ライフサイエンスコーパス: ALS

1 ALS is characterized by a motor unit (MU)-dependent vuln

2 ALS mutant SOD1 induced reductions in Miro1 levels were

3 ALS patients are hypermetabolic with increased resting e

4 ALS-affected motor neurons exhibit aberrant localization

5 ALS-linked mutations in Matrin 3 led to its re-distribut

6 genome-wide association study data of 1,234 ALS cases and 2,850 controls.

7 applied our algorithm to WGS data from 3001 ALS patients who have been tested for the presence of th

8 457 (8.95%) of 4925 ALS cases carried the C9orf72 repeat expansion.

9 ers of cerebellar atrophy were found for AD, ALS, FTD, MSA, and PSP.

10 vival (HR = 0.59; 95% CI: 0.42, 0.83), after ALS diagnosis.

11 onal logistic models and with survival after ALS diagnosis using Cox proportional hazards models.

12 All ALS-FUS variants impaired anterograde and retrograde FAT

13 al and cognitive syndrome in bvFTD with ALS (ALS-FTD) is indistinguishable from that of bvFTD alone.

14 is detectable in spinal tap biofluid from an ALS rat model, where its levels change as disease progre

15 ) mice expressing a conditional allele of an ALS-linked SOD1 mutation were crossed with Tph2-Cre mice

16 in both disorders supporting the idea of an ALS/FTD continuum.

17 sses the connection between autoimmunity and ALS/FTD, and explores the possibility that C9orf72 and o

18 ndings suggest differences between bvFTD and ALS-FTD.

19 in patients (P = 0.028 and 0.051 in cLBP and ALS, respectively) were similarly detected by SUVRoccip

20 xity of the pathogenic mechanisms of FTD and ALS and suggest promising molecular targets for future t

21 ecular basis underlying their role in PD and ALS.

22 sophila model expressing human wild-type and ALS-causative PFN1 mutants.

23 ine the protein interactome of wild-type and ALS-linked MATR3 mutations, we performed immunoprecipita

24 metabolic rate, however, did not reverse any ALS-related disease phenotypes such as motor dysfunction

25 Appel ALS score, ALS Functional Rating Scale-Revised, and McGi

26 y serve as prodromal symptoms decades before ALS diagnosis.

27 we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P=1 x 10(-

28 investigate the genetic relationship between ALS and schizophrenia using genome-wide association stud

29 ional pleiotropic genes associated with both ALS and neuropsychiatric disease in the Irish population

30 RNP granules formed by ALS-linked mutant TDP-43 are more viscous and exhibit di

31 i among all conditions studied (DM1, DM2, C9-ALS, polyglutamine diseases), reduction of polyglutamine

32 eaks in rat neurons, human cells and C9orf72 ALS patient spinal cord tissues.

33 urotoxicity in a Drosophila model of C9orf72 ALS.

34 ides characteristic of DM1, DM2, and C9orf72-ALS/FTD cells was drastically decreased.

35 s endothelial corneal dystrophy, and C9orf72-ALS/FTD.

36 r-captured spinal motor neurons from C9ORF72-ALS cases, we also demonstrate that the PI3K/Akt cell su

37 ations in the gene encoding TDP-43 can cause ALS.

38 multisystem degeneration that characterises ALS.

39 During the 10 years before diagnosis, ALS patients had increasing levels of LDL-C, HDL-C, apoB

40 ith disorders including Alzheimer's disease, ALS, and ischemic brain damage (elevated d-serine) and s

41 novel cellular pathology that distinguishes ALS and further support the importance of cortical dysfu

42 of SOD1(G93A) and TDP43(A315T), established ALS-related mutations, changed the subcellular expressio

43 ne synaptic dysfunction at NMJs experiencing ALS-related degradation and demonstrate the potential to

44 are common features of sporadic and familial ALS forms.

45 al in the SOD1(G93A) mouse model of familial ALS by 11 d.

46 Rmt in the G93A-SOD1 mouse model of familial ALS, since mutant SOD1 is known to accumulate in the IMS

47 al in the SOD1(G93A) mouse model of familial ALS.

48 mal control subjects, patients with familial ALS (fALS), sporadic ALS (sALS), ALS with frontotemporal

49 haploinsufficiency of TBK1 is causative for ALS and FTD regardless of the type of mutation.

50 dence for a novel gain-of-toxic function for ALS-linked FUS involving p38 MAPK activation.

51 ding protein with important implications for ALS.

52 n of complete locked-in states, at least for ALS.

53 t for Cu(II)(atsm) as a treatment option for ALS as well as insight to the CNS-selective effects of m

54 and can serve as a possible target pool for ALS treatment.

55 ntation as a future therapeutic strategy for ALS patients.

56 omising alternative therapeutic strategy for ALS that involves targeting ataxin-2.

57 lar PPIA is a promising druggable target for ALS and support further studies to develop a therapy to

58 inase emerged as a potential drug target for ALS therapy.

59 These findings suggest that therapies for ALS may need to be tailored for different cell types and

60 itive-behavioural symptoms span a range from ALS to frontotemporal dementia, present an opportunity t

61 motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the diseases.

62 cells in both fALS and sALS, as well as FTD-ALS patients.

63 sALS), ALS with frontotemporal dementia (FTD-ALS), and Alzheimer's disease (AD), and found profound a

64 dementia/amyotrophic lateral sclerosis (FTD/ALS, n = 252), Creutzfeldt-Jakob disease (CJD, n = 239),

65 l insight into the early pathogenesis of FUS-ALS.

66 Using our new FUSDelta14 ALS mouse-antibody system we show that neurodegeneration

67 [NFL] concentrations and survival in genetic ALS.

68 Hereditary ALS is strongly associated with variants in the human C9

69 non-TDP-43 mouse models of ALS and in human ALS patients, this phenotype is largely unexplored with

70 Blood DC analysis can be used to identify ALS patients with an altered course of inflammatory cell

71 In ALS, CHIT1 CSF levels were higher compared with Con (p<0

72 often present as the initial abnormality in ALS, an early harbinger of dysfunction and aberrant firi

73 that increased RNA polymerase II activity in ALS/FTLD may lead to increased repetitive element transc

74 becoming a common pathological alteration in ALS, representing one of the earliest defects observed i

75 olated from SOD1 G93A transgenic mice and in ALS mutant SOD1 transfected cortical neurons, but the un

76 of NFL to serve as a diagnostic biomarker in ALS and the prognostic value of cerebrospinal fluid NFL

77 pies to preserve and/or restore breathing in ALS patients.

78 al to preserve/restore breathing capacity in ALS.SIGNIFICANCE STATEMENT Since neuromuscular disorders

79 l individuals and to track immune changes in ALS and determine whether these changes correlate with d

80 Language impairments were more common in ALS-FTD than bvFTD: agrammatism (p<0.017) and impaired s

81 xamine the prognostic significance of CRP in ALS.

82 f neurons and glial cells that degenerate in ALS.

83 l protein synthesis and axon degeneration in ALS and can serve as a possible target pool for ALS trea

84 Serum CHIT1 levels were not different in ALS compared with any other study group.

85 ortance of RNA metabolism and SG dynamics in ALS/FTD pathogenesis.

86 ed protein agents of neuronal dysfunction in ALS diseases.

87 gets for addressing metabolic dysfunction in ALS.

88 nderstanding of the role of fasciculation in ALS remains incomplete, fasciculations derive from ectop

89 sm, and alcoholism, occur more frequently in ALS kindreds than in controls.

90 rongly with endocytic proteins, including in ALS patient tissue.

91 e molecular pathways known to be involved in ALS.

92 we investigated [Ca2+]c and Miro1 levels in ALS mutant SOD1 expressing neurons.

93 ific surface residues on profilin mutated in ALS patients.

94 an increased burden of TIA1 LCD mutations in ALS patients compared to controls (p = 8.7 x 10(-6)).

95 The identification of TIA1 mutations in ALS/FTD reinforces the importance of RNA metabolism and

96 r PPIA is a mediator of neuroinflammation in ALS.

97 nerability of corticospinal motor neurons in ALS.

98 pses were also significantly reduced only in ALS patients.

99 nisms underlying phrenic motor plasticity in ALS may guide development of new therapies to preserve a

100 sis and prediction of disease progression in ALS and, therefore, seems suitable as a supplemental mar

101 The failure of this system in ALS may translate into the split hand presentation, gait

102 cline was lower in plasma creatinine than in ALS functional rating scale-Revised (ALSFRS-R; p<0.001).

103 ing selective loss of specific cell types in ALS are not known.

104 es explaining up to 0.12% of the variance in ALS (P=8.4 x 10(-7)).

105 ndeed, treatment of a rat model of inherited ALS (caused by a mutation in Sod1) with ASOs against Sod

106 tudy, all 202 patients included in the Irish ALS Register between January 1, 2012, and January 31, 20

107 erapeutic strategy, not only for SOD1-linked ALS, but possibly also for sporadic ALS.

108 Many ALS/FTD linked genes play a direct role in autophagy/lys

109 s such, approaches to achieve meaningful MCR-ALS models are characterized.

110 ased model freedom, proper deployment of MCR-ALS requires careful consideration of the model paramete

111 ve resolution-alternating least-squares (MCR-ALS) was applied to LC-DAD, LC-FLD, and fused LC-DAD-FLD

112 ve resolution-alternating least-squares (MCR-ALS) was applied to the UVRR spectra, as well as off-lin

113 ve resolution-alternating least-squares (MCR-ALS), to circumvent this issue while retaining the advan

114 of previously reported techniques, that MCR-ALS can produce similar results to PCA-ILS and may serve

115 control samples (34 in plasma, 39 in mucosal ALS; 13 in both sample sets).

116 rofilin1 mutant mouse line may provide a new ALS model with the opportunity to gain unique perspectiv

117 ith alternating least-squares algorithm (NMF-ALS) to solve spectral overlaps.

118 Here we studied a novel ALS/FTD family and identified the P362L mutation in the

119 We identify five potential novel ALS-associated loci using conditional false discovery ra

120 velop key features resembling key aspects of ALS, highlighting its relevance to study disease pathoge

121 llmark pathological feature in most cases of ALS is nuclear depletion and cytoplasmic accumulation of

122 gation is a component of nearly all cases of ALS, targeting ataxin-2 could represent a broadly effect

123 bly diffuse fasciculation, characteristic of ALS.

124 A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (

125 Consideration of ALS as a primary neurodegenerative disorder of the human

126 nule homeostasis constitute a cornerstone of ALS/FTLD pathogenesis.

127 role of premorbid BMI in the development of ALS and survival after diagnosis remains unclear.

128 Although the etiology of ALS remains poorly understood, abnormal protein aggregat

129 In contrast, the expression of ALS-causative human PFN1 mutants causes a less pronounce

130 e been identified as a consistent feature of ALS, studies directly examining interhemispheric neural

131 tivated microglia are a universal feature of ALS/FTD pathology; however, their role in disease pathog

132 expression, a novel pathological feature of ALS/FTLD.

133 gressive, but relatively homogeneous form of ALS.

134 xicity in the context of a prominent form of ALS.

135 dence, prevalence, phenotype and genetics of ALS and outline the core operating principles that under

136 mmatory reaction that is a major hallmark of ALS.

137 tein fused in sarcoma (FUS) are hallmarks of ALS and frontotemporal dementia subtypes.

138 The history of ALS drug discovery is fraught with many stops and starts

139 The different increase of ALS incidence in men and women points to an effect of ex

140 The APC model revealed that the increase of ALS incidence is attributable to a birth cohort effect i

141 s to understand the underlying mechanisms of ALS and identify potential therapeutic targets.

142 Here, we show that misfolding of ALS-linked SOD1 mutants and wild-type (wt) SOD1 exposes

143 Using a mouse model of ALS expressing mutant superoxide dismutase 1 (SOD1(G93A)

144 tive effect in the SOD1(G93A) mouse model of ALS, and a humanised form of this antibody (ozanezumab)

145 been reported in non-TDP-43 mouse models of ALS and in human ALS patients, this phenotype is largely

146 valuated in patients and in animal models of ALS, but have been proven disappointing in part because

147 nd RNA mislocalization as common outcomes of ALS pathogenic mutations.

148 ding protein 43 (TDP-43) in the pathology of ALS and other neurodegenerative diseases.

149 eted form of mutant SOD1 in the pathology of ALS.

150 sses are hallmarks of the pathophysiology of ALS and other neurodegenerative diseases.

151 ons and understanding the pathophysiology of ALS.

152 nsions in the ataxin-2 gene increase risk of ALS.

153 oreover, DCs derived from a subpopulation of ALS patients produced higher levels of IL-8 and CCL-2 up

154 harmacological approach for the treatment of ALS.

155 e is relevant in explaining the variation of ALS incidence rates over time in the overall population

156 In C9orf72 carriers with ALS or ALS-FTD, changes in corticospinal tractography measures

157 lores the possibility that C9orf72 and other ALS/FTD genes may have a "dual effect" on both neuronal

158 mental structural study on eleven new ANG-PD/ALS variants which will have implications in understandi

159 , 2014, with definite, probable, or possible ALS as defined by El Escorial criteria were invited to p

160 5 patients with ALS drawn from 3 prospective ALS registers (Ireland, Italy and the Netherlands), and

161 In a rat ALS model (SOD1(G93A) ) we previously demonstrated that

162 underlies the pathogenesis of TDP-43-related ALS, the roles of wild-type TDP-43 in mitochondria are u

163 sport of mitochondria in mutant SOD1-related ALS we investigated [Ca2+]c and Miro1 levels in ALS muta

164 lay, site of onset, and score on the Revised ALS Functional Rating Scale.

165 th familial ALS (fALS), sporadic ALS (sALS), ALS with frontotemporal dementia (FTD-ALS), and Alzheime

166 nset, survival, ALS Functional Rating Scale (ALS-FRS) scores and respiratory function were analysed.

167 approach to amyotrophic lateral scleorosis (ALS)/frontotemporal dementia (FTD).

168 patients with amyotrophic lateral sclerosis (ALS) [5, 6].

169 patients with amyotrophic lateral sclerosis (ALS) although it is reported by most of these patients.

170 patients with amyotrophic lateral sclerosis (ALS) and developmental delay, intellectual disability an

171 se that cause amyotrophic lateral sclerosis (ALS) and fragile X syndrome, is challenging for short-re

172 Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) share overlapping

173 prevalence in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

174 cases of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

175 etic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the mechanisms

176 es, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

177 thogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

178 thogenesis of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Lobar Dementia (FTLD).

179 y reaction in amyotrophic lateral sclerosis (ALS) and is toxic for motor neurons.

180 al neurons in amyotrophic lateral sclerosis (ALS) and to neocortical hyperexcitability, a prominent f

181 erpinnings of amyotrophic lateral sclerosis (ALS) are complex and incompletely understood, although c

182 of heritable amyotrophic lateral sclerosis (ALS) binds to the central channel of the nuclear pore an

183 Amyotrophic lateral sclerosis (ALS) has an immune component, but previous human studies

184 to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-sensitive a

185 Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is characterized by

186 Amyotrophic lateral sclerosis (ALS) is a devastating and incurable neurodegenerative di

187 Amyotrophic lateral sclerosis (ALS) is a heterogeneous degenerative motor neuron diseas

188 Amyotrophic lateral sclerosis (ALS) is a multifactorial lethal motor neuron disease wit

189 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative condition primar

190 Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerative disease c

191 Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disorder

192 Amyotrophic lateral sclerosis (ALS) is debilitating neurodegenerative disease character

193 biomarker in amyotrophic lateral sclerosis (ALS) is needed.

194 ase course of amyotrophic lateral sclerosis (ALS) is rapid and, because its pathophysiology is unclea

195 t-derived MNs.Amyotrophic lateral sclerosis (ALS) leads to selective loss of motor neurons.

196 Amyotrophic lateral sclerosis (ALS) may be associated with low body mass index (BMI) at

197 ouse model of amyotrophic lateral sclerosis (ALS), a disease in which corticospinal neurons exhibit s

198 lial forms of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by progr

199 biomarkers of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease, we measur

200 le sclerosis, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease.

201 ein FUS cause amyotrophic lateral sclerosis (ALS), but the biophysical properties of these proteins h

202 e of familial amyotrophic lateral sclerosis (ALS), but the mechanisms underlying repeat-induced disea

203 prevalent in amyotrophic lateral sclerosis (ALS), but there is limited information on its associatio

204 ders, such as amyotrophic lateral sclerosis (ALS), end life via respiratory failure, the ability to h

205 euron disease amyotrophic lateral sclerosis (ALS), especially at the genetic level.

206 mentia (FTD), amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), progressive supranu

207 patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between th

208 se (LOAD) and amyotrophic lateral sclerosis (ALS), two major neurodegenerative diseases, in single-nu

209 r hallmark of amyotrophic lateral sclerosis (ALS), which is currently untreatable.

210 s of sporadic amyotrophic lateral sclerosis (ALS), while rarely documented, reflect failure of adapti

211 ial defects in Amytrophic Lateral Sclerosis (ALS)- and Alzheimer's disease (AD)-linked neurons.

212 s promoted by amyotrophic lateral sclerosis (ALS)-linked mutations, but the cellular functions affect

213 from advanced amyotrophic lateral sclerosis (ALS)-two of them in permanent CLIS and two entering the

214 ative disease amyotrophic lateral sclerosis (ALS).

215 use model for amyotrophic lateral sclerosis (ALS).

216 OD1 all cause amyotrophic lateral sclerosis (ALS).

217 physiology of amyotrophic lateral sclerosis (ALS).

218 al markers of amyotrophic lateral sclerosis (ALS).

219 f survival in amyotrophic lateral sclerosis (ALS).

220 rited form of amyotrophic lateral sclerosis (ALS).

221 generation in Amyotrophic lateral sclerosis (ALS).

222 use models of amyotrophic lateral sclerosis (ALS).

223 patients with amyotrophic lateral sclerosis (ALS).

224 ative disease amyotrophic lateral sclerosis (ALS).

225 al feature of amyotrophic lateral sclerosis (ALS).

226 sociated with Amyotrophic Lateral Sclerosis (ALS, motor neurone disease) (sporadic and familial) and

227 Appel ALS score, ALS Functional Rating Scale-Revised, and McGill Quality

228 sensor, we utilize the ambient light sensor (ALS) of the smartphone as light intensity detector and i

229 However, the observation that some ALS-linked PFN1 mutants fail to alter cellular actin org

230 These SOD1-specific ALS natural history data will be important for the desig

231 CSF of SOD1(G93A) mice and rats and sporadic ALS patients, suggesting that our findings may be releva

232 patients with familial ALS (fALS), sporadic ALS (sALS), ALS with frontotemporal dementia (FTD-ALS),

233 1-linked ALS, but possibly also for sporadic ALS.

234 gregation of RRM2 fragments seen in sporadic ALS patients.

235 he TDP-43 pathological signature of sporadic ALS is restricted to cortical areas as well as to subcor

236 ars with a diagnosis of familial or sporadic ALS were randomly assigned (1:1), centrally according to

237 uron loss, questioning its validity to study ALS.

238 Age of onset, survival, ALS Functional Rating Scale (ALS-FRS) scores and respira

239 ivascular end-feet astrocytes in symptomatic ALS mice may represent BSCB repair processes, supporting

240 n (IGVL) genes among patients with systemic (ALS) and localized (ALL) amyloidosis and to assess for a

241 V from target regions (cLBP study, thalamus; ALS study, precentral gyrus) was normalized with the SUV

242 Together these results provide evidence that ALS mutant SOD1 inhibits axonal transport of mitochondri

243 We have previously shown that ALS-associated mutations in Cu/Zn superoxide dismutase 1

244 They further suggest that ALS-linked mutations in PFN1 may perturb cellular microt

245 The ALS Functional Rating Scale (ALSFRS-R) and King's stage

246 Although the ALS-like phenotype of SOD1(G93A) mice is instigated by e

247 ALS Functional Rating Score-Revised and the ALS Milano-Torino Staging system at baseline and 6, 12,

248 y, secretion of wild-type human SOD1 and the ALS-linked mutant in human cells also require the diacid

249 udy, disease progression was assessed by the ALS Functional Rating Score-Revised and the ALS Milano-T

250 (log[NFL]) concentrations were higher in the ALS and FTD groups compared with the motor neuropathies

251 and implementation of clinical trials in the ALS(SOD1) patient population.

252 ression level of wild-type PFN1, but not the ALS-linked PFN1 mutants, increased microtubule growth ra

253 mpairment, as measured by total score on the ALS Functional Rating Scale-Revised, at first evaluation

254 isms of neurodegeneration that contribute to ALS pathogenesis.

255 g has emerged as a mechanism contributing to ALS pathology.

256 little is known about their contribution to ALS.

257 d further link cellular transport defects to ALS.

258 highlights the contribution of microglia to ALS/FTD pathogenesis, discusses the connection between a

259 veloping therapeutic strategies for treating ALS.SIGNIFICANCE STATEMENT It is not known why certain c

260 avelling the molecular mechanisms underlying ALS.

261 Functional studies in various ALS models are revealing a complex scenario where distin

262 of BMI and BMI change at different ages with ALS risk using unconditional logistic models and with su

263 extensive reductions of VMHC associated with ALS in brain regions of the precentral and postcentral g

264 olipoprotein metabolisms are associated with ALS risk and may serve as prodromal symptoms decades bef

265 middle age may be positively associated with ALS risk.

266 vioural and cognitive syndrome in bvFTD with ALS (ALS-FTD) is indistinguishable from that of bvFTD al

267 In C9orf72 carriers with ALS or ALS-FTD, changes in corticospinal tractography me

268 CHIT1 concentrations were correlated with ALS disease progression and severity but not with the su

269 63.5 [9.9] years) and 119 participants with ALS (50 women [42.0%] and 69 men [68.0%]; mean [SD] age,

270 al inflammatory markers in participants with ALS and healthy control individuals and to track immune

271 A total of 394 patients with ALS (168 women and 226 men; mean [SD] age at diagnosis,

272 n an independent cohort of 116 patients with ALS (50 women and 66 men; mean [SD] age at diagnosis, 67

273 A total of 77 patients with ALS (61.4%) and 51 control participants (38.6%) reported

274 cs of pNfH in CSF and serum of patients with ALS and controls were calculated and compared using rece

275 concentrations are elevated in patients with ALS and correlate with the disease progression rate.

276 These findings suggest that patients with ALS and elevated serum CRP levels progress more rapidly

277 ed pluripotent stem cells from patients with ALS and FUS mutations, the authors demonstrate that axon

278 al CSF SOD1 protein content in patients with ALS caused by different SOD1 mutations.

279 Serum CRP levels in the 394 patients with ALS correlated with severity of functional impairment, a

280 raphic/clinical data from 4925 patients with ALS drawn from 3 prospective ALS registers (Ireland, Ita

281 Nearly all patients with ALS have aggregates of the RNA-binding protein TDP-43 in

282 1 concentrations in the CSF of patients with ALS may reflect the extent of microglia/macrophage activ

283 30, 2015, in a large cohort of patients with ALS observed by an Italian tertiary multidisciplinary ce

284 K1 missense mutations found in patients with ALS or FTD is prevented by missing data demonstrating co

285 A total of 479 patients with ALS were alive and had not undergone tracheostomy at the

286 ica evaluated records from 175 patients with ALS with genetically confirmed SOD1 mutations, cared for

287 In the spinal cord of patients with ALS, but not Con, AD or CJD cases, CHIT1 was expressed i

288 ltifactorial nature of pain in patients with ALS, different treatments have been suggested, ranging f

289 icacy compared with placebo in patients with ALS.

290 urements were available for 78 patients with ALS.

291 CC subregions II, III and V in patients with ALS.

292 and efficacy of ozanezumab in patients with ALS.

293 of cerebrospinal fluid NFL in patients with ALS.

294 of individualised medicine for patients with ALS.

295 and second-degree relatives of patients with ALS.

296 a population-based registry of patients with ALS.

297 lopment of better treatments for people with ALS.

298 If replicated with ALS patients in CLIS, these positive results could indic

299 ation of rs10463311 spanning GPX3-TNIP1 with ALS (p = 1.3 x 10(-8)), with replication support from tw

300 redominant PBA) more prevalent in women with ALS.