ライフサイエンスコーパス: motor neuron disease

1 ovement (including parkinsonism and signs of motor neuron disease).

2 nea, apnea of prematurity, spinal injury, or motor neuron disease).

3 seases, including parkinsonian syndromes and motor neuron disease.

4 e of previous reports of macroglossia in ALS/motor neuron disease.

5 el of amyotrophic lateral sclerosis, a fatal motor neuron disease.

6 g five patients without ante-mortem signs of motor neuron disease.

7 ible by including tests of subclinical upper motor neuron disease.

8 ic lateral sclerosis (FALS), a rapidly fatal motor neuron disease.

9 mutation in Vps54 (GARP protein) that causes motor neuron disease.

10 vo, we used Caenorhabditis elegans models of motor neuron disease.

11 ot all cases of frontotemporal dementia with motor neuron disease.

12 actin is disrupted by a mutation that causes motor neuron disease.

13 iments were performed on a cellular model of motor neuron disease.

14 ubclinical upper motor neuron involvement in motor neuron disease.

15 ikely to be pathophysiologically relevant to motor neuron disease.

16 bvFTD-SP and a family history of dementia or motor neuron disease.

17 on between C9ORF72 mutations and presence of motor neuron disease.

18 muscle in a pattern matching mouse models of motor neuron disease.

19 ory insufficiency, such as spinal injury and motor neuron disease.

20 akness, or symptoms that initially suggested motor neuron disease.

21 for therapeutic purposes for SOD1 associated motor neuron disease.

22 molog of DAF-16, FOXO3a, in model systems of motor neuron disease.

23 utase in astrocytes expedites progression of motor neuron disease.

24 rse myelitis and pancreatitis; and 0.009 for motor neuron disease.

25 the pathological mechanisms of degenerative motor neuron disease.

26 c presentation of CMT4J clinically resembles motor neuron disease.

27 utory risk factors rather than causative for motor neuron disease.

28 d spasticity, is the most common adult-onset motor neuron disease.

29 -43 as a candidate gene in familial cases of motor neuron disease.

30 as multiple sclerosis, Alzheimer disease and motor neuron disease.

31 r palsy syndrome, corticobasal syndrome, and motor neuron disease.

32 with serious neurological diseases, such as motor neuron disease.

33 common autosomal recessive childhood form of motor neuron disease.

34 eases and spinal muscular atrophy, a non-ALS motor neuron disease.

35 ations in its gene are associated with lower motor neuron disease.

36 review examines the problem as it relates to motor neuron disease.

37 lations of neurofilaments that accompany ALS/motor neuron disease.

38 referential degeneration of motor neurons in motor neuron disease.

39 he above-mentioned genes in microcephaly and motor neuron disease.

40 ase 1; G59S p150(glued)) that cause familial motor neuron disease.

41 ds for copper and which is inactive, develop motor neuron disease.

42 th such mutations and in most forms of human motor neuron disease.

43 hogenesis of stroke, Alzheimer's disease and motor neuron disease.

44 n upstream event triggering neurotoxicity in motor neuron disease.

45 DP-43 toxicity-induced genome instability in motor neuron disease.

46 nein motor machinery are sufficient to cause motor neuron disease.

47 or VEGF as a neurotrophic/survival factor in motor neuron disease.

48 ynactin-mediated transport can lead to human motor neuron disease.

49 otor neuropathy and LMN variants of familial motor neuron disease.

50 A), the most common lethal genetic childhood motor neuron disease.

51 eases including Alzheimer's, Parkinson's and motor neuron disease.

52 (ALS) is the most common adult degenerative motor neuron disease.

53 on-regulating protein to the pathogenesis of motor neuron disease.

54 nervous system damage in patients with rare motor neuron disease.

55 ity was conserved across these two models of motor neuron disease.

56 ave implicated miRNAs in the pathogenesis of motor neuron disease.

57 LN2 mutations failed to manifest any sign of motor neuron disease.

58 tissues developed normally and aged without motor neuron disease.

59 hich is dysfunctional in some forms of upper motor neuron disease.

60 d suggests a novel mechanism for early-onset motor neuron disease.

61 unction, by itself, is insufficient to cause motor neuron disease.

62 onent of a molecular pathway associated with motor neuron disease.

63 ses: amyotrophic lateral sclerosis and lower motor neuron disease.

64 Spinal muscular atrophy (SMA) is a motor neuron disease.

65 t and sometimes features of parkinsonism and motor neuron disease.

66 groups included five patients with comorbid motor neuron disease.

67 tion of the central nervous system or spinal motor neuron disease.

68 t cause of frontotemporal dementia (FTD) and motor neuron disease.

69 nditure will be beneficial in the setting of motor neuron disease.

70 ost common and devastating childhood genetic motor-neuron disease.

71 signaling might have therapeutic efficacy in motor neuron diseases.

72 llular pathways that have been implicated in motor neuron diseases.

73 nt leading to weakness and muscle atrophy in motor neuron diseases.

74 nfers protection against the known causes of motor neuron diseases.

75 eimer's, spinocerebellar ataxia, and several motor neuron diseases.

76 on the pathogenic cascade in SBMA and other motor neuron diseases.

77 ve of various developmental neuropathies and motor neuron diseases.

78 well as potential disease genes for non-SMN motor neuron diseases.

79 or (VEGF)] as contributors to, or causes of, motor neuron diseases.

80 tion as a potential therapeutic approach for motor neuron diseases.

81 on and the individual response to therapy in motor neuron diseases.

82 with sporadic amyotrophic lateral sclerosis/motor neuron disease].

83 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer's disea

84 ne patients had frontotemporal dementia with motor neuron disease, 19 had frontotemporal dementia alo

85 FTLD-TDP (55 nine type A including one with motor neuron disease, 27 type B including 21 with motor

86 vFTD; 5.2% of all bvFTD cases), 8 with bvFTD/motor neuron disease (32% bvFTD/motor neuron disease cas

87 th non-C9ORF72 amyotrophic lateral sclerosis/motor neuron disease (36.3 months, P < 0.05).

88 Although SMA is often considered to be a motor neuron disease, accumulating evidence suggests tha

89 bly and aggregation in cells affected by the motor neuron disease ALS.

90 -binding and strengthen the link between two motor neuron diseases, ALS and spinal muscular atrophy (

91 The fatal adult motor neuron disease amyotrophic lateral sclerosis (ALS)

92 FTD overlaps extensively with the motor neuron disease amyotrophic lateral sclerosis (ALS)

93 at mutations in dynactin can cause the human motor neuron disease amyotrophic lateral sclerosis.

94 of sites in SOD1 are known to cause a fatal motor neuron disease, amyotrophic lateral sclerosis, and

95 models of primary muscle disease and in the motor neuron disease, amyotrophic lateral sclerosis.

96 SOD1(G93A) mouse model for neurodegenerative motor neuron disease, amyotrophic lateral sclerosis.

97 s mutated in two autosomal dominant forms of motor neuron disease: amyotrophic lateral sclerosis and

98 cent progress to investigate common forms of motor neuron disease: amyotrophic lateral sclerosis, her

99 Vapb are associated with autosomal dominant motor neuron diseases: amyotrophic lateral sclerosis and

100 ions, 36% of cases with clinical evidence of motor neuron disease and 7% of the entire cohort.

101 iseases including Creutzfeldt-Jakob disease, motor neuron disease and Alzheimer's disease.

102 rative diseases such as Parkinson's disease, motor neuron disease and Creutzfeldt-Jakob disease.

103 in mu binding protein-2 (Ighmbp2) gene cause motor neuron disease and dilated cardiomyopathy (DCM) in

104 was more heterogeneous, including cases with motor neuron disease and extrapyramidal syndromes.

105 Mutations in Dctn1 are associated with motor neuron disease and frontal temporal dementia, thus

106 trophic lateral sclerosis is the most common motor neuron disease and is still incurable.

107 reviously unrecognized treatment options for motor neuron disease and motor axonal regeneration.

108 SMA is the most common inherited motor neuron disease and occurs in approximately 1:6000

109 is the underlying mechanism in SOD1-related motor neuron disease and should be considered before app

110 the spinal cord can be sufficient to induce motor neuron disease and that the activities of chaperon

111 Spinal muscular atrophy (SMA) is a motor neuron disease and the leading genetic cause of in

112 uss strategies to model different aspects of motor neuron disease and the specific neurons involved i

113 s (ALS), the most common form of adult-onset motor neuron disease and the third most common neurodege

114 Las1L are associated with congenital lethal motor neuron disease and X-linked intellectual disabilit

115 s1 gene has been linked to congenital lethal motor neuron disease and X-linked intellectual disabilit

116 larval system as a viable model for studying motor neuron diseases and for investigating time-depende

117 emporal lobar degeneration cases (FTLD-TDP), motor neuron disease, and amyotrophic lateral sclerosis.

118 s neurological conditions, including stroke, motor neuron disease, and cocaine addiction.

119 dysfunction, including Parkinson's disease, motor neuron disease, and inherited peripheral neuropath

120 d DSB repair and persistent DDR signaling in motor neuron disease, and suggest that DSB repair-target

121 While motor neuron diseases are currently incurable, induced p

122 Motor neuron diseases are neurological disorders charact

123 nduction block, vasculitic neuropathies, and motor neuron disease as paraneoplastic disorders.

124 ether as part of the same syndrome, the term motor neuron disease, as an over-arching label, was not

125 ntotemporal lobar degeneration are incurable motor neuron diseases associated with muscle weakness, p

126 es will lead to an improved understanding of motor neuron disease biology and may provide novel targe

127 use not only of frontotemporal dementia with motor neuron disease but also of late onset psychosis.

128 ess, 46 patients, including 22 familial, had motor neuron disease but no mutation in C9ORF72.

129 neuropathological phenotypes consistent with motor neuron disease by 20 months of age, ALS2(-/-) mice

130 DCTN1 mutations, previously associated with motor neuron disease, can underlie the selective vulnera

131 isolated motor neurons from SOD1-associated motor neuron disease cases suggest key genes are also di

132 8 with bvFTD/motor neuron disease (32% bvFTD/motor neuron disease cases), 2 with semantic dementia (5

133 l and bulbar muscular atrophy is an X-linked motor neuron disease caused by a CAG repeat expansion in

134 muscular atrophy is an X-linked degenerative motor neuron disease caused by an abnormal expansion in

135 Spinal muscular atrophy (SMA) is a motor neuron disease caused by deficiency of the ubiquit

136 ular atrophy (SMA) is an autosomal recessive motor neuron disease caused by deletion or mutation of S

137 Spinal muscular atrophy (SMA) is a motor neuron disease caused by dysfunction of the surviv

138 pinal muscular atrophy (SMA) is an inherited motor neuron disease caused by homozygous loss of the Su

139 Spinal muscular atrophy (SMA) is a motor neuron disease caused by loss-of-function mutation

140 Spinal muscular atrophy is a common motor neuron disease caused by low survival motoneuron (

141 significantly influenced the progression of motor neuron disease caused by mutant SOD1(G93A) express

142 tudies in a family with an inherited form of motor neuron disease caused by mutation in the p150Glued

143 y (SBMA), an adult-onset, slowly progressive motor neuron disease caused by polyglutamine expansion i

144 inal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion m

145 suggest a microtubule-dependent mechanism in motor neuron disease caused by TDP-43-dependent alterati

146 trophy (SMA) is a common autosomal-recessive motor neuron disease caused by the homozygous loss of th

147 Spinal muscular atrophy (SMA) is a motor neuron disease caused by the loss of survival moto

148 pinal muscular atrophy (SMA) is an inherited motor neuron disease caused by the mutation of the survi

149 inal muscular atrophy (SMA) is a progressive motor neuron disease causing loss of motor function and

150 hic lateral sclerosis (ALS) is a devastating motor neuron disease causing paralysis and death from re

151 ic lateral sclerosis (ALS) is a degenerative motor neuron disease, causing muscle paralysis and death

152 he clinical and scientific network of German motor neuron disease centers (ALS/MND-NET).

153 nt 3) in four siblings with infantile spinal motor neuron disease, cerebellar atrophy, progressive mi

154 tic paraplegias (HSPs) are neurodegenerative motor neuron diseases characterized by progressive age-d

155 family with a late-onset phenotype including motor neuron disease, cognitive decline resembling front

156 ifferential vulnerability to degeneration in motor neuron disease could give important clues to the m

157 Thus, adult-onset motor neuron disease does not require aggregation or los

158 or tracts and also to have shown evidence of motor neuron disease during life.

159 developed clinical features consistent with motor neuron disease during the period of follow-up.

160 neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal l

161 a, Alzheimer's disease, Parkinson's disease, motor neuron disease, epilepsy and Guillain-Barre syndro

162 a, Alzheimer's disease, Parkinson's disease, motor neuron disease, epilepsy, and Guillain-Barre syndr

163 a, Alzheimer's disease, Parkinson's disease, motor neuron diseases, epilepsy or Guillain-Barre.

164 a, Alzheimer's disease, Parkinson's disease, motor neuron diseases, epilepsy, or Guillain-Barre.

165 ll affected members of an autosomal dominant motor neuron disease family.

166 teral sclerosis (ALS) is a devastating fatal motor neuron disease, for which there is currently no cu

167 tive and behavioural impairment (MNDcbi)) or motor neuron disease-frontotemporal dementia (MND-FTD).

168 non-fluent aphasia, and FTD overlapping with motor neuron disease [FTD-MND]), followed by a meta-anal

169 , and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and on

170 UK a new programme looking at the causes of motor neuron disease has recently been sanctioned.

171 death of motor neurons in this common adult motor neuron disease has remained a mystery.

172 rms of spinal muscular atrophy, a pure lower motor neuron disease, have been characterized clinically

173 ubule-binding domain of p150Glued results in motor neuron disease; here we investigate the effects of

174 Traditionally, SMA has been described as a motor neuron disease; however, there is a growing body o

175 e spinal cord significantly delayed onset of motor neuron disease in ALS.

176 utant mice manifest a severe and early-onset motor neuron disease in an autosomal recessive manner, d

177 l dementia and amyotrophic lateral sclerosis/motor neuron disease in both familial and sporadic cases

178 a fully penetrant, autosomal recessive lower motor neuron disease in domestic cats that clinically re

179 ble of inducing fatal progressive spongiform motor neuron disease in mice that is largely mediated by

180 se Charcot-Marie-Tooth disease in humans and motor neuron disease in mice.

181 man neural stem cell (NSC) grafts ameliorate motor neuron disease in SOD1 transgenic rodents.

182 s are both essential elements in therapy for motor neuron disease in the SOD1(G93A) mice.

183 t not wild type, dynactin p150(Glued) causes motor neuron disease in these animals that are character

184 n of amyotrophic lateral sclerosis (ALS) and motor neuron disease in unique populations could provide

185 uld become a strategic therapeutic target in motor neuron diseases in which aberrant activation of th

186 some dominantly inherited familial forms of motor neuron disease including amyotrophic lateral scler

187 ect side-arm interactions, are a hallmark of motor-neuron diseases including amyotrophic lateral scle

188 some dominantly inherited familial forms of motor neuron disease, including amyotrophic lateral scle

189 milial frontotemporal lobar degeneration and motor neuron disease, including cases previously identif

190 potential disease modifier across different motor neuron diseases, including SMA.

191 yotrophic lateral sclerosis (ALS) is a fatal motor neuron disease inherited in a small subset of pati

192 sclerosis (ALS), the most common adult-onset motor neuron disease is caused by a selective loss of mo

193 Of these four subtypes, motor neuron disease is more commonly associated with ty

194 e critical biochemical target of riluzole in motor neuron disease is not known, but the pharmacologic

195 In addition to cerebellar ataxia, motor neuron disease is often seen in SCA2, and ATXN2 CA

196 The mechanism by which VAPB mutations cause motor neuron disease is unclear, but studies of the most

197 A major question in the pathogenesis of motor neuron disease is why motor neurons are selectivel

198 rophic lateral sclerosis (known in the UK as motor neuron disease) is a devastating illness with unce

199 Amyotrophic lateral sclerosis (ALS; motor neuron disease) is a relentlessly progressive diso

200 hic lateral sclerosis (ALS), the most common motor neuron disease, is caused by a selective loss of m

201 erosis (ALS) is a heterogeneous degenerative motor neuron disease linked to numerous genetic mutation

202 Although SMA is primarily a motor neuron disease, metabolism abnormalities such as m

203 e deficits, shortened lifespans, and develop motor neuron disease, mimicking the human disease.

204 SBMA), or Kennedy's disease, is a late-onset motor neuron disease (MND) caused by an abnormal expansi

205 Motor neuron disease (MND) is a common neurodegenerative

206 rganophosphorus (OP) compounds contribute to motor neuron disease (MND) is supported by association o

207 measurements of progression in patients with motor neuron disease (MND), as tools for future clinical

208 ing evidence of mitochondrial dysfunction in motor neuron disease (MND), but the molecular basis of t

209 r degeneration (FTLD), and 259 patients with motor neuron disease (MND), for whom genomic DNA was ava

210 are accompanied by histological features of motor neuron disease (MND), the term FTLD-MND is used.

211 c cause of frontotemporal dementia (FTD) and motor neuron disease (MND).

212 been linked to an autosomal dominant form of motor neuron disease (MND).

213 negative inclusions (FTLD-U) with or without motor neuron disease (MND).

214 d cognitive and/or behavioural impairment in motor neuron disease (MND).

215 cortical areas are functionally abnormal in motor neuron disease (MND, amyotrophic lateral sclerosis

216 We revealed that motor-neuron disease (MND)-linked RNA-binding proteins (

217 otrophic lateral sclerosis (ALS, also called motor neuron disease, MND) are severe neurodegenerative

218 Motor neuron diseases (MNDs) are neurodegenerative disor

219 Motor neuron diseases (MNDs) are progressive neurodegene

220 The molecular and cellular bases of motor neuron diseases (MNDs) are still poorly understood

221 Motor neuron diseases (MNDs) encompass an extensive and

222 es neurological symptoms and dysfunctions in motor neuron diseases (MNDs) such as amyotrophic lateral

223 otrophic lateral sclerosis (ALS) and related motor neuron diseases (MNDs).

224 tion does not delay disease progression in a motor neuron disease mouse model overexpressing a human

225 iants (corticobasal degeneration, n = 9; and motor neuron disease, n = 9), although most cases presen

226 ular atrophy (SMA) is an autosomal-recessive motor neuron disease of high incidence and severity and

227 modulation will help slow the progression of motor neuron disease, offering a novel treatment paradig

228 omosome 9-linked frontotemporal dementia and motor neuron disease offers the opportunity for greater

229 a, Alzheimer's disease, Parkinson's disease, motor neuron diseases or epilepsy.

230 Childhood onset motor neuron diseases or neuronopathies are a clinically

231 'ALS' OR 'Amyotrophic Lateral Sclerosis' OR 'Motor Neuron Disease' OR 'MND'.

232 a, Alzheimer's disease, Parkinson's disease, motor neuron diseases, or epilepsy.

233 greater understanding of the pathogenesis of motor neuron disease, our knowledge of the progressive b

234 ion of this structure as a primary driver in motor neuron disease pathogenesis remains uncertain.

235 ders discussed in the present review are the motor neuron diseases, peripheral neuropathies, myasthen

236 The amyotrophic lateral sclerosis/motor neuron disease phenotype is not yet well character

237 sor MR imaging alterations were specific for motor neuron disease phenotypes, with clinically overt u

238 several core behavioral features of FTD with motor neuron disease, possibly due to functional changes

239 d relatively uniform underlying pathologies: motor neuron disease predicted ubiquitinated inclusions,

240 TDP-43 in a family with dominantly inherited motor neuron disease provides evidence of a direct link

241 Although KD/SBMA has been thought of as a motor neuron disease, recent evidence indicates a key ro

242 relevance of abnormal energy homeostasis to motor neuron disease remains unclear.

243 n neurons display correction of both DCM and motor neuron disease, resulting in an essentially wild-t

244 Examination of transgenic models of motor neuron disease shows that prominent aggregates of

245 utant G93A develop a delayed and progressive motor neuron disease similar to human amyotrophic latera

246 Two models of familial motor neuron disease, SOD1(G93A) and TAU(P301L), transge

247 The motor neuron disease spinal muscular atrophy (SMA) cause

248 The inherited motor neuron disease spinal muscular atrophy (SMA) is ca

249 The inherited motor neuron disease spinal muscular atrophy (SMA) is ca

250 The motor neuron disease spinal muscular atrophy (SMA) is ca

251 The childhood motor neuron disease spinal muscular atrophy (SMA) resul

252 motor neuron (SMN) gene causes the childhood motor neuron disease spinal muscular atrophy (SMA).

253 e primary pathological targets in the lethal motor neuron diseases spinal muscular atrophy (SMA) and

254 Mutations in the SMN1 gene result in the motor neuron disease, spinal muscular atrophy (SMA).

255 urvival motor neuron (SMN) protein cause the motor neuron disease, spinal muscular atrophy (SMA).

256 is currently no treatment for the inherited motor neuron disease, spinal muscular atrophy (SMA).

257 f-function of HSJ1 is linked to a pure lower motor neuron disease, strongly suggesting that HSJ1 also

258 use of neurotrophic factors in degenerative motor neuron diseases such as amyotrophic lateral sclero

259 ets, and mutations in these proteins lead to motor neuron diseases, such as hereditary spastic parapl

260 We observed parallels to progressive motor neuron disease symptoms in these animals.

261 ral sclerosis (ALS) is the most common adult motor neuron disease that affects approximately 2/100,00

262 hic lateral sclerosis (ALS) is a progressive motor neuron disease that culminates in paralysis and de

263 B gene is associated with a familial form of motor neuron disease that has been classified as Amyotro

264 Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that has sporadic and inherited for

265 hows that deficiency in ALS2 causes an upper motor neuron disease that in humans closely resembles a

266 otrophic lateral sclerosis (FALS) is a fatal motor neuron disease that is caused by mutations in the

267 ausative for autosomal recessive early-onset motor neuron disease that is thought to predominantly af

268 Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that leads to loss of motor functio

269 Spinal muscular atrophy is an inherited motor neuron disease that results from a deficiency of t

270 n cell disease are autosomal recessive fetal motor neuron diseases that are caused by mutations in an

271 severity of spinal muscular atrophy (SMA), a motor-neuron disease that is the leading genetic cause o

272 In motor neuron disease, the focus of therapy is to prevent

273 In the primary lateral sclerosis variant of motor neuron disease, there is selective destruction of

274 al sclerosis (ALS) are among the most common motor neuron diseases to afflict the human population.

275 Eleven of these cases had characteristic motor neuron disease-type inclusions in the dentate gyru

276 d the onset and progression of the fulminant motor neuron disease typical of the rat SOD1 G93A model

277 ) is a spontaneous, relentlessly progressive motor neuron disease, usually resulting in death from re

278 neurologic function in animals with diffuse motor neuron disease via enhancement of host neuron surv

279 A family history of motor neuron disease was documented in one case.

280 th both social and language dysfunction, and motor neuron disease was more likely to emerge in these

281 Motor neuron disease was present in 55 patients (14%).

282 weakness occurred in 60% of patients, while motor neuron disease was the referring diagnosis in 30%.

283 d motor neurons is required for the onset of motor neuron disease, we generated chimeric mice in whic

284 the pathological role of mutant profilin1 in motor neuron disease, we generated transgenic lines of m

285 e crude and age-adjusted incidence rates for motor neuron disease were 1.08 and 1.50, respectively.

286 Parkinson's disease, multiple sclerosis, and motor neuron disease were not increased in persons livin

287 level sufficient to cause fatal, early-onset motor neuron disease when expressed ubiquitously, but di

288 isorders such as Huntington's disease and in motor neuron disease, where cellular stress disrupts fun

289 ases including Alzheimer's, Parkinson's, and motor neuron diseases, which may relate to its functions

290 female with atypical frontotemporal dementia-motor neuron disease who underwent temporal lobe resecti

291 Amyotrophic lateral sclerosis (ALS) is a motor neuron disease whose pathophysiological deficits,

292 hy type 1 (SMA1) is a progressive, monogenic motor neuron disease with an onset during infancy that r

293 impairment (MNDci)), behavioural impairment (motor neuron disease with behavioural impairment (MNDbi)

294 e with behavioural impairment (MNDbi), both (motor neuron disease with cognitive and behavioural impa

295 entified patients with cognitive impairment (motor neuron disease with cognitive impairment (MNDci)),

296 nked to amyotrophic lateral sclerosis and to motor neuron disease with FTLD.

297 sing ALS-linked mutants of SOD1 that develop motor neuron disease with many of the key pathological h

298 ateral sclerosis, is a progressive and fatal motor neuron disease with no effective medicine.

299 l sclerosis (ALS) is a multifactorial lethal motor neuron disease with no known treatment.

300 yotrophic lateral sclerosis (ALS) is a fatal motor neuron disease, with astrocytes implicated as cont