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

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

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

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

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

8 ubclinical upper motor neuron involvement in motor neuron disease.

9 ikely to be pathophysiologically relevant to motor neuron disease.

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

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

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

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

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

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

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

17 for therapeutic purposes for SOD1 associated motor neuron disease.

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

19 utase in astrocytes expedites progression of motor neuron disease.

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

21 the pathological mechanisms of degenerative motor neuron disease.

22 c presentation of CMT4J clinically resembles motor neuron disease.

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

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

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

26 -43 as a candidate gene in familial cases of motor neuron disease.

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

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

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

30 common autosomal recessive childhood form of motor neuron disease.

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

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

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

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

35 referential degeneration of motor neurons in motor neuron disease.

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

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

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

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

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

41 n upstream event triggering neurotoxicity in motor neuron disease.

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

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

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

45 as a mechanism for neuronal degeneration in motor neuron disease.

46 in a Sprague-Dawley rat results in ALS-like motor neuron disease.

47 ases, including Alzheimer's disease (AD) and motor neuron disease.

48 5 motor cortex samples from subjects with no motor neuron disease.

49 g to its evaluation in humans suffering from motor neuron disease.

50 osomal loci associated with several types of motor neuron disease.

51 ings at MR imaging in the detection of upper motor neuron disease.

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

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

54 tissues developed normally and aged without motor neuron disease.

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

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

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

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

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

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

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

62 groups included five patients with comorbid motor neuron disease.

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

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

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

66 seases, including parkinsonian syndromes and motor neuron disease.

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

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

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

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

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

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

73 signaling might have therapeutic efficacy in motor neuron diseases.

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

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

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

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

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

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

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

81 didates for other inherited neuropathies and motor neuron diseases.

82 s and have implications for the treatment of motor neuron diseases.

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

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

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

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

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

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

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

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

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

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

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

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

95 been implicated in the familial form of the motor neuron disease amyotrophic lateral sclerosis (Lou

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

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

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

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

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

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

102 In 43 of 50 patients with motor neuron disease and 14 of 14 control subjects, matc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 The mechanisms of neuronal degeneration in motor neuron disease are not fully understood.

122 While motor neuron diseases are currently incurable, induced p

123 Motor neuron diseases are neurological disorders charact

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

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

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 ociation with amyotrophic lateral sclerosis (motor neuron disease), but none were seen in brainstem o

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

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

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

133 8 with bvFTD/motor neuron disease (32% bvFTD/motor neuron disease cases), 2 with semantic dementia (5

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

135 pinobulbar muscular atrophy is a progressive motor neuron disease caused by abnormal polyglutamine tr

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

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

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

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

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

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

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

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

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

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

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

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

148 inal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by the expansion of a polygl

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

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

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

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

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

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

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

156 lateral sclerosis (ALS) is a form of chronic motor neuron disease characterized by combined upper and

157 e develop amyotrophic lateral sclerosis-like motor neuron disease characterized by selective spinal m

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

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

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

161 In motor neuron diseases, Cu/Zn superoxide dismutase and su

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

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

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

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

166 eroxide dismutase (SOD1) result in the fatal motor neuron disease familial amyotrophic lateral sclero

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

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

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

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

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

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

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

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

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

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

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

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

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

180 al spinal muscular atrophy (SMA) is a common motor neuron disease in humans and in its most severe fo

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

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

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

184 did not modify the onset and progression of motor neuron disease in SOD1-mutant mice.

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

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

187 nt SOD1 plays no role in the pathogenesis of motor neuron disease in these mouse models.

188 Motor neuron disease in these rats depended on high leve

189 Here, we demonstrate motor neuron disease in transgenic mice expressing a SOD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 Motor neuron disease (MND) is a common neurodegenerative

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

211 ALS) develop a rapidly progressive and fatal motor neuron disease (MND) similar to amyotrophic latera

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

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

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

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

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

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

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

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

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

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

222 Motor neuron diseases (MNDs) are neurodegenerative disor

223 Motor neuron diseases (MNDs) are progressive neurodegene

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

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

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

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

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

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

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

231 Childhood onset motor neuron diseases or neuronopathies are a clinically

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

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

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

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

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

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

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

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

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

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

242 lzheimer's disease, Parkinson's disease, and motor neuron disease share a propensity to occur with in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 (ALS) is a rapidly progressive, adult-onset motor neuron disease that arises as a dominantly inherit

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

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

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

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

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

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

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

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

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

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

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

273 Here we show linkage of a lower motor neuron disease to a region of 4 Mb at chromosome 2

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 tions in the ALS2 gene linked to early-onset motor neuron disease uniformly produce loss of activity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 We suggest that motor neuron disease with early involvement of vertical

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

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

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

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

299 pression of IL-3 in transgenic mice causes a motor neuron disease with several features of amyotrophi

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