ライフサイエンスコーパス: motor dysfunction

1 oms (e.g. epilepsy, intellectual disability, motor dysfunction).

2 e and understand the factors contributing to motor dysfunction.

3 neuron loss was observed in cases with major motor dysfunction.

4 elease dopamine formulations) for addressing motor dysfunction.

5 survivors of TBI are cognitive deficits and motor dysfunction.

6 f midbrain dopaminergic neurons resulting in motor dysfunction.

7 educing the risk of cerebral palsy and major motor dysfunction.

8 or diagnosis of intensive care unit-acquired motor dysfunction.

9 15T, or M337V TDP-43 transgenes cause severe motor dysfunction.

10 ognitive disorders (HAND) persist along with motor dysfunction.

11 early-onset and progressive neurological and motor dysfunction.

12 A accelerated neurodegeneration and worsened motor dysfunction.

13 sis compared to WT cells and correlated with motor dysfunction.

14 inating in both gastrointestinal sensory and motor dysfunction.

15 oning the medial forebrain bundle attenuated motor dysfunction.

16 e inflammation, decreased nerve function and motor dysfunction.

17 this combination produced dopamine loss and motor dysfunction.

18 erized by severe neurological impairment and motor dysfunction.

19 and visual tests, but not by the severity of motor dysfunction.

20 or cortex were correlated with the extent of motor dysfunction.

21 s of aging including skin, bone, immune, and motor dysfunction.

22 ed that loss of ICC could be responsible for motor dysfunction.

23 at neuropsychological risk for cognitive and motor dysfunction.

24 CC may be responsible for the development of motor dysfunction.

25 ng muscarinic blockade were not due to gross motor dysfunction.

26 uting a low GBEF value to an irreversible GB motor dysfunction.

27 totic neurons resulted in symptoms of severe motor dysfunction.

28 opamine synthesis prevents the appearance of motor dysfunction.

29 bit normal hippocampal function but moderate motor dysfunction.

30 gra pars compacta (SN) leads to debilitating motor dysfunction.

31 pamine levels, and consequent extrapyramidal motor dysfunction.

32 e characterized by cognitive, behavioral and motor dysfunction.

33 aracteristic neuropathology, and progressive motor dysfunction.

34 retardation, absence of speech, seizures and motor dysfunction.

35 contribute to the clinical manifestations of motor dysfunction.

36 pears rigid and inflexible, exacerbating the motor dysfunction.

37 in HIV-infected subjects with cognitive and motor dysfunction.

38 characterized by loss of myelin and clinical motor dysfunction.

39 ent spinal motor neuron loss and progressive motor dysfunction.

40 ognitive disorders (HAND) persist along with motor dysfunction.

41 velopmental delay, cognitive impairment, and motor dysfunction.

42 decreased neurotransmitter levels and severe motor dysfunction.

43 rentiation disruption contributes to lasting motor dysfunction.

44 iurnal patterns in neurodegenerative-related motor dysfunction.

45 through chronic pain, sensory deficits, and motor dysfunction.

46 ntia, marked TDP-43 pathology and late-onset motor dysfunction.

47 neuronal oscillatory activity are related to motor dysfunction.

48 arly-onset seizures, intellectual delay, and motor dysfunction.

49 cluding autism, intellectual disability, and motor dysfunction.

50 promote the recovery of respiratory and limb motor dysfunction.

51 visual, language, executive, behavioural, or motor dysfunction.

52 or neurons, results in life-long progressive motor dysfunction.

53 on of variation between disease duration and motor dysfunction.

54 oxylase (AADC) deficiency suffer from severe motor dysfunction.

55 ture, reduced ATP production, and flight and motor dysfunction.

56 bute to behavioral deficits in AS, including motor dysfunction.

57 r that results in debilitating cognitive and motor dysfunction.

58 isease and can be an onset symptom preceding motor dysfunction.

59 with the persistence of neuropathic pain and motor dysfunction.

60 ich contributes to parkinsonian activity and motor dysfunction.

61 progressive multiple sclerosis ameliorating motor dysfunction.

62 se clinical features including cognitive and motor dysfunction.

63 udate nucleus were inversely correlated with motor dysfunction.

64 is frequently associated with cognitive and motor dysfunction.

65 nd mild social interaction deficits, but not motor dysfunction.

66 n effects on clinical measures of apathy and motor dysfunction.

67 compacta and age-dependent L-DOPA-sensitive motor dysfunction.

68 and communication, stereotypic behaviors and motor dysfunction.

69 cturnal activity but are fertile and show no motor dysfunction.

70 ration independently predicted cognitive and motor dysfunction.

71 ns of GPe-STN network activity are linked to motor dysfunction.

72 xon regeneration often result in devastating motor dysfunction.

73 ated cannabinoid withdrawal, hypothermia, or motor dysfunction.

74 Mecp2-null mice in dopamine deregulation and motor dysfunction.

75 tipation, hypohidrosis and hyposmia, without motor dysfunction.

76 pamine levels, and consequent extrapyramidal motor dysfunction.

77 le atrophy, and debilitating and often fatal motor dysfunction.

78 hic neuronal loss that leads to cognitive or motor dysfunction.

79 outputs and thereby contribute to PD-related motor dysfunctions.

80 dity of neuropsychiatric disorder-associated motor dysfunctions.

81 multiple symptoms, including the well-known motor dysfunctions.

82 d symptoms were disfigurement (44 patients), motor dysfunction (33), and pain (26).

83 urodegenerative diseases are associated with motor dysfunction, a powerful readout for the disease.

84 2 in the writhing assay and without inducing motor dysfunction after sc administration in mice.

85 over, mod2B administration markedly improved motor dysfunction and a prolonged lifespan in Sandhoff d

86 Paroxetine attenuated motor dysfunction and body weight loss and improved gluc

87 ient in betaPP survive and breed but exhibit motor dysfunction and brain gliosis, consistent with a p

88 orated multiple RTT-like features, including motor dysfunction and breathing irregularities, in both

89 Although CCI induced significant motor dysfunction and cognitive deficits, no differences

90 duces more severe alpha-synuclein pathology, motor dysfunction and cognitive impairment when compared

91 Motor dysfunction and cognitive impairment, suggested by

92 ams contribute to altered neural maturation, motor dysfunction and death.

93 e been shown to correlate with cognitive and motor dysfunction and deficits in social behavior.

94 in a young boy who suffered from progressive motor dysfunction and developmental delay.

95 3 protein in Drosophila motor neurons led to motor dysfunction and dramatic reduction of life span.

96 ritical modulators of PD pathogenesis and/or motor dysfunction and dyskinesia: RGSs 4, 6, 9, and 10.

97 ng neuronal loss, mitochondrial enlargement, motor dysfunction and early death.

98 eads to neurological debilitation, including motor dysfunction and frank dementia.

99 hypoxia 6 weeks after PFF injection reversed motor dysfunction and halted further DA neurodegeneratio

100 The phenotype includes smooth muscle motor dysfunction and hypertensive sphincter resulting f

101 as to determine whether lack of awareness of motor dysfunction and lack of insight into mental dysfun

102 lated pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity.

103 apeutic applicability of D-520 in addressing motor dysfunction and neuroprotection in PD and PDD, as

104 ings highlight the association between early motor dysfunction and olfactory impairment, emphasising

105 expression in SCA1 Purkinje neurons improves motor dysfunction and partially restores Purkinje neuron

106 iptomic dysregulation even after substantial motor dysfunction and pathology were observed.

107 Slc38a3-cKO pups fail to thrive, exhibiting motor dysfunction and preweaning lethality.

108 aenorhabditis elegans led to reduced growth, motor dysfunction and reduced lifespan.

109 lateral sclerosis (ALS), before the onset of motor dysfunction and remains at the high levels through

110 Loss of Pum1 caused progressive motor dysfunction and SCA1-like neurodegeneration with m

111 istic gait disorder that reflects cerebellar motor dysfunction and sensory loss.

112 early lethality and precipitates age-related motor dysfunction and stress sensitivity, that is rescue

113 The disconnect between motor dysfunction and symptoms continues to promote care

114 erative disease characterized by progressive motor dysfunction and the loss of large motor neurons in

115 We examined cognitive and motor dysfunction and the relationship of behavior defic

116 ynaptic activity in mice induced ataxia-like motor dysfunctions and loss of motor precision.

117 These mice developed motor dysfunctions and progressive neurodegeneration in

118 apoptotic protease activation), behavioral (motor dysfunction), and metabolic (glucose intolerance a

119 uman GEMIN5, leads to developmental defects, motor dysfunction, and a reduced lifespan.

120 istal sciatic nerve, counteracts progressive motor dysfunction, and ameliorates neuropathic symptoms

121 sorders characterized by mental retardation, motor dysfunction, and autistic behaviors.

122 op throughout the body causing pain, sensory/motor dysfunction, and death.

123 roblems, including behavioral abnormalities, motor dysfunction, and dementia.

124 ed with developmental delay, lack of speech, motor dysfunction, and epilepsy.

125 xpression of the HuD ortholog, elav, induces motor dysfunction, and its knockdown improves motor func

126 notypes, including developmental regression, motor dysfunction, and learning and memory deficits.

127 at birth, but subsequently developed severe motor dysfunction, and perished at approximately 3 weeks

128 opathic effects including neurodegeneration, motor dysfunction, and premature death.

129 CS all lead to juvenile lethality, profound motor dysfunction, and significantly reduced Na(+) chann

130 nt were the WM tracts most closely linked to motor dysfunction, and temporal and frontal cortex were

131 the rehabilitation process of subjects with motor dysfunction, and this will contribute to the devel

132 cterized by autism, intellectual disability, motor dysfunction, anxiety, epilepsy, recurrent respirat

133 in MSA, suggesting that in MSA cognitive and motor dysfunction are decoupled; (iv) plasma neurofilame

134 but mouse models recapitulating PAF without motor dysfunction are lacking.

135 her regions of the brain, and additional non-motor dysfunctions are common.

136 t seek the mechanisms by which cognitive and motor dysfunctions arise from cerebellar degeneration.

137 pha-synuclein (alphaSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease

138 fficiency caused cognitive, psychiatric, and motor dysfunctions, as well as cortical hyperexcitabilit

139 histological evidence of cord damage and in motor dysfunction assessed 4 weeks later.

140 se models induces dose-dependent, late-onset motor dysfunction associated with loss of proprioceptive

141 Plasticity and repetitive motor dysfunction associated with mGluR5 action were mea

142 protein spinophilin in mediating repetitive motor dysfunction associated with mGluR5 function.

143 Recent studies suggest that motor dysfunction associated with the chronic nonphysiol

144 5 mg/kg) significantly attenuated neurologic motor dysfunction at 24 h (p<0.01) and 2 weeks (p<0.05)

145 el evidence for the existence of subclinical motor dysfunction at a pre-clinical stage of SCA6.

146 movement test robustly detected significant motor dysfunction at day 1, 3, and 7 post-injury that po

147 ema had significantly greater frequencies of motor dysfunction at follow-up compared with patients in

148 encephalopathy, global developmental delay, motor dysfunction, autistic features and sleep disturban

149 g is initially normal but, with the onset of motor dysfunction, becomes disrupted, accompanied by abn

150 ice not only does not reverse neurologic and motor dysfunction, but further worsens overall liver fun

151 ter injury is often accompanied by orofacial motor dysfunction, but little is known about the structu

152 Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamin

153 he striatum precedes symptoms in a number of motor dysfunctions, but it is unclear whether this is pa

154 hanges in dopamine release may contribute to motor dysfunctions characterizing senescence.

155 ed children suffer from blindness, epilepsy, motor dysfunction, cognitive decline, and premature deat

156 unction, a history of tremor, or evidence of motor dysfunction consistent with parkinsonism were soli

157 dback as a potential initiating event in ALS motor dysfunction, coupled with the ability of modified

158 s a synucleinopathy that is characterized by motor dysfunction, death of midbrain dopaminergic neuron

159 is a neurodegenerative condition featured by motor dysfunction, death of midbrain dopaminergic neuron

160 ated with an increased risk of cognitive and motor dysfunction, dementia, depression, and stroke.

161 degenerative disease characterized by severe motor dysfunction due to progressive degeneration of mes

162 Motor dysfunction (e.g., bradykinesia) and motivational

163 e treatment did result in significantly less motor dysfunction, even when no differences in levels of

164 randial colonic tone are reduced, reflecting motor dysfunctions, even in NTC.

165 Limited motor dysfunction (Expanded Disability Status Scale scor

166 logy, inflammation in the gut and brain, and motor dysfunctions, for which AEP is indispensable.

167 val scales measuring composite cognitive and motor dysfunction from pooled bedside neurocognitive exa

168 valuation of esophageal symptoms, esophageal motor dysfunction, gastroesophageal reflux disease, and

169 atal mice recapitulates SMA-like progressive motor dysfunction, growth impairment, and shortened life

170 ed-G59S mutant dynactin p150(Glued) develops motor dysfunction >8 months before loss of motor neurons

171 Brainstem or motor dysfunction had resolved in 44 of 57 (77%) at 2 mo

172 treatment) remains unknown, although spastic motor dysfunction has been related to the hyperexcitabil

173 ecp2 from the cortex or basal ganglia causes motor dysfunction, hypoactivity, and tremor, which are a

174 nt transgenic rats exhibit L-DOPA-responsive motor dysfunction, impaired striatal dopamine release as

175 NS, and delayed the onset and progression of motor dysfunction, improved body weight gain and surviva

176 n homolog significantly improves Htt-induced motor dysfunction in a fly model of HD.

177 agonist at this receptor subtype, attenuates motor dysfunction in a Parkinson's disease-relevant anim

178 n the severity of neurochemical deficits and motor dysfunction in a primate model of Parkinson's dise

179 ramatically protected from neurotoxicity and motor dysfunction in a striatal-specific model of HD eli

180 ssion of inflammatory cytokines and improved motor dysfunction in a systemic NMO mouse model.

181 tion in early stages and results in moderate motor dysfunction in adulthood.

182 chronic gastric hypersensitivity and gastric motor dysfunction in adults even in the absence of signi

183 rain abnormality that not only contribute to motor dysfunction in autism, but also deficits in social

184 on represents the first neuroimaging data of motor dysfunction in children with autism, providing ins

185 ucidating how these mechanisms contribute to motor dysfunction in conditions such as cerebral palsy a

186 nd identifies key mechanisms contributing to motor dysfunction in conditions such as cerebral palsy a

187 the present study we sought to characterize motor dysfunction in CRPS patients using kinematic analy

188 The spectrum of gastric motor dysfunction in diabetes mellitus continues to be e

189 s striatal dopamine metabolism, and prevents motor dysfunction in female mice treated with the MPTP,

190 es depletion of neurotransmitters and severe motor dysfunction in infants and children.

191 ve, late onset neuromuscular disease causing motor dysfunction in men.

192 ingERp57 in the nervous system led to severe motor dysfunction in mice associated with a loss of neur

193 tically protected from neurodegeneration and motor dysfunction in mouse models of HD.

194 Deep brain stimulation (DBS) relieves motor dysfunction in Parkinson's disease, and other move

195 dbrain dopamine neurons (mDANs) causes major motor dysfunction in Parkinson's disease, which makes ce

196 receptors contributes to the pathogenesis of motor dysfunction in Parkinson's disease.

197 ternal brain states are believed to underlie motor dysfunction in Parkinson's disease.

198 ta-band oscillations, imbalanced firing, and motor dysfunction in Parkinson's disease.

199 ht have the potential not only to ameliorate motor dysfunction in PD patients but also to modify dise

200 In addition to the well known motor dysfunction in PD patients, cognitive deficits and

201 ss of locus coeruleus neurons contributes to motor dysfunction in PD.

202 g that these mazes could be used to quantify motor dysfunction in PD.

203 mice provides a model for understanding the motor dysfunction in POMA.

204 -12 months, transgenic mice began to display motor dysfunction in rotarod testing.

205 rade axonal transport may critically mediate motor dysfunction in SBMA, but the site(s) where AR disr

206 generation, neuromuscular junction loss, and motor dysfunction in TDP-43 mice.

207 sgenic mouse model that develops progressive motor dysfunction in the absence of protein aggregation

208 e symptoms such as fatigue and cognitive and motor dysfunction in the chronic phase of TBI, where obj

209 ating neuroprotection in both and preventing motor dysfunction in the LOF mutant mouse.

210 ibitors can significantly delay the onset of motor dysfunction in the SOD1-G93A transgenic mouse mode

211 L-DOPA treatment improves motor dysfunction in these "MitoPark" mice, but this dec

212 gray matter, and averted neuronal damage and motor dysfunction in Type-B EAE mice.

213 of levodopa could significantly improve the motor dysfunction in UQCRC1 p.Tyr314Ser mutant knock-in

214 The stress-induced motor dysfunction in V408A mice is similar to that of fa

215 ia (BG) circuits contribute to cognitive and motor dysfunctions in alcohol use disorder.

216 loss of DA innervation is required to reveal motor dysfunctions in PD.

217 is characterized by extensive motor and non-motor dysfunction, including gait disturbance, which is

218 oxic stress preceded axonal degeneration and motor dysfunction, indicating a critical role for PI31 i

219 lated RNA is sufficient to cause substantial motor dysfunction, indicating that disruption of TDP43 f

220 c, deletion of Scyl1 was sufficient to cause motor dysfunction, indicating that SCYL1 acts in a neura

221 ium spiny neuron D(2)R signaling) suppresses motor dysfunction induced by L-DOPA or D(2)R-selective a

222 was to characterize the effect of FLX on the motor dysfunctions induced by a low dose of TBZ (0.75 mg

223 cy (m-/p+) for Ube3a resembles human AS with motor dysfunction, inducible seizures, and a context-dep

224 a neurodevelopmental disorder that manifests motor dysfunction, intellectual disability, autism, and

225 Motor dysfunction is an important cause of oropharyngeal

226 hip between patterned Purkinje cell loss and motor dysfunction is not straightforward.

227 Assessment of colonic motor dysfunction is rarely done because of inadequate m

228 Significant motor dysfunction is seen with no changes in learning an

229 Motor dysfunction is usually caused by weakness and the

230 a disorder associated with breast cancer and motor dysfunction, is a neuron-specific nuclear RNA bind

231 is effective in the short-term in relieving motor dysfunction, it does not stop the progressive disa

232 he longitudinal trajectory of HIV-associated motor dysfunction, its neural substrates and impact on q

233 he longitudinal trajectory of HIV-associated motor dysfunction, its neural substrates, and impact on

234 lateral sclerosis (ALS), display progressive motor dysfunction leading to paralysis and premature dea

235 f age, the Gigyf2(+/-) mice begin to exhibit motor dysfunction manifested as decreased balance time o

236 ons, underlying diseases, and rectal sensory-motor dysfunction may all contribute to its increased pr

237 Motor dysfunction may also accompany this condition.

238 f ALS-related phenotypes including kyphosis, motor dysfunctions, muscle weakness/atrophy, motor neuro

239 vous system of mice was sufficient to induce motor dysfunction, neurodegeneration, mitochondrial abno

240 shed neurodegenerative phenotypes, including motor dysfunction, neuromuscular junction defects, and s

241 earning and memory deficits) and peripheral (motor dysfunction) neurotoxic effects at concentrations/

242 ted loss and atrophy of striatal neurons and motor dysfunction, normalized expression of the striatal

243 hin the BGTC circuit that contributes to the motor dysfunction observed in PD.

244 azepine, and tamoxifen could also rescue the motor dysfunction of 7-mo-old FTLD-U mice.

245 hat recapitulate the disease progression and motor dysfunction of HD also exhibit sleep and circadian

246 of the subthalamic nucleus in mediating the motor dysfunction of Parkinson's disease and for pioneer

247 procedure that has been shown to reduce the motor dysfunction of patients with advanced Parkinson's

248 y extended lifespan and delayed the onset of motor dysfunction of SOD1 mutants, suggesting that Bax a

249 c diseases frequently experience sensory and motor dysfunctions of the urinary bladder.

250 In Parkinson's disease (PD), motor dysfunctions only become apparent after extensive

251 ty in HTT's CAG repeat as a driver of age of motor dysfunction onset, but currently, the relationship

252 e any ALS-related disease phenotypes such as motor dysfunction or decreased lifespan.

253 .001) and neuroinflammation and ameliorated motor dysfunction (P = .024).

254 antly more epidural hematoma (p < 0.001) and motor dysfunction (p = 0.049) as well as deep wound infe

255 ved vehicle continued to exhibit significant motor dysfunction (P< 0.01).

256 in cortical layer V and spinal ventral horn, motor dysfunction, paralysis, and death.

257 auses motor neuron degeneration, progressive motor dysfunction, paralysis, and death.

258 's disease is a genetic disorder that causes motor dysfunction, personality changes, dementia, and pr

259 tein also exhibit neurodegenerative changes, motor dysfunction, perturbed energy metabolism, and elev

260 oth the hyperactive and hypoactive phases of motor dysfunction preceded the detection of nuclear micr

261 ion of the drug repaglinide delayed onset of motor dysfunction, reduced striatal atrophy, and prolong

262 ral abnormalities that promote the resultant motor dysfunctions remain elusive.

263 Complex motor dysfunction remains common in HIV and is associate

264 Complex motor dysfunction remains common in HIV and is associate

265 3A) ALS mice prolonged survival, ameliorated motor dysfunction, rescued motor neuron loss, and reduce

266 s associated with increased vulnerability to motor dysfunction secondary to dopamine depletion.

267 chronic gastric hypersensitivity and gastric motor dysfunction seen in FD patients can be modeled in

268 -1 and GlyR alpha2 pre-mRNA may underlie the motor dysfunction seen in POMA.

269 rodegeneration characterized by vision loss, motor dysfunction, seizures, and often early death.

270 stic features of macrocephaly, cognitive and motor dysfunction, subcutaneous and visceral lipomas and

271 MKK7 cKO mice at 8 months showed motor dysfunctions such as weakness of hind-limb and gai

272 n projecting to the striatum, which leads to motor dysfunctions, such as bradykinesia (slowed movemen

273 t was initiated before or after the onset of motor dysfunction, suggesting a potential for such antid

274 A steady progression of motor dysfunction takes place in Huntington's disease (H

275 ontain crucial information about subclinical motor dysfunction that can be used to diagnose patients

276 y event in SMA and may be a primary cause of motor dysfunction that is amenable to therapeutic interv

277 d that Atp13a2 null mice develop age-related motor dysfunction that is preceded by neuropathological

278 r emotional stress causes episodes of severe motor dysfunction that manifest as ataxia and dystonia.

279 Building on success in rehabilitation for motor dysfunction, the delivery of vagus nerve stimulati

280 Perinatal loss of alpha1ACT leads to motor dysfunction through disruption of neurogenesis and

281 encephalomyelitis (EAE) model, with reduced motor dysfunction to allow unconfounded testing of allod

282 The relation of esophageal motor dysfunction to outcomes from antireflux surgery re

283 a are linked to ailments from behavioral and motor dysfunctions to microcephaly.

284 roprioceptors alleviates both early and late motor dysfunction, underscores the importance of conside

285 induced dopaminergic neuron degeneration and motor dysfunction via disruption of DAT function and the

286 s that reliably capture non-length dependent motor dysfunction, vocal fold weakness and respiratory d

287 In addition, motor dysfunction was markedly accelerated in G93A SOD1

288 Neurotoxicity (primarily grade 1 motor dysfunction) was reported in 14% patients and corr

289 lity solely to the patient's environment and motor dysfunction, we investigate whether a secondary fu

290 tage of disease, Purkinje cell pathology and motor dysfunction were completely reversible.

291 Motor dysfunctions were chiefly associated with the ante

292 ts in the immune system and gastrointestinal motor dysfunctions, whereas in an initial study we showe

293 mplex, with its characteristic cognitive and motor dysfunction, which is caused by HIV itself.

294 patients in this study had mild to moderate motor dysfunctions, which did not prevent them from perf

295 e impairment, cerebellar atrophy/hypoplasia, motor dysfunction with ataxia and dystonia, and nystagmu

296 f CP, defined as a nonprogressive congenital motor dysfunction with hypertonia or dyskinesia.

297 peats manifested progressive behavioural and motor dysfunction with neuron loss and gliosis in striat

298 ) mutation that recapitulate the progressive motor dysfunction with tremor, dystonia and ataxia seen

299 Significant disability arises from limb motor dysfunction, with a minority of patients requiring

300 fts, resulting in significant improvement in motor dysfunctions without tumor formation.