ライフサイエンスコーパス: dyslexia

1 on in 99 elementary school children (26 with dyslexia).

2 tion deficits (WRD; sometimes referred to as dyslexia).

3 uals with language-related disorders such as dyslexia.

4 phrenia and that of structural correlates in dyslexia.

5 nto-parietal attention network characterizes dyslexia.

6 that weakness in V5/MT may not be causal to dyslexia.

7 sputedly the most efficient intervention for dyslexia.

8 fferences show causes rather than effects of dyslexia.

9 ains unknown, apart from a suggested role in dyslexia.

10 ysiology and reading skills in children with dyslexia.

11 nificantly predicted future reading gains in dyslexia.

12 , reliably predicted future reading gains in dyslexia.

13 an predict future long-term reading gains in dyslexia.

14 nisms underlying cerebral lateralization and dyslexia.

15 developmental disorders including autism and dyslexia.

16 clusion, a hallmark symptom in developmental dyslexia.

17 rity of children who would otherwise develop dyslexia.

18 ility genes and clarify the genetic bases of dyslexia.

19 -learning eye-movement control in hemianopic dyslexia.

20 nymous visual field disorders and hemianopic dyslexia.

21 ere impairment of reading, called hemianopic dyslexia.

22 for alleviating the phonological deficit in dyslexia.

23 el of current reading ability independent of dyslexia.

24 and related to atypical brain morphology in dyslexia.

25 visual crowding, compared to adults without dyslexia.

26 obiological influences on the development of dyslexia.

27 ons of hypoactivation and hyperactivation to dyslexia.

28 most widely accepted areas of difficulty in dyslexia.

29 ocessing deficits are not a causal factor in dyslexia.

30 ptual and cognitive deficits associated with dyslexia.

31 ute early on to the phonological disorder in dyslexia.

32 otential relevance of these brain changes to dyslexia.

33 ility, or more specific neural correlates of dyslexia.

34 ain development are increasingly reported in dyslexia.

35 with developmental language disorder and/or dyslexia.

36 ar processing, contribute to the etiology of dyslexia.

37 nguage, spelling, and reading disability, or dyslexia.

38 nguage acquisition place a child at risk for dyslexia.

39 al intervention in adults with developmental dyslexia.

40 reading and picture naming in developmental dyslexia.

41 omal regions implicated in susceptibility to dyslexia.

42 g, spelling and language measures related to dyslexia.

43 gical processing in children and adults with dyslexia.

44 tic naming and the double-deficit subtype of dyslexia.

45 isorders ranging from Parkinson's disease to dyslexia.

46 unctional neural mechanisms in children with dyslexia.

47 a neurobiological etiology of developmental dyslexia.

48 ccount for the perceptual errors observed in dyslexia.

49 ial programs can be effective in identifying dyslexia.

50 etween these neurobiological disruptions and dyslexia.

51 investigate such perceptual organization in dyslexia.

52 sual deficit in a global integration task in dyslexia.

53 kills, one of the key component processes in dyslexia.

54 f one of the genes involved in developmental dyslexia.

55 ts functional disconnection in developmental dyslexia.

56 cale selection are impaired in developmental dyslexia.

57 ative hand skill measure in individuals with dyslexia.

58 nd appropriate treatment recommendations for dyslexia.

59 ecific computational deficit associated with dyslexia.

60 etion within the DCDC2 gene, a risk gene for dyslexia.

61 siently restore this activity in adults with dyslexia.

62 dulations, regardless of hereditary risk for dyslexia.

63 children may reveal early neural markers for dyslexia.

64 eptual learning as a factor in developmental dyslexia.

65 children at high and low hereditary risk for dyslexia.

66 le-brain functional connectivity analysis of dyslexia.

67 EAD1" or "regulatory element associated with dyslexia 1."

68 r amyotrophic lateral sclerosis 5 (ALS5) and dyslexia-1 (DYX1) and TMOD4 a candidate gene for limb gi

69 children with a normal IQ and developmental dyslexia (16 male, three female; age range, 6-16 years;

70 tional MRI was performed on 20 children with dyslexia (8-12 years old) during phonological processing

71 It is possible that in dyslexia a persistent sensory deficit in monitoring the

72 in modern societies, but many children have dyslexia, a difficulty in learning to read.

73 Dyslexia, a disorder of reading and spelling, is a heter

74 SD patients often present with surface dyslexia, a relatively selective impairment in reading l

75 Developmental dyslexia, a severe and persistent reading and spelling i

76 nts in reading and writing characteristic of dyslexia, a view consistent with the recently appreciate

77 Language-based learning disorders such as dyslexia affect millions of people, but there is little

78 Developmental dyslexia affects 5%-10% of the population, resulting in

79 Reviews on cortical visual impairment, dyslexia, Aicardi syndrome, and neuronal ceroid lipofusc

80 young children, older adults and people with dyslexia all exhibit increased visual crowding, compared

81 Developmental dyslexia, an unexplained difficulty in learning to read,

82 We selected five pairs of children with dyslexia and (younger) typically developing readers matc

83 15q11.2(BP1-BP2) deletion) have a history of dyslexia and dyscalculia, even after adjusting for IQ in

84 pen our understanding of the neural basis of dyslexia and highlight the importance of synchrony betwe

85 s in typical child readers and children with dyslexia and identify novel electrophysiological markers

86 ms in three genes previously associated with dyslexia and implicated in neuronal migration (DYX1C1, D

87 itory modality is a feature of developmental dyslexia and it may also affect reading-related cognitiv

88 r neural migration genes are associated with dyslexia and may contribute to auditory processing defic

89 reports of reduced behavioral adaptation in dyslexia and may reveal a difference in brain functions

90 DYX1C1 has been associated with dyslexia and neuronal migration in the developing neocor

91 useful to clarify the benefits of LCPUFAs in dyslexia and other closely related conditions.

92 en identified in patients with developmental dyslexia and psychomotor retardation.

93 X1C1) gene has recently been associated with dyslexia and reading scores in several population sample

94 Thus, in contrast to patients with surface dyslexia and semantic impairment from anterior temporal

95 vious studies have implicated this region in dyslexia and some speculations are made in this regard.

96 terize a previously unidentified subgroup of dyslexia and suggest that measurement of flicker fusion

97 e of the KIAA0319 gene in the development of dyslexia and suggest that this gene influences reading a

98 t may be critical for reading improvement in dyslexia and that may differ from typical reading develo

99 n the temporo-parietal lobe in developmental dyslexia and that the altered cerebral structural symmet

100 f improvement was shallower for readers with dyslexia and the segment size where performance became a

101 phonological processing is characteristic of dyslexia and thought to be a basis for difficulty in lea

102 he relation between behavioral predictors of dyslexia and white matter organization in left arcuate f

103 sabilities, and learning difficulties (e.g., dyslexia) and were absent for sensory or motor/physical

104 in attention deficit hyperactivity disorder, dyslexia, and fetal alcohol spectrum disorder.

105 age include developmental language disorder, dyslexia, and motor-speech disorders such as articulatio

106 m, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millio

107 ntify infants and young children at risk for dyslexia, and preventive intervention is often effective

108 h Omega-3 LC-PUFA found for ADHD, Dyspraxia, Dyslexia, and related conditions might extend to the gen

109 These results suggest that deficits in dyslexia are associated with a failure of the neural mec

110 Deficits in dyslexia are attributed to an intact declarative learnin

111 ncluding schizophrenia, autism, ADD/ADHD and dyslexia are believed to originate during gestation and

112 lecular evidence that cerebral asymmetry and dyslexia are linked.

113 y neuroanatomical abnormalities that precede dyslexia are not in the reading network itself, but rath

114 sults suggest that domains common to SSD and dyslexia are pleiotropically influenced by a putative qu

115 Readers with dyslexia are purported to have a selective visual impair

116 Although the causes of dyslexia are still debated, all researchers agree that t

117 ns the motion processing deficit observed in dyslexia as the consequence of a lack, or poor quality,

118 ered neocortical activation, suggesting that dyslexia associated genes might play as yet unspecified

119 These results link the function of the dyslexia-associated gene Dcdc2 to spike timing through a

120 Variants in dyslexia-associated genes, including DCDC2, have been li

121 esearch mainly focused on pathomechanisms of dyslexia at the cerebral cortex level, several lines of

122 A matched control group of children with dyslexia attending the same schools who did not use the

123 egrity in kindergartners who are at risk for dyslexia because of poor phonological awareness.

124 ould be used as screening tool for detecting dyslexia before a child begins to fail at school.

125 rimary progressive aphasia and developmental dyslexia both manifest with phonological disturbances an

126 Individuals with autism and individuals with dyslexia both show reduced use of previous sensory infor

127 l magnocellular dysfunction is not causal to dyslexia but may instead be consequential to impoverishe

128 hat segmentation is impaired in readers with dyslexia but only on tasks containing motion information

129 sing deficits and language disorders such as dyslexia; but whether the former cause the latter, or si

130 h in children with and without developmental dyslexia by measuring auditory brainstem responses to a

131 a neural correlate previously implicated in dyslexia by neuroimaging evidence.

132 tic basis of composite phenotypes related to dyslexia, by providing evidence for major-gene modes of

133 and picture naming deficits in developmental dyslexia can be reduced to a common neurological impairm

134 that the perceptual deficits associated with dyslexia can be understood computationally as a deficit

135 genome-wide association study (GWAS) on 2274 dyslexia cases and 6272 controls, testing associations a

136 Developmental dyslexia, characterized by unexplained difficulty in rea

137 hogenesis of such disorders as developmental dyslexia, congenital amusia and tinnitus.

138 An understanding of the role of genetics in dyslexia could help to diagnose and treat susceptible ch

139 Developmental dyslexia (DD) and specific language impairment (SLI) are

140 Developmental dyslexia (DD) is a learning disorder affecting the abili

141 ly studied candidate genes for developmental dyslexia (DD) owing to its important role in neuronal mi

142 h pedigree of eight cases with developmental dyslexia (DD) revealed several regions shared by the aff

143 Individuals with developmental dyslexia (DD) show a disruption in posterior left-hemisp

144 Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task mod

145 People with dyslexia differ in their individual profiles across a ra

146 els for component phenotypes associated with dyslexia: digit span and a nonword-repetition task.

147 ction in disorders such as schizophrenia and dyslexia, diseases in which sex differences in incidence

148 ay be a mechanism for why some children with dyslexia do not respond to intervention.

149 speech (AOS), and left parietal symptoms of dyslexia, dysgraphia, and dyscalculia.

150 l dystrophy (DHRD), and one form of familial dyslexia (DYX-3).

151 Next we examine the cognitive model of dyslexia, especially the phonological theory, and review

152 Adults and children with developmental dyslexia exhibit reduced parietotemporal activation in f

153 Individuals with dyslexia exhibited impaired voice-recognition abilities

154 In contrast, children with developmental dyslexia exhibited impairment in their ability to modify

155 For every stimulus type, individuals with dyslexia exhibited significantly diminished neural adapt

156 mulus repetition in adults and children with dyslexia for a wide variety of stimuli, spoken words, wr

157 paired reading development, individuals with dyslexia frequently exhibit behavioral deficits in perce

158 ional neuroimaging studies, individuals with dyslexia frequently exhibit both hypoactivation, often i

159 ognitive neuroscience measures could prevent dyslexia from occurring in the majority of children who

160 within the reading system; in developmental dyslexia, functional imaging is being used to identify t

161 In patients with acquired dyslexia, functional imaging is demonstrating re-organis

162 demonstrate that suppression of a candidate-dyslexia gene causes deficits on tasks of rapid stimulus

163 ng Kiaa0319 RNAi and suggests that different dyslexia genes may cause different deficits in the speec

164 d selectively for a 30-Hz stimulation in the dyslexia group.

165 IC in the control group were not seen in the dyslexia group.

166 IFO-ILF in the control group but not in the dyslexia group.

167 of known reading regions (seeds) among three dyslexia groups characterized by (a) no remediation (cur

168 rontal gyrus was significantly weaker in all dyslexia groups, irrespective of remediation status/lite

169 ur results contribute to the hypothesis that dyslexia has a developmental neurobiological basis by li

170 Treatment of dyslexia has been advanced through neuroscience, yet fur

171 r to depend upon magnocellular pathways, and dyslexia has been associated with deficits in this pathw

172 Dyslexia has been frequently linked to cerebral cortex a

173 he perception of rapidly presented sounds in dyslexia has been interpreted as evidence of a prolonged

174 Dyslexia has been reported in every culture studied, and

175 k involved in reading and its dysfunction in dyslexia has been well studied, it is unknown whether dy

176 Neuroimaging in children with dyslexia has revealed reduced engagement of the left tem

177 s resulting in selective reading difficulty (dyslexia) has remained elusive.

178 Patients with surface dyslexia have disproportionate difficulty pronouncing ir

179 we show that male adults with developmental dyslexia have reduced structural connectivity between th

180 use of reading difficulties in developmental dyslexia; however, existing evidence also implicates deg

181 sess three leading theories of developmental dyslexia: (i) the phonological theory, (ii) the magnocel

182 typically developing readers, children with dyslexia improved their reading of novel words presented

183 ss gray matter volume (GMV) in developmental dyslexia in bilateral temporoparietal and left occipitot

184 functions and may be linked to epilepsy and dyslexia in humans.

185 vestigated the functional anatomy of surface dyslexia in SD using functional magnetic resonance imagi

186 ted by neuropsychological studies of surface dyslexia in semantic dementia and the connectionist tria

187 t of a focal cortical thickness reduction in dyslexia in the subregion of ventral occipitotemporal co

188 meliorate clinical conditions (e.g., autism, dyslexia) in which multisensory temporal function may be

189 of a QTL influencing multiple components of dyslexia, in particular the reading of irregular words (

190 ave identified several candidate regions for dyslexia, including one on chromosome 3 segregating in a

191 Dyslexia, incomplete homonymous hemianopia, preserved co

192 8p QTL is probably a general risk factor for dyslexia, influencing several reading-related processes.

193 uggesting future directions for the study of dyslexia intervention paradigms.

194 behavioral plasticity in adult developmental dyslexia involves two distinct neural mechanisms, each o

195 Dyslexia is a common and complex disorder with evidence

196 Dyslexia is a common neurodevelopmental disorder caused

197 Developmental dyslexia is a common reading disorder that negatively im

198 Dyslexia is a developmental disorder in reading that exh

199 Developmental dyslexia is a learning disability that specifically affe

200 Developmental dyslexia is a neurodevelopmental condition which causes

201 Dyslexia is a neurodevelopmental disorder that is charac

202 Dyslexia is a prevalent reading disability whose underly

203 Developmental dyslexia is a reading disorder, yet deficits also manife

204 It is well established that dyslexia is a significantly heritable trait with a neuro

205 Developmental dyslexia is a specific disorder of reading and spelling

206 Dyslexia is a specific impairment in reading that affect

207 Dyslexia is a specific learning disability that is neuro

208 Dyslexia is a widespread condition characterized by diff

209 the altered cerebral structural symmetry in dyslexia is associated with abnormal development of cell

210 The phonological deficit in dyslexia is associated with altered low-gamma oscillator

211 ortex, much in the same way as developmental dyslexia is associated with hypoactivation of this area.

212 One hypothesis posits that dyslexia is caused by deficits in the motion processing

213 has been well studied, it is unknown whether dyslexia is caused by structural abnormalities in the re

214 Work confirms that, neurobiologically, dyslexia is characterised by dysfunction of the normal l

215 Developmental dyslexia is characterized by a phonological processing d

216 Developmental dyslexia is characterized by the inability to acquire ty

217 Developmental dyslexia is defined as a specific and significant impair

218 Although dyslexia is diagnosed through reading difficulty, there

219 blem in studying children with developmental dyslexia is how to separate inefficiency in learning on

220 uroimaging tests reviewed here indicate that dyslexia is indeed associated with cerebellar impairment

221 Dyslexia is one of the most prevalent childhood cognitiv

222 readers.SIGNIFICANCE STATEMENT Developmental dyslexia is one of the most widespread learning disabili

223 support a conclusion that the impairment in dyslexia is phonologic in nature and that these brain ac

224 Our perspective on dyslexia is that some of the brain changes cause phonolo

225 A core difficulty in developmental dyslexia is the accurate specification and neural repres

226 has suggested that a fundamental deficit in dyslexia is the inability to process sensory input that

227 Dyslexia is the most common developmental language disor

228 ilities (such as IQ, language impairment and dyslexia) is expected to provide new insights into the b

229 Reading disability (RD), or dyslexia, is a common heterogeneous syndrome with a larg

230 Reading disability (RD), or dyslexia, is a complex cognitive disorder manifested by

231 We first review the core concepts of dyslexia: its definition, prevalence, and developmental

232 eflected functional atypicalities related to dyslexia itself, independent of current reading ability,

233 The reported neuroanatomical differences in dyslexia may be causal to the reading problems, followin

234 Children with dyslexia may read poorly for several reasons.

235 Finally, within children with dyslexia, measures of cortical representation of the phr

236 Some or all of the subtypes of dyslexia might have partly or wholly distinct genetic ca

237 n children with dyslexia (n = 25) or without dyslexia (n = 20) to discover whether initial behavioral

238 ngitudinal study over 2.5 y in children with dyslexia (n = 25) or without dyslexia (n = 20) to discov

239 AA0319, have been previously associated with dyslexia, neuronal migration, and ciliary function.

240 s have seldom been explored in developmental dyslexia nor its subtypes.

241 Dyslexia often arises from impaired phonological awarene

242 Children with dyslexia often exhibit increased variability in sensory

243 identified a risk haplotype associated with dyslexia on chromosome 6p22.2 which spans the TTRAP gene

244 ral connectivity are related to the cause of dyslexia or if they are consequences of reading difficul

245 tnessed an explosion in our understanding of dyslexia (or specific reading disability), the most comm

246 four genes thus far linked to developmental dyslexia participate in brain development, and abnormali

247 tigates cortical signatures of developmental dyslexia, particularly from the perspective of behaviora

248 of variance); dark adaptation improved in 5 dyslexia patients after supplementation with a docosahex

249 g different reading experiences, rather than dyslexia per se, whereas the neuroanatomical precursors

250 fraction of the differences being driven by dyslexia per se.

251 a specific genotype, rather than the entire dyslexia population, contributing to the large variabili

252 Two other behavioral predictors of dyslexia, rapid naming and letter knowledge, did not cor

253 olymorphisms (SNPs) that was associated with dyslexia (reading disability) in two independent samples

254 e of relative hand skill in individuals with dyslexia [reading disability (RD)].

255 eptual distortions experienced by those with dyslexia reflect a disturbance in the basic mechanisms s

256 In contrast, areas of hypoactivation in dyslexia reflected functional atypicalities related to d

257 Thus, areas of hyperactivation in dyslexia reflected processes related to the level of cur

258 in the D6S464-D6S273 region for a number of dyslexia-related cognitive deficits.

259 enotypes were constructed to span a range of dyslexia-related cognitive processes.

260 tual inference reveals that individuals with dyslexia rely more on information about the immediate pa

261 The biological basis for developmental dyslexia remains unknown.

262 results indicate that the GMV differences in dyslexia reported here and in prior studies are in large

263 bility in impairment of motion thresholds in dyslexia reported in the literature.

264 other psychophysical tasks typically used in dyslexia research.

265 DD, and observed significant associations of dyslexia risk with PGSs for attention deficit hyperactiv

266 t contribution of common genetic variants to dyslexia risk, and novel genomic overlaps with psychiatr

267 With the scientific underpinnings of dyslexia serving as a foundation, we turn our attention

268 Children with dyslexia showed a correlation between the magnitude of i

269 eviously identified as enhancing the risk of dyslexia showed a reduced left-hemispheric asymmetry of

270 Physiologically, children with dyslexia showed increased activity in multiple brain are

271 nomalous expression of cerebral asymmetry in dyslexia similar to that of the planum temporale, which

272 ved across children with evidence of classic dyslexia, specific comprehension deficit, and language l

273 usceptibility locus and a linkage region for dyslexia, speech-sound disorder and reading.

274 elligence, testing them for association with dyslexia status in our sample.

275 regions in men with persistent developmental dyslexia, suggesting that the anatomical disconnection o

276 One theory of dyslexia suggests that the phonological awareness defici

277 The dyslexia susceptibility 1 candidate 1 (DYX1C1) gene has

278 The KIAA0319 gene is one of the most robust dyslexia susceptibility factors but its function remains

279 p quantitative-trait loci (QTLs) influencing dyslexia susceptibility have targeted specific chromosom

280 l cooperative associations may be present in dyslexia that are indicative of poor perceptual integrat

281 n as a core neurophysiological difference in dyslexia that may underlie impaired reading development.

282 st a structural basis of behavioral risk for dyslexia that predates reading instruction.

283 ical mechanism leading to the development of dyslexia: the risk haplotype on chromosome 6p22.2 down-r

284 enge is to find ways that allow a child with dyslexia to read more words in less time, because readin

285 We bring considerations from dyslexia to suggest that the claim can be extended furth

286 From this, we propose that dyslexia training programs should take into account the

287 We studied the neural mechanisms underlying dyslexia using a simple frequency-discrimination task.

288 discrimination in children with and without dyslexia, using magnocellular and parvocellular visual s

289 Individuals with developmental dyslexia vary in their ability to improve reading skills

290 e formal literacy training began until after dyslexia was diagnosed.

291 In addition, the diagnosis of lifelong dyslexia was established by clinical means.

292 In individuals with dyslexia, we found preserved integration of visual speec

293 neurotypical participants, individuals with dyslexia weighted earlier stimuli less heavily, whereas

294 r reading skills in adults and children with dyslexia were associated with greater repetition-induced

295 sent data support the phonological theory of dyslexia, while acknowledging the presence of additional

296 g task and in young adults with a history of dyslexia who are well compensated for their disorder.

297 mining iFC can reveal cortical signatures of dyslexia with particular promise for monitoring neural c

298 zophrenia patients met criteria for acquired dyslexia, with 50% reading below eighth grade level desp

299 tential to reconcile influential theories of dyslexia within a predictive coding framework of brain f

300 cal processing predicted which children with dyslexia would improve reading skills 2.5 y later with >