ライフサイエンスコーパス: lateral sclerosis

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

2 f the corticofugal hypothesis of amyotrophic lateral sclerosis.

3 ion-like protein associated with amyotrophic lateral sclerosis.

4 elated neurodegenerative disease amyotrophic lateral sclerosis.

5 urodegenerative diseases such as amyotrophic lateral sclerosis.

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

7 lded aggregates in patients with amyotrophic lateral sclerosis.

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

9 ach to evaluate in patients with amyotrophic lateral sclerosis.

10 to the onset and progression of amyotrophic lateral sclerosis.

11 of Parkinson disease compared to amyotrophic lateral sclerosis.

12 egenerative disorders, including amyotrophic lateral sclerosis.

13 etabolism in the pathogenesis of amyotrophic lateral sclerosis.

14 issues and a Drosophila model of amyotrophic lateral sclerosis.

15 jects with Alzheimer disease and amyotrophic lateral sclerosis.

16 cated in human diseases, such as amyotrophic lateral sclerosis.

17 tween the studied biomarkers and amyotrophic lateral sclerosis.

18 encing as a treatment option for amyotrophic lateral sclerosis.

19 he most common cause of familial amyotrophic lateral sclerosis.

20 lopment of and predisposition to amyotrophic lateral sclerosis.

21 eases, including Parkinson's and amyotrophic lateral sclerosis.

22 of the neurodegenerative disease amyotrophic lateral sclerosis.

23 s of frontotemporal dementia and amyotrophic lateral sclerosis.

24 nd TAR DNA-binding protein 43 in amyotrophic lateral sclerosis.

25 have been identified in familial amyotrophic lateral sclerosis.

26 pathological conditions such as amyotrophic lateral sclerosis.

27 ies, traumatic brain injury, and amyotrophic lateral sclerosis.

28 rovascular diseases (1%; n = 2), amyotrophic lateral sclerosis (0.5%; n = 1) and cerebellar degenerat

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

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

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

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

33 les of 4 patients with confirmed amyotrophic lateral sclerosis (ALS) and 6 healthy controls.

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

35 odegenerative diseases including Amyotrophic Lateral Sclerosis (ALS) and Alzheimer's, Huntington's, a

36 lammation has been implicated in amyotrophic lateral sclerosis (ALS) and can be visualized using tran

37 ickness at the clinical onset of amyotrophic lateral sclerosis (ALS) and explore motor manifestation

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

39 t common known genetic cause for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

40 the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

41 e most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

42 pansions (HREs) in C9orf72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

43 G4C2 HRE) in C9orf72 that causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

44 the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

45 most prevalent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

46 4)C(2)) repeats in C9ORF72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

47 ues of Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

48 the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

49 degenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

50 ount for almost half of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

51 omains (PrLDs) that aggregate in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

52 In amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

53 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

54 ism in UNC13A is associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

55 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

56 Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

57 ion is a pathogenic signature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

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

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

60 The amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD

61 rodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

62 ping neurodegenerative disorders amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

63 affected neurons of people with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degener

64 neurodegenerative diseases like amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementi

65 in the majority of patients with amyotrophic lateral sclerosis (ALS) and in approximately 50% of pati

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

67 , frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) are

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

69 tress that is strongly linked to amyotrophic lateral sclerosis (ALS) and other neurological disorders

70 esents the defining pathology in amyotrophic lateral sclerosis (ALS) and related proteinopathies.

71 lmark of degenerating neurons in amyotrophic lateral sclerosis (ALS) and subsets of frontotemporal de

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

73 rodegenerative disorders such as amyotrophic lateral sclerosis (ALS) are limited, and optimising thei

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

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

76 rontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) by analyzing whole-genome sequen

77 Patients with amyotrophic lateral sclerosis (ALS) can have abnormal TDP-43 aggrega

78 Amyotrophic lateral sclerosis (ALS) can overlap genetically, patholo

79 temporal dementia and those with amyotrophic lateral sclerosis (ALS) carrying FUS mutations.

80 Mutations causing amyotrophic lateral sclerosis (ALS) clearly implicate ubiquitously e

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

82 ing studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD1 mutations.

83 most recent research concerning amyotrophic lateral sclerosis (ALS) emphasizes the role of glia in d

84 proximately 35% of patients with amyotrophic lateral sclerosis (ALS) exhibit mild cognitive deficits

85 arge-scale sequencing efforts in amyotrophic lateral sclerosis (ALS) have implicated novel genes usin

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

87 electric shocks with the risk of amyotrophic lateral sclerosis (ALS) in a pooled case-control study (

88 euroanatomical staging scheme of amyotrophic lateral sclerosis (ALS) indicates that a cortical lesion

89 Amyotrophic lateral sclerosis (ALS) is a complex disease with numero

90 Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerati

91 Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerati

92 Amyotrophic lateral sclerosis (ALS) is a fatal and incurable neurode

93 Amyotrophic lateral sclerosis (ALS) is a fatal disease involving mot

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

95 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

96 Background Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

97 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

98 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

99 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

100 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative dis

101 Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder

102 Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease

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

104 Amyotrophic lateral sclerosis (ALS) is a multifactorial, multisystem

105 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease c

106 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease c

107 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease i

108 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease o

109 Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron di

110 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerati

111 Amyotrophic lateral sclerosis (ALS) is a progressive neuromuscular d

112 Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurode

113 Amyotrophic lateral sclerosis (ALS) is an incurable neurological dis

114 Amyotrophic Lateral Sclerosis (ALS) is an inexorably progressive neu

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

116 rontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is incompletely understood.

117 rontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is not understood.

118 estion regarding the etiology of amyotrophic lateral sclerosis (ALS) is whether the various gene muta

119 ransgenic (NTg) and a transgenic amyotrophic lateral sclerosis (ALS) mouse model, superoxide dismutas

120 logic role of skeletal muscle in amyotrophic lateral sclerosis (ALS) onset and progression.

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

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

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

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

125 Amyotrophic lateral sclerosis (ALS) presents with focal muscle weakn

126 Although the aetiology of amyotrophic lateral sclerosis (ALS) remains poorly understood, impai

127 Paralysis occurring in amyotrophic lateral sclerosis (ALS) results from denervation of skel

128 In amyotrophic lateral sclerosis (ALS) spinal motor neurons (SpMN) prog

129 dividuals who are diagnosed with amyotrophic lateral sclerosis (ALS) today face the same historically

130 tial causal effect of smoking on amyotrophic lateral sclerosis (ALS) using the Project MinE data invo

131 ve and behavioural impairment in amyotrophic lateral sclerosis (ALS) with frontotemporal dementia (AL

132 n fused in sarcoma (FUS) lead to amyotrophic lateral sclerosis (ALS) with varying ages of onset, prog

133 f respiratory muscle weakness in amyotrophic lateral sclerosis (ALS) would identify disease mechanism

134 he RNA-binding protein FUS cause amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative

135 d frequently in individuals with amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disea

136 Amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disea

137 implicated in playing a role in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease cha

138 rodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), a relentlessly progressive and

139 th and without diagnoses of OAG, amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), Parki

140 degenerative diseases, including amyotrophic lateral sclerosis (ALS), and is characterised by activat

141 D), stroke, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), and other neuroinflammatory con

142 uch as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD).

143 utrient metabolism is altered in amyotrophic lateral sclerosis (ALS), as early as childhood, suggesti

144 motoneuron (MN) degeneration in amyotrophic lateral sclerosis (ALS), but actual proof of hyperexcita

145 f neurological diseases, notably amyotrophic lateral sclerosis (ALS), but most likely also other dise

146 n suggested as a risk factor for amyotrophic lateral sclerosis (ALS), but only retrospective studies

147 d as a susceptibility factor for amyotrophic lateral sclerosis (ALS), but results are conflicting and

148 Mutations in UBQLN2 cause amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD),

149 to the pathogenesis of familial amyotrophic lateral sclerosis (ALS), however the relative toxicities

150 In amyotrophic lateral sclerosis (ALS), immune cells and glia contribut

151 approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing

152 Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative di

153 od-spinal cord barrier (BSCB) in Amyotrophic Lateral Sclerosis (ALS), mainly by endothelial cell (EC)

154 ney disease (CKD), epilepsy, and amyotrophic lateral sclerosis (ALS), mantis-ml achieved an average a

155 us system (CNS) diseases such as amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Parkins

156 on-invasive ventilation (NIV) in amyotrophic lateral sclerosis (ALS), the question of enteral nutriti

157 SG formation is associated with amyotrophic lateral sclerosis (ALS), understanding the connection be

158 discover novel genes underlying amyotrophic lateral sclerosis (ALS), we aggregated exomes from 3,864

159 ppaB activity in pathogenesis of amyotrophic lateral sclerosis (ALS), we generated transgenic mice wi

160 Parallel proteomics with amyotrophic lateral sclerosis (ALS)-associated C9ORF72 dipeptides un

161 e transport requires ANXA11, and amyotrophic lateral sclerosis (ALS)-associated mutations in ANXA11 i

162 gnostic categories and targeting Amyotrophic Lateral Sclerosis (ALS)-associated pathways may pave the

163 In addition, expression of an amyotrophic lateral sclerosis (ALS)-associated superoxide dismutase

164 et in mice expressing a familial amyotrophic lateral sclerosis (ALS)-causing mutant SOD1 produces lon

165 s expressing either wild-type or amyotrophic lateral sclerosis (ALS)-linked mutant FUS.

166 ndamental question to comprehend amyotrophic lateral sclerosis (ALS).

167 Sarcoma (FUS) cause early-onset amyotrophic lateral sclerosis (ALS).

168 ase, polyglutamine diseases, and amyotrophic lateral sclerosis (ALS).

169 bar muscular atrophy (SBMA), and amyotrophic lateral sclerosis (ALS).

170 neurodegenerative disorders like amyotrophic lateral sclerosis (ALS).

171 he pathogenesis and treatment of amyotrophic lateral sclerosis (ALS).

172 the neurodegenerative cascade in amyotrophic lateral sclerosis (ALS).

173 end points in clinical trials in amyotrophic lateral sclerosis (ALS).

174 l lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS).

175 occurring large animal model of amyotrophic lateral sclerosis (ALS).

176 th or cause sporadic or familial amyotrophic lateral sclerosis (ALS).

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

178 vely degenerate in patients with amyotrophic lateral sclerosis (ALS).

179 sm has been repeatedly linked to amyotrophic lateral sclerosis (ALS).

180 1 (SOD1) cause familial forms of amyotrophic lateral sclerosis (ALS).

181 rophy are consistent features of amyotrophic lateral sclerosis (ALS).

182 non-coding regions of FUS cause amyotrophic lateral sclerosis (ALS).

183 in the neurodegenerative disease amyotrophic lateral sclerosis (ALS).

184 elevant regions in patients with amyotrophic lateral sclerosis (ALS).

185 have been found in patients with Amyotrophic lateral sclerosis (ALS).

186 with both sporadic and familial amyotrophic lateral sclerosis (ALS).

187 a role in the pathophysiology of amyotrophic lateral sclerosis (ALS).

188 neurons (MNs) is the hallmark of amyotrophic lateral sclerosis (ALS).

189 potential therapeutic target in amyotrophic lateral sclerosis (ALS).

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

191 the commonest cause of familial amyotrophic lateral sclerosis (ALS).

192 asticity may extend longevity in amyotrophic lateral sclerosis (ALS).

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

194 he initiation and progression of amyotrophic lateral sclerosis (ALS).

195 hat accompany motoneuron loss in amyotrophic lateral sclerosis (ALS).

196 are highly conserved features in amyotrophic lateral sclerosis (ALS).

197 rts of individuals with sporadic amyotrophic lateral sclerosis (ALS).

198 al lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).

199 euroinflammation is important in amyotrophic lateral sclerosis (ALS).

200 D1) are associated with familial amyotrophic lateral sclerosis (ALS).

201 at may contribute to the risk of amyotrophic lateral sclerosis (ALS).

202 degenerative diseases, including amyotrophic lateral sclerosis (ALS).

203 en linked to the pathogenesis of amyotrophic lateral sclerosis (ALS).

204 manifest pathological changes in amyotrophic lateral sclerosis (ALS).

205 In a subgroup of patients with amyotrophic lateral sclerosis (ALS)/Frontotemporal dementia (FTD), t

206 the most common genetic cause of amyotrophic lateral sclerosis (ALS)/frontotemporal dementia (FTD).

207 LN2 mutations result in familial amyotrophic lateral sclerosis (ALS)/frontotemporal dementia in human

208 differ between individuals with amyotrophic lateral sclerosis (ALS, n = 59) versus NC.

209 nd neurological diseases such as amyotrophic lateral sclerosis and Alzheimer's disease.

210 were noted between patients with amyotrophic lateral sclerosis and controls.

211 ases, such as Alzheimer disease, amyotrophic lateral sclerosis and even schizophrenia.

212 prevalent defect associated with amyotrophic lateral sclerosis and frontotemporal degeneration(1).

213 f72 in normal physiology, and in amyotrophic lateral sclerosis and frontotemporal degeneration.

214 a patient derived iPSC model of amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD)

215 thin C9orf72 are associated with amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD).

216 urodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD).

217 tive diseases, including C9orf72 Amyotrophic Lateral Sclerosis and Frontotemporal Dementia (ALS/FTD).

218 gene is a main cause of familial amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD

219 2 cause the most common familial amyotrophic lateral sclerosis and frontotemporal dementia (collectiv

220 eutic target for C9orf72-related amyotrophic lateral sclerosis and frontotemporal dementia and other

221 hy is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia where cyto

222 etic variant that contributes to amyotrophic lateral sclerosis and frontotemporal dementia(1,2).

223 43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia, how aggre

224 es is implicated in the diseases amyotrophic lateral sclerosis and frontotemporal dementia.

225 ene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia.

226 odegenerative diseases including amyotrophic lateral sclerosis and frontotemporal dementia.

227 Amyotrophic lateral sclerosis and frontotemporal lobar degeneration

228 rvous systems of mouse models of amyotrophic lateral sclerosis and human patients with amyotrophic la

229 le, an FDA-approved drug used in amyotrophic lateral sclerosis and known to block persistent and resu

230 e of frontotemporal dementia and amyotrophic lateral sclerosis and no mutation in known amyotrophic l

231 rsible TDP-43 aggregates form in amyotrophic lateral sclerosis and other neurodegenerative conditions

232 s a novel therapeutic target for amyotrophic lateral sclerosis and related disorders with Tar DNA-bin

233 ed as a mechanistic link between amyotrophic lateral sclerosis and spinal muscular atrophy (SMA), and

234 ffects the metabolic pathways in amyotrophic lateral sclerosis and whether these pathways can be mani

235 ntation and IL-13 inhibition for amyotrophic lateral sclerosis) and influences on longevity (leukemia

236 0.5-1% of ALS (Amyotrophic Lateral Sclerosis) and Parkinson's disease (PD) are asso

237 as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, and demyelinating diseases such as mu

238 's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease.

239 Frontotemporal dementia and amyotrophic lateral sclerosis are clinically and pathologically over

240 such as muscle fasciculations in amyotrophic lateral sclerosis, as suggested by our computational mod

241 SPA1A reduced aggregation of the amyotrophic lateral sclerosis-associated protein variant superoxide

242 chromatin accessibility of genes involved in lateral sclerosis, basal transcription factors, and fola

243 lls from a patient with sporadic amyotrophic lateral sclerosis but can be applied more generally to m

244 a negative prognostic factor in amyotrophic lateral sclerosis, but there is no evidence regarding wh

245 f the neurodegenerative disorder amyotrophic lateral sclerosis (C9-ALS) and is linked to the unconven

246 entia, Huntington's disease, and amyotrophic lateral sclerosis-characteristic protein aggregates obse

247 l phenotypes (Alzheimer disease, amyotrophic lateral sclerosis, depression, insomnia, intelligence, n

248 t the corticofugal hypothesis of amyotrophic lateral sclerosis experimentally.

249 es in transgenic mouse models of amyotrophic lateral sclerosis expressing mutant forms of either Tar

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

251 its occurrence within neurons in amyotrophic lateral sclerosis, frontotemporal dementia, and other ne

252 enerative diseases, particularly amyotrophic lateral sclerosis, frontotemporal dementias and Alzheime

253 rodegenerative diseases, such as amyotrophic lateral sclerosis, frontotemporal lobar degeneration, an

254 clerosis and human patients with amyotrophic lateral sclerosis/frontotemporal dementia.

255 causing Parkinson's disease and amyotrophic lateral sclerosis/frontotemporal dementia/myopathy, resp

256 (PD) and frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS) are insidious and incurable

257 ecline in the total score on the Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFR

258 Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised item s

259 y frontotemporal dementia and/or amyotrophic lateral sclerosis genes (TBK1, OPTN and SQSTM1) suggests

260 eral frontotemporal dementia and amyotrophic lateral sclerosis genes, including TBK1, OPTN and SQSTM1

261 ative genes and risk factors for amyotrophic lateral sclerosis have been identified.

262 (residues 286-331 containing the amyotrophic lateral sclerosis hereditary mutation A315E), which form

263 tions, meningitis, encephalitis, amyotrophic lateral sclerosis, Huntington disease, dementia, intelle

264 development for the treatment of amyotrophic lateral sclerosis, Huntington's disease, and Alzheimer's

265 number of human diseases such as amyotrophic lateral sclerosis, Huntington's disease, and Alzheimer's

266 tified that C9orf72 and sporadic amyotrophic lateral sclerosis induced astrocytes have distinct metab

267 Amyotrophic lateral sclerosis is a deleterious neurodegenerative dis

268 Amyotrophic lateral sclerosis is a rapidly progressing and fatal dis

269 rbances in the kinome network in amyotrophic lateral sclerosis is needed to properly target specific

270 Amyotrophic lateral sclerosis is the most common degenerative disord

271 e of frontotemporal dementia and amyotrophic lateral sclerosis, is translated through repeat-associat

272 sm on the disease progression in amyotrophic lateral sclerosis, it is vital to understand how the ene

273 d mSOD1 might play a role in the amyotrophic lateral sclerosis-linked aggregation of SOD1.

274 erexpression of zebrafish and an Amyotrophic Lateral Sclerosis mouse model, SOD1 G93A.

275 e abuse, temporal lobe epilepsy, amyotrophic lateral sclerosis, multiple system atrophy, and other ne

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

277 entations, potentially mimicking amyotrophic lateral sclerosis or distal hereditary motor neuropathy

278 milies with a high prevalence of amyotrophic lateral sclerosis or frontotemporal dementia, indicating

279 diminish the risk of developing amyotrophic lateral sclerosis or frontotemporal dementia, or to slow

280 s, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disea

281 the multiple roles of kinases in amyotrophic lateral sclerosis pathogenesis.

282 motor neurons specifically from amyotrophic lateral sclerosis patients carrying C9orf72 hexanucleoti

283 induced astrocytes from C9orf72 amyotrophic lateral sclerosis patients compared to normal controls,

284 Recent studies carried out on amyotrophic lateral sclerosis patients suggest that the disease migh

285 Primary lateral sclerosis (PLS) is a neurodegenerative disorder

286 cohort of patients with ALS (n=82), primary lateral sclerosis (PLS, n=10), ALS-mimic conditions (n=1

287 ing effect of HCFD for the whole amyotrophic lateral sclerosis population.

288 otor neuron-predominant forms of amyotrophic lateral sclerosis remains a significant challenge in the

289 lerosis, Parkinson's disease and amyotrophic lateral sclerosis remains elusive despite decades of res

290 tected CB2 upregulation in human amyotrophic lateral sclerosis spinal cord tissue and may thus become

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

292 otemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis) study is a prospective, multicentre,

293 jority of patients with sporadic amyotrophic lateral sclerosis (up to 97%) and a substantial proporti

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

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

296 South-East England Register for Amyotrophic Lateral Sclerosis, we performed a retrospective longitud

297 individuals and in patients with amyotrophic lateral sclerosis, we show that the piezoelectric thin f

298 ned odds ratio (for AD, FTD, and amyotrophic lateral sclerosis, which shares clinicopathological over

299 tential therapeutic strategy for amyotrophic lateral sclerosis with defective RNA metabolism.

300 a dipeptide repeat derived from amyotrophic lateral sclerosis with frontotemporal dementia (ALS/FTD)