ライフサイエンスコーパス: autistic

1 at the same bias did not appear to emerge in autistic adolescents in this study may explain some of t

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

3 sitively related to anxiety symptoms, and in autistic adults, perseveration (indexed by both task err

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

5 g methods to classify 22 autistic and 22 non-autistic adults.

6 ised machine learning methods to classify 22 autistic and 22 non-autistic adults.

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

8 ery limited or no therapeutic effects on the autistic and cognitive phenotypes in the Fmr1 KO2 mice,

9 the age of brain cortical morphology in both autistic and healthy individuals.

10 tional brain features related to age in both autistic and healthy populations.

11 d comparably at a sensorimotor level in both autistic and neurotypical individuals with varying level

12 For both autistic and non-autistic individuals, transgender and g

13 dose of bryostatin-1 effectively rescued the autistic and non-spatial learning deficit cognitive phen

14 Autistic and typical participants were presented with se

15 dentified but were not formally diagnosed as autistic, and 59 were not diagnosed or self-identified,

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

17 FOXP1 haploinsufficiency is characterized by autistic behavior, language impairment, and intellectual

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

19 Here we demonstrated that autistic behavioral and electrophysiological phenotypes

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

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

22 rare disease marked by early-life seizures, autistic behaviors, and intellectual disability.

23 microbiota is sufficient to induce hallmark autistic behaviors.

24 hat trigger impaired synaptic maturation and autistic behaviors.

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

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

27 characterized by intellectual disability and autistic behaviors.

28 actors that may be associated with childhood autistic behaviors.

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

30 losure encourages development and attenuates autistic behaviors.

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

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

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

34 volume declined with age at a slower rate in autistic boys and girls relative to typically developing

35 vity has been found in the amniotic fluid of autistic boys, based on measuring prenatal androgens and

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

37 vidence for altered visual processing in the autistic brain exists.

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

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

40 s best predicts the morphological age of the autistic brain.

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

42 are associated with fiber development in the autistic brain.

43 has revealed that a substantial fraction of autistic brains possess distinct transcriptomic signatur

44 me lncRNAs show altered expression levels in autistic brains, but their roles in ASD pathogenesis are

45 ime looking at the face, but weaker when the autistic child spent more time looking at the face.

46 ges of approximately 2.5 to 7.0 years in 125 autistic children and 69 typically developing control pa

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

48 resonance imaging studies suggest that young autistic children have alterations in white matter struc

49 d a smaller cohort of 30 age- and IQ-matched autistic children on the same task, we found some early

50 Autistic children performed far worse in temporal discri

51 entences with weak cross-modal coordination, autistic children produced similar levels of cross-modal

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

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

54 Autistic children were found to have slower development

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

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

57 In autistic children, perseverative errors were positively

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

59 nition in human technology; (2) tradeoffs of autistic cognition with social skills; and (3) a model o

60 The blanket dismissal of assisted autistic communication is therefore unwarranted.

61 Autistic cortico-cortical interactions vary by context,

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

63 of pervasive developmental disorder (PDD) or autistic disorder (AD) according to International Classi

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

65 ovo mutations (DNMs) from 1628 subjects with autistic disorder (AD), 1873 from 1564 subjects with per

66 The secondary outcome was autistic disorder (AD).

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

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

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

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

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

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

75 that increases in these indices characterize autistic facial expression, compared with neurotypical i

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

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

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

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

80 obal developmental delay, motor dysfunction, autistic features and sleep disturbances.

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

82 However, the pathogenic origin of the autistic features of CDD remains unknown.

83 Autistic features of these mice represent powerful tools

84 All patients had autistic features, and autism spectrum disorder (ASD) wa

85 ed by epilepsy, intellectual disability, and autistic features, and CDKL5-deficient mice exhibit a co

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

87 sability, muscle weakness and abnormal tone, autistic features, behavioral abnormalities, and variabl

88 tellectual disability with language deficit, autistic features, behavioural abnormalities, epilepsy,

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

90 ual disability (ID), motor and speech delay, autistic features, hypotonia, feeding difficulties, spas

91 ASD or autistic features, language and motor delay, and variabl

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

93 eizures, severe intellectual disability, and autistic features.

94 ns in CTCF cause intellectual disability and autistic features.

95 evelopment of ID accompanied by epilepsy and autistic features.

96 th ID frequently accompanied by epilepsy and autistic features.

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

98 t since birth), intellectual disability, and autistic features.

99 al cortex (PFC) of Shank3-deficient mice and autistic human postmortem brains.

100 esponses to sulforaphane in both healthy and autistic humans, and providing guidance for biomedical i

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

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

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

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

105 This finding may inform how autistic individuals are perceived in their daily conver

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

107 Within autistic individuals depletion upregulated fronto-thalam

108 Some autistic individuals exhibit abnormal development of the

109 Autistic individuals experience significantly elevated r

110 ants, we directly tested the hypothesis that autistic individuals have atypical white matter developm

111 important to identify sources of trauma for autistic individuals in order to reduce their occurrence

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

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

114 Autistic individuals showed abnormally increased task-dr

115 Autistic individuals showed on average more perseveratio

116 ly imitate unusual movement kinematics while autistic individuals tended to fail.

117 from the experimental condition in which non-autistic individuals tended to successfully imitate unus

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

119 In the uncinate fasciculus, autistic individuals who decreased in autism symptom sev

120 Furthermore, in the sagittal stratum, autistic individuals who increased in autism severity ov

121 For example, autistic individuals with disproportionate megalencephal

122 the positive effects of repeated oxytocin on autistic individuals' facial expressions and demonstrate

123 Support should be collaborative, with autistic individuals, families, and service providers ta

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

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

126 e considered, along with the perspectives of autistic individuals, in both research and practice.

127 motor, temporal and prefrontal cortex in the autistic individuals, relative to the control groups.

128 For both autistic and non-autistic individuals, transgender and gender-diverse ind

129 hite matter structure that differ from older autistic individuals.

130 ative agency in a sample of nine nonspeaking autistic letterboard users.

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

132 t-refractory epilepsy, cognitive impairment, autistic-like behavior, and premature death.

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

134 astrocytes, defined by Gfap, failed to cause autistic-like behavioral abnormalities.

135 malities, improve cognitive deficits, revert autistic-like behaviors and protect against seizures.

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

137 se inhibition of NMDAR signaling ameliorates autistic-like behaviors in GABAergic knockout mice, as w

138 uronal net-enwrapped parvalbumin neurons and autistic-like behaviors in MIA/HI offspring.

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

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

141 f MIA and neonatal hypoxia ischemia produces autistic-like behaviors in the offspring, and has synerg

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

143 Conversely, HI neither provoked autistic-like behaviors nor concealed them in the MIA of

144 Instead, the dual MIA/HI insult added autistic-like behaviors with diminished synaptic density

145 We found that MIA induced autistic-like behaviors without microglial activation bu

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

147 y disorder (CDD) is a rare disease marked by autistic-like behaviors, intellectual disability, and se

148 d inhibitory synaptic functions, engendering autistic-like behaviors.

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

150 onocytic infiltrates, perineuronal nets, and autistic-like behaviors.

151 al neurogenesis, leading to macrocephaly and autistic-like behaviors.

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

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

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

155 a formal autism diagnosis, but experiencing autistic-like difficulties, use similar compensatory str

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

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

158 aling and circuit hyperexcitability underlie autistic-like features in mouse models of CDD and provid

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

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

161 loss of CDKL5 in GABAergic neurons leads to autistic-like phenotypes in mice accompanied by excessiv

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

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

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

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

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

167 rotypical individuals with varying levels of autistic-like traits.

168 s in a phenotype of extreme macrocephaly and autistic-like traits.

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

170 Here, we describe a severely autistic male patient carrying a single amino acid subst

171 Here we used functional MRI to scan autistic males (n = 19) without intellectual disability

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

173 2; Experiment 1) and in clinically diagnosed autistic participants (n = 29; Experiment 2).

174 ating paradigm with a group of 18 adolescent autistic participants and 18 typically developing contro

175 effect was present for both neurotypical and autistic participants, indicating similarities in their

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

177 About one-third of autistic people have limited ability to use speech.

178 anding of how to model heterogeneity between autistic people will facilitate progress towards precisi

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

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

181 smissed the possibility that any nonspeaking autistic person who communicates with assistance could b

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

183 necessary and sufficient to transduce MIA to autistic phenotype in male offspring.

184 everse the compromised brain development and autistic phenotype pointing to new possibilities for pre

185 stration of ATP to P2rx7 WT dams also evoked autistic phenotype, but not in KO dams, implying that P2

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

187 igated whether bryostatin-1 might affect the autistic phenotypes and other behaviors, including open

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

189 Given the known heterogeneity within the autistic population, it is crucial to design tests of se

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

191 for the two SSBI phenotypes from parents to autistic probands.

192 his reduction was positively correlated with autistic quotient scores, consistent with an atypical vi

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

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

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

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

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

198 rldwide via social media and the UK National Autistic Society formed a convenience sample.

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

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

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

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

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

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

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

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

207 ttention deficit hyperactivity disorder, and autistic spectrum disorder.

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

209 The autistic spectrum is characterized by profound impairmen

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

211 Recently, it has been suggested that the autistic spectrum might be characterized by alterations

212 convergence in post-mortem brain tissue from autistic subjects.

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

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

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

216 Autistic symptom severity appears to be more stable, wit

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

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

219 Autistic symptom severity was indexed using the Autism D

220 relationship between diffusion measures and autistic symptom severity.

221 which absence of the callosum might generate autistic symptomatology?

222 l cases of Phelan-McDermid syndrome, causing autistic symptoms and a severe delay in motor skill acqu

223 ionship between ophthalmologic disorders and autistic symptoms and severity.

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

225 Autistic symptoms in this NF1 cohort demonstrated a robu

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

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

228 ht be responsible for later manifestation of autistic symptoms.

229 ental diseases with neurological defects and autistic symptoms.

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

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

232 personalised-medicine approaches to specific autistic syndromes.

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

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

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

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

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

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

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

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

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

242 The relation between autistic traits and brain mechanisms underlying spontane

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

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

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

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

247 ponsiveness Scale-II (SRS-2) as a measure of autistic traits and social impairment.

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

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

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

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

252 olites were associated with higher scores of autistic traits as measured by the SRS-2 in boys, but no

253 21 children with genetic data, parents rated autistic traits at 6 years of age.

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

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

256 participants with an above-median number of autistic traits benefited more from the presence of high

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

258 diagnosed autism and significantly stronger autistic traits compared to controls, as well as a signi

259 ationship between gestational phthalates and autistic traits in 3- to 4-y-old Canadian children.

260 More pronounced autistic traits in a group of healthy control subjects w

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

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

263 al neuromotor development during infancy and autistic traits in childhood.

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

265 ur findings suggest that a greater number of autistic traits in neurotypical individuals is associate

266 eye contact during verbal communication and autistic traits in neurotypical people.

267 we investigated whether a greater number of autistic traits in neurotypical subjects is associated w

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

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

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

271 etween nonoptimal neuromotor development and autistic traits in the general population.

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

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

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

275 ontact with a speaker predicted the level of autistic traits measured by Autism-spectrum Quotient (AQ

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

277 Autistic traits span a wide spectrum of behavioral depar

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

279 Autistic traits vary along a continuum extending into th

280 lation between overall motor development and autistic traits was .35 (SE = .21, p < .001).

281 motor development was 20% (SE = .21) and of autistic traits was 68% (SE = .26).

282 Autistic traits were measured using the Social Responsiv

283 insufficiency causes a severe NDD defined by autistic traits, cognitive impairment, and epilepsy.

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

285 s related to autism (self-report measures of autistic traits, empathy, systemizing, and sensory sensi

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

287 n average, higher on self-report measures of autistic traits, systemizing, and sensory sensitivity, a

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

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

290 and those for ADHD both were associated with autistic traits.

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

292 ociations of PRSs with neuromotor scores and autistic traits.

293 k between endocrine-disrupting chemicals and autistic traits.

294 the presence of the most clinically relevant autistic traits.

295 sociation between neuromotor development and autistic traits.

296 nd/or global developmental delay; hypotonia; autistic traits; movement disorders; growth abnormalitie

297 ole of Cav1.2 channel signals in autism, the autistic TS2-neo mouse has been generated bearing the G4

298 Autistic type problems and irritability also appear to s

299 ses characteristic of fluent spelling in non-autistic typists.

300 tly classify individuals' diagnostic status (autistic versus control; 87% accuracy).