of amyotrophic lateral sclerosis (ALS).

202 binding protein (RBP) TAF15 is implicated in amyotrophic lateral sclerosis (ALS).

203 een implicated in both familial and sporadic amyotrophic lateral sclerosis (ALS).

204 c cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).

205 in many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS).

206 crucial step in the onset and progression of amyotrophic lateral sclerosis (ALS).

207 have been identified in patients affected by amyotrophic lateral sclerosis (ALS).

208 ort is an early neuropathological feature of amyotrophic lateral sclerosis (ALS).

209 rited forms of the neurodegenerative disease amyotrophic lateral sclerosis (ALS).

210 ng and in SOD1(G93A) mice, a mouse model for amyotrophic lateral sclerosis (ALS).

211 utations in the gene encoding SOD1 all cause amyotrophic lateral sclerosis (ALS).

212 tification of early physiological markers of amyotrophic lateral sclerosis (ALS).

213 ght to have a role in the pathophysiology of amyotrophic lateral sclerosis (ALS).

214 sma creatinine is a predictor of survival in amyotrophic lateral sclerosis (ALS).

215 otor neuron toxicity in an inherited form of amyotrophic lateral sclerosis (ALS).

216 is one of the causes of neurodegeneration in Amyotrophic lateral sclerosis (ALS).

217 candidates associated with the prognosis of amyotrophic lateral sclerosis (ALS); however, there is s

218 as RNase 5) are known to be associated with Amyotrophic Lateral Sclerosis (ALS, motor neurone diseas

219 nding domain results in the juvenile form of amyotrophic lateral sclerosis (ALS16), and a 20 amino-ac

220 spastic paraplegia (HSP) and juvenile onset amyotrophic lateral sclerosis (ALS5).

221 olog ubiquilin 2 is associated with familial amyotrophic lateral sclerosis, also contributes to defec

222 pathways and therapeutic targets shared with amyotrophic lateral sclerosis and Alzheimer disease.

223 including frontotemporal lobar degeneration, amyotrophic lateral sclerosis and Alzheimer's disease (A

224 ve diseases, including Huntington's disease, amyotrophic lateral sclerosis and Alzheimer's disease.

225 ponent of neurodegenerative diseases such as amyotrophic lateral sclerosis and Alzheimer's, Parkinson

226 athological hallmark in approximately 95% of amyotrophic lateral sclerosis and approximately 60% of f

227 eat expansions that cause C9orf72-associated amyotrophic lateral sclerosis and frontotemporal dementi

228 the C9orf72 gene is the most common cause of amyotrophic lateral sclerosis and frontotemporal dementi

229 f many neurodegenerative diseases, including amyotrophic lateral sclerosis and frontotemporal dementi

230 nded hexanucleotide repeat in C9orf72 causes amyotrophic lateral sclerosis and frontotemporal dementi

231 sion in an intron of the C9orf72 gene causes amyotrophic lateral sclerosis and frontotemporal dementi

232 ORF72 are the most frequent genetic cause of amyotrophic lateral sclerosis and frontotemporal dementi

233 f72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementi

234 nC9orf72 is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementi

235 ene are the commonest known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementi

236 we find, launching from Drosophila models of amyotrophic lateral sclerosis and frontotemporal dementi

237 ety of neurodegenerative diseases, including amyotrophic lateral sclerosis and frontotemporal lobar d

238 mer's, Huntington's and Parkinson's disease, amyotrophic lateral sclerosis and multiple sclerosis.

239 logical phenotypes for C. elegans models for amyotrophic lateral sclerosis and Parkinson's disease, a

240 ing protein and alpha-synuclein, involved in amyotrophic lateral sclerosis and Parkinson's disease, r

241 sues from a TDP-43 transgenic mouse model of amyotrophic lateral sclerosis and patients with sporadic

242 sodium pumps in movement disorders, such as amyotrophic lateral sclerosis and rapid-onset dystonia p

243 lular aggregation of TDP-43 is a hallmark of amyotrophic lateral sclerosis and ubiquitin-positive fro

244 as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal lobar

245 ions, including stroke, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease,

246 muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy ty

247 muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy ty

248 encouraging results in experimental stroke, amyotrophic lateral sclerosis, and neurotrauma models.

249 l disorders (including autism, epilepsy, and amyotrophic lateral sclerosis) are underpinned by synapt

250 The neuropathological overlap with amyotrophic lateral sclerosis, associated with some shar

251 ally investigated whether spread of a mutant amyotrophic lateral sclerosis-associated cytosolic super

252 d mutants of OPTN, E50K and M98K, but not an amyotrophic lateral sclerosis-associated mutant, E478G,

253 egeneration and to motor unit dismantling in amyotrophic lateral sclerosis at late disease stage.

254 2), Huntington's disease, and C9orf72-linked amyotrophic lateral sclerosis (C9-ALS).

255 potential treatments for C9ORF72-associated amyotrophic lateral sclerosis (c9ALS) approach clinical

256 In SOD1(G86R) mice, an animal model of amyotrophic lateral sclerosis, conduritol B epoxide pres

257 n identified as causing a subset of familial amyotrophic lateral sclerosis (fALS) and more rarely cau

258 lin 1 (PFN1) gene are causative for familial amyotrophic lateral sclerosis (fALS).

259 s carrying SOD1 mutations linked to familial amyotrophic lateral sclerosis (fALS/SOD1).

260 in muscle innervation, which degenerates in amyotrophic lateral sclerosis from the early disease sta

261 rum of multisystem proteinopathies including amyotrophic lateral sclerosis, frontotemporal lobar dege

262 ure in neurodegenerative diseases, including amyotrophic lateral sclerosis, frontotemporal lobar deme

263 amilial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neithe

264 f FTD cases (n = 128), and of FTD cases with Amyotrophic Lateral Sclerosis (FTD-ALS; n = 7) to those

265 sease (AD, n = 289), frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS, n = 252), Creutz

266 Main Outcomes and Measures: Amyotrophic lateral sclerosis function, measured using t

267 n immune metrics with changes on the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (A

268 assay genetic variation in a panel of known amyotrophic lateral sclerosis genes in 1126 patient samp

269 Recently, an additional connection to amyotrophic lateral sclerosis has emerged from studies o

270 on leading to frontotemporal dementia and/or amyotrophic lateral sclerosis have highly variable ages

271 nd psychological well-being in patients with amyotrophic lateral sclerosis-induced locked-in state an

272 tions in the ALS2 gene result in early-onset amyotrophic lateral sclerosis, infantile-onset ascending

273 Because amyotrophic lateral sclerosis is a fatal adult-onset neu

274 Amyotrophic lateral sclerosis is a progressive adult-ons

275 Amyotrophic lateral sclerosis is a progressive neurodege

276 Amyotrophic lateral sclerosis is characterised by the pr

277 ndings show that the genetic architecture of amyotrophic lateral sclerosis is complex and that variat

278 inhibitor (designated HTB1M) of two familial amyotrophic lateral sclerosis-linked SOD1 mutants, SOD1(

279 : A cross-sectional baseline analysis of the Amyotrophic Lateral Sclerosis Multicenter Cohort Study o

280 in neurological diseases, including ataxias, amyotrophic lateral sclerosis, nucleotide expansion diso

281 ative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and

282 s of the CNS, including Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and

283 le of the sodium pump in diseases, including amyotrophic lateral sclerosis, parkinsonism, epilepsy, a

284 no-L-alanine (BMAA), a probable cause of the amyotrophic lateral sclerosis/parkinsonism-dementia comp

285 S mice are promising tools for understanding amyotrophic lateral sclerosis pathogenesis and testing n

286 f gangliosides in the cerebrospinal fluid of amyotrophic lateral sclerosis patients in early disease

287 Analysis of functionally linked amyotrophic lateral sclerosis proteins revealed recruitm

288 gregation in Charcot-Marie-Tooth disease and amyotrophic lateral sclerosis, respectively.

289 ic stroke, brain trauma, multiple sclerosis, amyotrophic lateral sclerosis, sepsis, ischemic and repe

290 ber of settings, including a murine model of amyotrophic lateral sclerosis (SOD1G93A), middle cerebra

291 me of defective autophagy in the broader FTD/amyotrophic lateral sclerosis spectrum of neurodegenerat

292 n degenerative motor neuron diseases such as amyotrophic lateral sclerosis, spinal muscular atrophy,

293 e partially reminiscent of those observed in amyotrophic lateral sclerosis, such as ubiquitin and p62

294 ry pathway while in Huntington's disease and amyotrophic lateral sclerosis they form in different cel

295 te our findings in transgenic mice and human amyotrophic lateral sclerosis tissues.

296 ia with oculomotor apraxia type 2 (AOA2) and amyotrophic lateral sclerosis type 4 (ALS4).

297 , 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerati

298 Mutations in FUS are causative for amyotrophic lateral sclerosis with a dominant mode of in

299 disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis with associated frontotemp

300 with Lewy bodies; Huntington's disease; and amyotrophic lateral sclerosis with dementia, as well as