ライフサイエンスコーパス: autistic

1 ct worsens with age, becoming most severe in autistic 3- and 4-year-olds.

2 eloping children, a finding also reported in autistic adults and adolescents.

3 traumatic stress disorder, social anxiety in autistic adults, and anxiety associated with a life-thre

4 c children, but -to a less extent- higher in autistic adults.

5 in the amygdala with a 3T MRI scanner in 16 autistic and 17 control adult human participants.

6 We recruited 20 autistic and 20 typically developing children.

7 We tested autistic and age- and ability-matched typical children i

8 ch and song were compared in low-functioning autistic and age-matched control children using passive

9 Therefore, we sought to determine whether autistic and antisocial traits exhibit dissociable corti

10 total = 742 scans), and provided ratings of autistic and antisocial traits.

11 Recent gene expression data comparing autistic and control brains suggest that the normal diff

12 frontal gyrus were indistinguishable between autistic and control groups.

13 Using assessments of both subclinical autistic and subclinical antisocial traits within a larg

14 Autistic and typical participants were presented with se

15 haracterized as a function of development in autistic and typically developing children.

16 bing MEF2C function in neocortex can produce autistic- and ID-like behaviors in mice.

17 thesis of a female protective effect against autistic behavior and can be used to inform and interpre

18 social, and motor skills and development of autistic behavior.

19 Here we demonstrated that autistic behavioral and electrophysiological phenotypes

20 Male preponderance in autistic behavioral impairment has been explained in ter

21 ncentrations were also associated with fewer autistic behaviors (beta = -2.0; 95% CI: -4.4, 0.4).

22 The three oldest TTDN1 patients displayed autistic behaviors in contrast to the characteristic fri

23 Some EDCs were associated with autistic behaviors in this cohort, but our modest sample

24 In contrast, fewer autistic behaviors were observed among children born to

25 characterized by intellectual disability and autistic behaviors, holds promise for revealing the mole

26 actors that may be associated with childhood autistic behaviors.

27 ial Responsiveness Scale (SRS), a measure of autistic behaviors.

28 1; 95% CI: 0.8-7.3) was associated with more autistic behaviors.

29 fy gestational EDC exposures associated with autistic behaviors.

30 ty genes to contribute to the development of autistic behaviors.

31 ssion of brain function and the emergence of autistic behaviors.

32 t was mediated by social ability rather than autistic behaviors.

33 characterized by intellectual disability and autistic behaviors.

34 quantify specific features that distinguish autistic behaviour associated with callosal agenesis fro

35 actors may partially explain the severity of autistic behaviours and/or provide a novel (tractable) t

36 ain changes occur during the period in which autistic behaviours are first emerging.

37 lopmental disorders with a high incidence of autistic behaviours, such as fragile X syndrome, has the

38 a disruption in inhibitory signaling in the autistic brain and forge a translational path between an

39 omplete absence of functional studies of the autistic brain during early development.

40 however, little is known concerning how the autistic brain processes spatio-temporal information con

41 nriched for genes upregulated in post-mortem autistic brain, including astrocyte and microglia marker

42 at altered connectivity is a hallmark of the autistic brain.

43 ional de-differentiation occurs elsewhere in autistic brain.

44 frontal and temporal cortex is attenuated in autistic brains.

45 occipital and cerebellar cortical regions in autistic brains.

46 ld increase in the odds of having a probable autistic child (adjusted odds ratio=3.89, 95% confidence

47 We defined a probable autistic child by a PDP score>98th percentile and SRS sc

48 its but are based mainly on studies of older autistic children and adults.

49 The families of autistic children have increased emotional and financial

50 s of total movement time reduction-appear in autistic children only when exposed to objects paired wi

51 Autistic children performed far worse in temporal discri

52 n left inferior frontal gyrus was reduced in autistic children relative to controls during speech sti

53 the left arcuate fasciculus was decreased in autistic children relative to controls, structural termi

54 If true, autistic children should show reduced central tendency t

55 maller illusory reversal was demonstrated in autistic children than in neurotypical children.

56 ested that central tendency was much less in autistic children than predicted by theoretical modellin

57 a social message otherwise neglected, helps autistic children to covertly imitate the actions of oth

58 oral processing of tactile stimuli exists in autistic children, and the altered processing may interf

59 al cortex with short-range FC being lower in autistic children, but -to a less extent- higher in auti

60 for de novo likely gene-disrupting indels in autistic children.

61 a crossed-hands illusion was investigated in autistic children.

62 ignalling is impaired in human epileptic and autistic conditions, and vertebrate ADARs may have a rel

63 We first demonstrate a robust, replicated autistic deficit in binocular rivalry [11], a basic visu

64 The association for the case subgroup autistic disorder (1,310 cases) was similar: 0.88 (0.72,

65 lastoid cell lines (LCLs) from children with autistic disorder (AD) show mitoplasticity (AD-A), presu

66 The prevalence of autistic disorder (AD), a serious developmental conditio

67 -functioning adult male subjects with DSM-IV Autistic Disorder (age 18-45 years; full scale IQ >70; A

68 We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, pa

69 The RR for autistic disorder after any procedure compared with spon

70 Overall, 103 of 6959 children (1.5%) with autistic disorder and 180 of 15,830 (1.1%) with mental r

71 Relative risks (RRs) for autistic disorder and mental retardation and rates per 1

72 sociated with a small increase in the RR for autistic disorder and mental retardation compared with I

73 ing the analysis to singletons, the risks of autistic disorder associated with ICSI using surgically

74 The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We fo

75 VF treatment overall was not associated with autistic disorder but was associated with a small but st

76 atistically significantly increased risks of autistic disorder following ICSI using surgically extrac

77 mated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95

78 The adjusted OR for autistic disorder in children of folic acid users was 0.

79 nception was associated with a lower risk of autistic disorder in the MoBa cohort.

80 rn in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic rela

81 with autism spectrum disorder (i.e., DSM-IV autistic disorder or Asperger's disorder) (n = 34) and m

82 were followed up for a clinical diagnosis of autistic disorder or mental retardation until December 3

83 ms with a diagnosis code in any position for autistic disorder or other specified pervasive developme

84 al development and MECP2 mutation causes the autistic disorder Rett syndrome.

85 Heritability of ASD and autistic disorder were estimated to be approximately 50%

86 ample had been diagnosed with ASDs: 114 with autistic disorder, 56 with Asperger syndrome, and 100 wi

87 8, 1.14) for all ASDs, 1.12 (0.97, 1.30) for autistic disorder, and 1.63 (1.30, 2.04) for ASD-NOS.

88 Participants had autistic disorder, Asperger syndrome, or pervasive devel

89 thers took folic acid, 0.10% (64/61,042) had autistic disorder, compared with 0.21% (50/24,134) in th

90 supplements showed no such association with autistic disorder, even though fish oil use was associat

91 en were diagnosed with ASD, of whom 5689 had autistic disorder.

92 otherwise specified (PDD-NOS), to 0.53, for autistic disorder.

93 ebo-controlled study of NAC in children with autistic disorder.

94 C for treating irritability in children with autistic disorder.

95 autism spectrum disorders (childhood autism [autistic disorder], Asperger syndrome, atypical autism,

96 t hub function shared across the spectrum of autistic disorders - whether caused by rare highly penet

97 and diagnostic criteria for the spectrum of autistic disorders will change and become more specific

98 logy of fragile X syndrome (FXS) and related autistic disorders.

99 ted that at-risk toddlers later diagnosed as autistic display deficient left hemisphere response to s

100 hip between the sex-different development of autistic features and CRMP4 deficiency.

101 s include leanness, intellectual disability, autistic features and developmental deficits.

102 l disorder Rett syndrome (RTT) presents with autistic features and is caused primarily by mutations i

103 er that is characterized by impaired memory, autistic features and mostly severe intellectual disabil

104 ns in CTCF cause intellectual disability and autistic features in humans.

105 Autistic features of these mice represent powerful tools

106 ) determining both callosal agenesis and its autistic features, and what are the proximal mechanisms

107 elopmental delay, coordination problems, and autistic features, have not been identified.

108 n in both child- and adulthood, and included autistic features, mood disorders, obsessive-compulsive

109 ge, the onset of anxiety, hand stereotypies, autistic features, seizures and autonomic dysfunction.

110 ed body weight, intellectual disability, and autistic features.

111 eizures, severe intellectual disability, and autistic features.

112 in a child with epileptic encephalopathy and autistic features.

113 ans causes BCAA deficiency and epilepsy with autistic features.

114 ns in CTCF cause intellectual disability and autistic features.

115 evelopment of ID accompanied by epilepsy and autistic features.

116 th ID frequently accompanied by epilepsy and autistic features.

117 rty-eight 6- to 12-year-old high-functioning autistic (HFA) children and 31 typically developing (TD)

118 bined with behavioral problems consisting of autistic, hyperactive and/or aggressive behavior.

119 suggests that female sex protects girls from autistic impairments and that girls may require greater

120 ologic load was associated with quantitative autistic impairments in females compared with males.

121 e the 90th percentile had significantly more autistic impairments than the siblings of male probands

122 TRPC6, a cation channel, in a non-syndromic autistic individual.

123 k, both of which were originally impaired in autistic individuals (judgement tendency: P = 0.019, d =

124 e been observed in the post-mortem tissue of autistic individuals [8, 9], and GABAergic signaling is

125 ese signals can be accessed effectively when autistic individuals are prompted and motivated to do so

126 ncrease in the burden of smaller hotspots in autistic individuals as compared to controls.

127 Within autistic individuals depletion upregulated fronto-thalam

128 Some autistic individuals exhibit abnormal development of the

129 median size 79 kbp, range 3-96 kbp) in 2,588 autistic individuals from simplex and multiplex families

130 Genome-wide studies of autistic individuals have implicated numerous minor risk

131 Poor performance by autistic individuals on this task has widely been interp

132 Several groups have reported that autistic individuals show reduced integration of sociall

133 icalities in Bayesian terms, suggesting that autistic individuals underuse predictive information or

134 render language processing more difficult in autistic individuals, hindering social communication.

135 sm, extends to the first-degree relatives of autistic individuals, implying heritable risk.

136 mortem cerebella from 14 neurotypical and 11 autistic individuals.

137 ance communication and social behavior among autistic individuals.

138 in vitro and is altered in schizophrenic and autistic individuals.

139 risk factors in humans, on measures of both autistic-like behavior and epilepsy in Sprague-Dawley ra

140 may represent neurobiological substrates of autistic-like behavior, particularly in males, and may s

141 exhibit learning and memory impairments, and autistic-like behaviors (increased repetitive behaviors,

142 and autonomic control, cognitive impairment, autistic-like behaviors and increased risk of seizures.

143 Established measures of emergent autistic-like behaviors and standardized tests of cognit

144 r maternal stress or terbutaline resulted in autistic-like behaviors in offspring (stereotyped/repeti

145 abnormal postnatal vocalizations, and other autistic-like behaviors in the mouse.

146 vidence supporting treatment of epilepsy and autistic-like behaviors linked to DS with CBD.

147 tions presumably underlie the development of autistic-like behaviors, a clear pattern of connectivity

148 f CTNNB1 gene in regulation of cognitive and autistic-like behaviors.

149 region commonly deleted in JBS patients with autistic-like behaviour.

150 Moreover, these autistic-like behaviours are accompanied by synaptic pat

151 The autistic-like behaviours displayed by the eIF4E-transgen

152 models have resulted in synaptic defects and autistic-like behaviours including anxiety, social inter

153 s of Tsc1 in mouse cerebellar PCs results in autistic-like behaviours, including abnormal social inte

154 n animal models of autism, ameliorating some autistic-like characteristics in the offspring.

155 t-reported externalizing, internalizing, and autistic-like child behavior.

156 and demonstrate that mice lacking CDKL5 show autistic-like deficits in social interaction, as well as

157 tant mouse models of co-morbid cognitive and autistic-like disabilities.

158 ccordingly, loss of CDKL5 in mice results in autistic-like features and impaired neuronal communicati

159 at increased expression of AT-1 can cause an autistic-like phenotype by affecting key neuronal metabo

160 es signal transduction pathways and mediates autistic-like phenotypes and together establish a causal

161 We investigated the potential reversal of autistic-like phenotypes in Eif4ebp2(-/-) mice by using

162 neurodevelopmental perturbations as well as autistic-like responses.

163 hese animals demonstrate cognitive deficits, autistic-like social behavior, aberrations in synaptic p

164 idiol (CBD) effectively reduced seizures and autistic-like social deficits in a well-validated mouse

165 metabolic activity patterns associated with autistic-like social deficits.

166 is a specific trait, such as intelligence or autistic-like social impairment, and the trait could be

167 atment with lower doses of CBD also improved autistic-like social interaction deficits in DS mice.

168 vation Scale for Infants was used to measure autistic-like traits and derive clusters at 12 months of

169 Scores on a measure of autistic-like traits at 12 months of age were used in a

170 l sample) had significantly higher levels of autistic-like traits compared with cluster 2.

171 The presence of autistic-like traits in relatives of individuals with au

172 Study findings suggest the emergence of autistic-like traits resembling a broader autism phenoty

173 established to evaluate core and associated autistic-like traits, including tests for social abnorma

174 fects of OXT were negatively correlated with autistic-like traits.

175 dent in subjects scoring high on measures of autistic-like traits.

176 Mutant mouse strains with "autistic-like" phenotypes (Fmr1(-/y) and Eif4e Ser209Ala

177 beta1 and FAK are significantly decreased in autistic lymphoblasts and that Src protein expression an

178 Additionally, six of seven autistic male siblings of probands in male-male multiple

179 ion is a central component of many models of autistic neurobiology.

180 However, autistic observers showed little or no adaptation, altho

181 ges in NCAM2 expression in Down syndrome and autistic patients may therefore contribute to abnormal n

182 ecent theoretical hypothesis suggesting that autistic perception relies less on prior knowledge repre

183 ent a direct link between GABA signaling and autistic perceptual symptomatology.

184 into question unwarranted assumptions about autistic persons and their language development and use.

185 function mutations in NHE9 may contribute to autistic phenotype by modulating synaptic membrane prote

186 How regional abnormalities relate to the autistic phenotype remains unclear.

187 ordant for ASD, ASD-associated traits and no autistic phenotype.

188 genetic variation on the presentation of an autistic phenotype.

189 tors (mGluRs) mGluR1 and mGluR5 reverses the autistic phenotypes in several ASD mouse models.

190 Studies of infant siblings of older autistic probands, who are at elevated risk for autism,

191 on to detail) placed synaesthetes within the autistic range.

192 inistration of oxytocin temporally mitigates autistic social behaviours in experimental settings, it

193 ions and is associated with the emergence of autistic social deficits in the second year of life.

194 ear that is associated with the emergence of autistic social deficits.

195 was linked to the emergence and severity of autistic social deficits.

196 D adults was associated with the severity of autistic socio-communicational core symptom, that of the

197 dynamics of binocular rivalry we observed in autistic spectrum conditions.

198 People with an autistic spectrum disorder (ASD) display a variety of ch

199 The pathophysiology of autistic spectrum disorder (ASD) is not fully understood

200 esults from some studies have suggested that autistic spectrum disorder may vary by season of birth,

201 rly in pathological bonding, such as that in autistic spectrum disorder or postpartum depression.

202 Autistic spectrum disorder was the most frequent diagnos

203 Seasonal variations were specific to autistic spectrum disorder, intellectual disabilities, a

204 in (components of) group psychology, seen in autistic spectrum disorder, schizophrenia, and borderlin

205 ttention deficit hyperactivity disorder, and autistic spectrum disorder.

206 implex families, each having a child with an autistic spectrum disorder.

207 CTTNBP2 has also been associated with autistic spectrum disorder.

208 re not increased in mothers of children with autistic spectrum disorder.

209 ed fixation of eyes in autism, children with autistic spectrum disorders (ASD) and typically developi

210 case reports suggest an association between autistic spectrum disorders (ASDs) and celiac disease (C

211 o mice, which are also associated with other autistic spectrum disorders.

212 It has been suggested that the autistic spectrum might be characterized by alterations

213 ion as a function of different levels of the autistic spectrum quotient; (AQ).

214 d cross-sectional and longitudinal sample of autistic subjects and age- and gender-matched typically

215 nce network and the default mode network, in autistic subjects and age-, gender-, and IQ-matched cont

216 similar threshold was estimated for sedated autistic subjects on the basis of differences between no

217 MS mRNA levels were significantly lower in autistic subjects, especially at younger ages, and this

218 f differences between nonsedated and sedated autistic subjects.

219 2 regulate two disease-related genes, Auts2 (Autistic Susceptibility Gene2) and Bhlhb5 (mutated in He

220 Cross-trajectory overlap between the autistic symptom severity and adaptive functioning group

221 ible suite of interventions that target both autistic symptom severity and adaptive functioning shoul

222 of "yoking" of developmental trajectories in autistic symptom severity and adaptive functioning.

223 Autistic symptom severity appears to be more stable, wit

224 ajectory groups provided the best fit to the autistic symptom severity data.

225 Sex was a significant predictor of autistic symptom severity group membership and age at di

226 Autistic symptom severity was indexed using the Autism D

227 relationship between diffusion measures and autistic symptom severity.

228 with current clinical presentation to assess autistic symptomatology, we found that 8/26 (about a thi

229 as highly predictive of clinical measures of autistic symptomatology.

230 which absence of the callosum might generate autistic symptomatology?

231 nal adjustment for children's IQ or comorbid autistic symptoms attenuated the association (increase i

232 severe hypothyroxinemia had higher scores of autistic symptoms by age 6 years (adjusted B=0.23, 95% C

233 s was highly correlated with the severity of autistic symptoms in ASC, as well as autistic traits acr

234 ypothyroxinemia (gestational weeks 6-18) and autistic symptoms in children.

235 arly gestation maternal hypothyroxinemia and autistic symptoms in offspring.

236 ignificantly associated with the severity of autistic symptoms in our clinical population, and was in

237 er pathways may precede the manifestation of autistic symptoms in the first year of life.

238 Autistic symptoms in this NF1 cohort demonstrated a robu

239 rthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome.

240 iation (increase in ADHD scores adjusted for autistic symptoms, 7% [95% CI, 1%-15%]; increase in ADHD

241 t mice recapitulate almost the full range of autistic symptoms, including impairments in social inter

242 ht be responsible for later manifestation of autistic symptoms.

243 art of the core neural substrates underlying autistic symptoms.

244 ental diseases with neurological defects and autistic symptoms.

245 my, which correlate with specific aspects of autistic symptoms.

246 nd Adaptive Behavior Scales and were free of autistic symptoms.

247 personalised-medicine approaches to specific autistic syndromes.

248 Objective: To characterize the quantitative autistic trait (QAT) burden in a pooled NF1 data set.

249 um disorder (ASD) and substantially elevated autistic trait burden in individuals with neurofibromato

250 90th and 95th percentiles of the population autistic trait distributions.

251 context- (female vs male touch) and trait- (autistic trait load) specific manner.

252 Higher autistic trait ratings were associated with thinner cort

253 DNA methylation and quantitatively measured autistic trait scores across our sample cohort.

254 noleic acid status were associated with more autistic traits (all P's < 0.05).

255 y comparing scores with standard measures of autistic traits (Autism Quotient (AQ)), neurodevelopment

256 creening using a population-based measure of autistic traits (CAST assessment), structured diagnostic

257 rity of autistic symptoms in ASC, as well as autistic traits across both ASC and control groups.

258 relationship between cortical morphology and autistic traits along a continuum in a large population-

259 ifferences in cortical morphology related to autistic traits along a continuum in a large population-

260 of future autistic traits and the change in autistic traits and adaptive behavior over the same time

261 and behavior (follow-up latency and baseline autistic traits and adaptive behavior scores) in two mea

262 t (IQ), early language ability, and baseline autistic traits and adaptive behavior scores] to be pred

263 After excluding children with the highest autistic traits and confirmed ASD, the association remai

264 sent study assesses the relationship between autistic traits and decision-making in a socioeconomic g

265 tempts, along with self-reported measures of autistic traits and empathy.

266 hermore, we identified several patients with autistic traits and motor delay carrying deleterious hom

267 The results reveal for the first time that autistic traits and positive psychotic experiences inter

268 work (FPTCN) was highly predictive of future autistic traits and the change in autistic traits and ad

269 d attempts to standardise the measurement of autistic traits and to set appropriate clinical threshol

270 omega-3 status was not associated with child autistic traits and, consistently, neither was prenatal

271 onclude that individuals with high levels of autistic traits are less likely to utilize ToM as a cogn

272 Child autistic traits at 6 years were assessed by using the So

273 measures of outcome--adaptive behaviors and autistic traits at least 1 y postscan (mean follow-up la

274 In both samples, we compared sibling autistic traits between female and male probands, who we

275 so correlated with individual differences in autistic traits but there were no correlations with beha

276 tion specifically affects the development of autistic traits in addition to general neurodevelopment.

277 acid status during pregnancy affects risk of autistic traits in childhood.

278 Our results demonstrate that higher autistic traits in healthy subjects are related to lower

279 able, patterns of inheritance of subclinical autistic traits in nonclinical samples are poorly unders

280 Recent research has identified autistic traits in some transgender persons.

281 nections was associated with the severity of autistic traits in the ASD group (all r >/= 0.21, P < .0

282 io during pregnancy was associated with more autistic traits in the offspring (beta = -0.008, 95% con

283 ernal fatty acid intake during pregnancy and autistic traits in the offspring.

284 on differed in relation to the self-reported autistic traits in the typically developing population.

285 Although this screening tool measures autistic traits in this population, sensitivity for scor

286 ction strength between networks with age and autistic traits indexed by the Social Responsiveness Sca

287 Children with more autistic traits showed widespread areas of decreased gyr

288 Autistic traits span a wide spectrum of behavioral depar

289 pport to an extension of the neurobiology of autistic traits to the general population.

290 , the influence of participant self-reported autistic traits was also investigated.

291 in the live interaction only; and increased autistic traits were associated with less looking at the

292 Autistic traits were measured using the Social Responsiv

293 so assessed associations between depression, autistic traits, empathy, and likelihood of suicidal ide

294 discrepancies regarding the distribution of autistic traits, sex predominance, and association betwe

295 :omega-6 ratio is associated with more child autistic traits, which is largely accounted for by highe

296 visual-motor activity displayed more severe autistic traits, while children with greater intrinsic v

297 this context are blunted in individuals with autistic traits.

298 ypical absences, intellectual disability and autistic traits.

299 iology of both autism spectrum disorders and autistic traits.

300 ad are also correlated with ASD severity and autistic traits.

301 sure neuroimmune activation in the brains of autistic volunteers and their age and sex-matched health