ライフサイエンスコーパス: amyotrophic

1 atin dynamics may be a treatment approach to amyotrophic lateral scleorosis (ALS)/frontotemporal deme

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

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

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

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

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

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

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

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

10 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

12 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

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

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

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

17 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

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

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

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

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

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

24 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

26 Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal D

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

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

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

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

31 Amyotrophic lateral sclerosis (ALS) and frontotemporal l

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Amyotrophic lateral sclerosis (ALS) has an immune compon

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

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

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

49 Amyotrophic Lateral Sclerosis (ALS) is a complex neurode

50 Amyotrophic lateral sclerosis (ALS) is a degenerative di

51 Amyotrophic lateral sclerosis (ALS) is a degenerative mo

52 Amyotrophic lateral sclerosis (ALS) is a devastating adu

53 Amyotrophic lateral sclerosis (ALS) is a devastating and

54 Amyotrophic lateral sclerosis (ALS) is a devastating neu

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

56 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

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

58 Amyotrophic lateral sclerosis (ALS) is a heterogeneous d

59 Amyotrophic lateral sclerosis (ALS) is a heterogeneous d

60 Amyotrophic lateral sclerosis (ALS) is a lethal neurodeg

61 Amyotrophic lateral sclerosis (ALS) is a multifactorial

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

63 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

64 Amyotrophic lateral sclerosis (ALS) is a progressive and

65 Amyotrophic lateral sclerosis (ALS) is a progressive and

66 Amyotrophic lateral sclerosis (ALS) is a progressive mot

67 Amyotrophic lateral sclerosis (ALS) is a progressive neu

68 Amyotrophic lateral sclerosis (ALS) is a progressive neu

69 Amyotrophic lateral sclerosis (ALS) is a progressive neu

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

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

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

73 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

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

75 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

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

77 Amyotrophic lateral sclerosis (ALS) is an idiopathic and

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

79 Amyotrophic lateral sclerosis (ALS) is characterized by

80 Amyotrophic lateral sclerosis (ALS) is debilitating neur

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

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

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

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

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

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

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

88 Amyotrophic lateral sclerosis (ALS) may be associated wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 3 (TDP-43) and RNA-binding protein FUS cause amyotrophic lateral sclerosis (ALS), but the biophysical

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Amyotrophic lateral sclerosis is a progressive adult-ons

227 Amyotrophic lateral sclerosis is a progressive neurodege

228 Amyotrophic lateral sclerosis is characterised by the pr

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

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

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

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

233 Analysis of functionally linked amyotrophic lateral sclerosis proteins revealed recruitm

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

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

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

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

238 , 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerati

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

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

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

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

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

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

245 762 (77%) recipients had cancer, 79 (8%) had amyotrophic lateral sclerosis, 44 (4.5%) had lung diseas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 presentation of motoneuron disorders such as amyotrophic lateral sclerosis.

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

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

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

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

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

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

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

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

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

282 treatment of neurodegenerative diseases like amyotrophic lateral sclerosis.

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

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

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

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

287 lateral sclerosis and patients with sporadic amyotrophic lateral sclerosis.

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

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

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

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

292 tracellular signaling function implicated in amyotrophic lateral sclerosis.

293 uroprotective properties approved for use in amyotrophic lateral sclerosis.

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

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

296 enuating the disease progression of familial amyotrophic lateral sclerosis.

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

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

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

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