ライフサイエンスコーパス: amyotrophic

1 brain data and clinical parameters (revised amyotrophic functional rating scale, slow vital capacity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 In amyotrophic lateral sclerosis (ALS) and frontotemporal d

24 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

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

27 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

28 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

30 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

31 Amyotrophic lateral sclerosis (ALS) and frontotemporal d

32 The amyotrophic lateral sclerosis (ALS) and frontotemporal d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Amyotrophic lateral sclerosis (ALS) can overlap genetica

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

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

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

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

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

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

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

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

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

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

60 Amyotrophic lateral sclerosis (ALS) is a complex disease

61 Amyotrophic lateral sclerosis (ALS) is a devastating neu

62 Amyotrophic lateral sclerosis (ALS) is a devastating neu

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

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

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

66 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

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

68 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

69 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

70 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

71 Amyotrophic lateral sclerosis (ALS) is a fatal neurodege

72 Amyotrophic lateral sclerosis (ALS) is a fatal neurologi

73 Amyotrophic lateral sclerosis (ALS) is a fatal neuromusc

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

75 Amyotrophic lateral sclerosis (ALS) is a multifactorial,

76 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

77 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

78 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

79 Amyotrophic lateral sclerosis (ALS) is a neurodegenerati

80 Amyotrophic lateral sclerosis (ALS) is a progressive mot

81 Amyotrophic lateral sclerosis (ALS) is a progressive neu

82 Amyotrophic lateral sclerosis (ALS) is a progressive neu

83 Amyotrophic lateral sclerosis (ALS) is a rapidly progres

84 Amyotrophic lateral sclerosis (ALS) is an incurable neur

85 Amyotrophic Lateral Sclerosis (ALS) is an inexorably pro

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

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

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

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

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

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

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

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

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

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

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

97 Amyotrophic lateral sclerosis (ALS) presents with focal

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

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

100 In amyotrophic lateral sclerosis (ALS) spinal motor neurons

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

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

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

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

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

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

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

108 Amyotrophic lateral sclerosis (ALS), a fatal neurodegene

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 nderlie neurodegenerative diseases including amyotrophic lateral sclerosis and frontotemporal dementi

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

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

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

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

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

204 Amyotrophic lateral sclerosis and frontotemporal lobar d

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

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

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

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

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

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

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

212 Frontotemporal dementia and amyotrophic lateral sclerosis are clinically and patholo

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

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

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

216 Amyotrophic Lateral Sclerosis Functional Rating Scale-Re

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

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

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

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

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

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

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

224 Amyotrophic lateral sclerosis is a deleterious neurodege

225 Amyotrophic lateral sclerosis is a rapidly progressing a

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

227 Amyotrophic lateral sclerosis is the most common degener

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 0.5-1% of ALS (Amyotrophic Lateral Sclerosis) and Parkinson's disease (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 ported in neurodegenerative diseases such as amyotrophic lateral sclerosis.

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

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

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

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

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

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

283 ty of neurodegenerative disorders, including amyotrophic lateral sclerosis.

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

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

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

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

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

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

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

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

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

293 milial form of the neurodegenerative disease amyotrophic lateral sclerosis.

294 pathogenesis of frontotemporal dementia and amyotrophic lateral sclerosis.

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

296 43 (TDP-43) have been identified in familial amyotrophic lateral sclerosis.

297 affected by pathological conditions such as amyotrophic lateral sclerosis.

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

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

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