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1 tion deficits (WRD; sometimes referred to as dyslexia).
2 cale selection are impaired in developmental dyslexia.
3 sputedly the most efficient intervention for dyslexia.
4 fferences show causes rather than effects of dyslexia.
5 ains unknown, apart from a suggested role in dyslexia.
6 ysiology and reading skills in children with dyslexia.
7 nificantly predicted future reading gains in dyslexia.
8 , reliably predicted future reading gains in dyslexia.
9 an predict future long-term reading gains in dyslexia.
10 nisms underlying cerebral lateralization and dyslexia.
11 developmental disorders including autism and dyslexia.
12 clusion, a hallmark symptom in developmental dyslexia.
13 rity of children who would otherwise develop dyslexia.
14 -learning eye-movement control in hemianopic dyslexia.
15 nymous visual field disorders and hemianopic dyslexia.
16 ere impairment of reading, called hemianopic dyslexia.
17 el of current reading ability independent of dyslexia.
18 ative hand skill measure in individuals with dyslexia.
19 and related to atypical brain morphology in dyslexia.
20 obiological influences on the development of dyslexia.
21 ons of hypoactivation and hyperactivation to dyslexia.
22 most widely accepted areas of difficulty in dyslexia.
23 ocessing deficits are not a causal factor in dyslexia.
24 ptual and cognitive deficits associated with dyslexia.
25 ute early on to the phonological disorder in dyslexia.
26 otential relevance of these brain changes to dyslexia.
27 ility, or more specific neural correlates of dyslexia.
28 ain development are increasingly reported in dyslexia.
29 with developmental language disorder and/or dyslexia.
30 ar processing, contribute to the etiology of dyslexia.
31 nguage, spelling, and reading disability, or dyslexia.
32 nguage acquisition place a child at risk for dyslexia.
33 al intervention in adults with developmental dyslexia.
34 reading and picture naming in developmental dyslexia.
35 omal regions implicated in susceptibility to dyslexia.
36 g, spelling and language measures related to dyslexia.
37 gical processing in children and adults with dyslexia.
38 tic naming and the double-deficit subtype of dyslexia.
39 unctional neural mechanisms in children with dyslexia.
40 a neurobiological etiology of developmental dyslexia.
41 ccount for the perceptual errors observed in dyslexia.
42 ial programs can be effective in identifying dyslexia.
43 etween these neurobiological disruptions and dyslexia.
44 investigate such perceptual organization in dyslexia.
45 sual deficit in a global integration task in dyslexia.
46 kills, one of the key component processes in dyslexia.
47 f one of the genes involved in developmental dyslexia.
48 ts functional disconnection in developmental dyslexia.
49 mal subjects and subjects with developmental dyslexia.
50 been reported in the brain in developmental dyslexia.
51 ry has been linked to both schizophrenia and dyslexia.
52 rganization of the cortical visual system in dyslexia.
53 where dysfunction may lead to developmental dyslexia.
54 ecific computational deficit associated with dyslexia.
55 etion within the DCDC2 gene, a risk gene for dyslexia.
56 dulations, regardless of hereditary risk for dyslexia.
57 children may reveal early neural markers for dyslexia.
58 eptual learning as a factor in developmental dyslexia.
59 children at high and low hereditary risk for dyslexia.
60 le-brain functional connectivity analysis of dyslexia.
61 uals with language-related disorders such as dyslexia.
62 phrenia and that of structural correlates in dyslexia.
63 nto-parietal attention network characterizes dyslexia.
64 that weakness in V5/MT may not be causal to dyslexia.
66 r amyotrophic lateral sclerosis 5 (ALS5) and dyslexia-1 (DYX1) and TMOD4 a candidate gene for limb gi
67 children with a normal IQ and developmental dyslexia (16 male, three female; age range, 6-16 years;
68 tional MRI was performed on 20 children with dyslexia (8-12 years old) during phonological processing
74 nts in reading and writing characteristic of dyslexia, a view consistent with the recently appreciate
75 Language-based learning disorders such as dyslexia affect millions of people, but there is little
80 recent data on the genetics of developmental dyslexia and consider broader issues involved in the sea
81 15q11.2(BP1-BP2) deletion) have a history of dyslexia and dyscalculia, even after adjusting for IQ in
82 pen our understanding of the neural basis of dyslexia and highlight the importance of synchrony betwe
83 ms in three genes previously associated with dyslexia and implicated in neuronal migration (DYX1C1, D
84 e hypothesis for an M pathway abnormality in dyslexia and imply a strong relationship between the int
85 e hypothesis for an M pathway abnormality in dyslexia and imply strong relationships between the inte
86 r neural migration genes are associated with dyslexia and may contribute to auditory processing defic
87 reports of reduced behavioral adaptation in dyslexia and may reveal a difference in brain functions
91 X1C1) gene has recently been associated with dyslexia and reading scores in several population sample
92 Thus, in contrast to patients with surface dyslexia and semantic impairment from anterior temporal
93 vious studies have implicated this region in dyslexia and some speculations are made in this regard.
94 e of the KIAA0319 gene in the development of dyslexia and suggest that this gene influences reading a
95 t may be critical for reading improvement in dyslexia and that may differ from typical reading develo
96 n the temporo-parietal lobe in developmental dyslexia and that the altered cerebral structural symmet
97 f improvement was shallower for readers with dyslexia and the segment size where performance became a
98 phonological processing is characteristic of dyslexia and thought to be a basis for difficulty in lea
99 he relation between behavioral predictors of dyslexia and white matter organization in left arcuate f
100 sabilities, and learning difficulties (e.g., dyslexia) and were absent for sensory or motor/physical
102 m, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millio
103 ntify infants and young children at risk for dyslexia, and preventive intervention is often effective
104 h Omega-3 LC-PUFA found for ADHD, Dyspraxia, Dyslexia, and related conditions might extend to the gen
107 ncluding schizophrenia, autism, ADD/ADHD and dyslexia are believed to originate during gestation and
109 y neuroanatomical abnormalities that precede dyslexia are not in the reading network itself, but rath
110 sults suggest that domains common to SSD and dyslexia are pleiotropically influenced by a putative qu
113 ns the motion processing deficit observed in dyslexia as the consequence of a lack, or poor quality,
114 ered neocortical activation, suggesting that dyslexia associated genes might play as yet unspecified
117 A matched control group of children with dyslexia attending the same schools who did not use the
119 rimary progressive aphasia and developmental dyslexia both manifest with phonological disturbances an
120 l magnocellular dysfunction is not causal to dyslexia but may instead be consequential to impoverishe
121 hat segmentation is impaired in readers with dyslexia but only on tasks containing motion information
122 ften have accompanying reading difficulties (dyslexia), but not all children with reading difficultie
123 sing deficits and language disorders such as dyslexia; but whether the former cause the latter, or si
124 h in children with and without developmental dyslexia by measuring auditory brainstem responses to a
125 tic basis of composite phenotypes related to dyslexia, by providing evidence for major-gene modes of
126 and picture naming deficits in developmental dyslexia can be reduced to a common neurological impairm
127 that the perceptual deficits associated with dyslexia can be understood computationally as a deficit
130 An understanding of the role of genetics in dyslexia could help to diagnose and treat susceptible ch
132 ly studied candidate genes for developmental dyslexia (DD) owing to its important role in neuronal mi
133 h pedigree of eight cases with developmental dyslexia (DD) revealed several regions shared by the aff
135 Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task mod
137 els for component phenotypes associated with dyslexia: digit span and a nonword-repetition task.
138 ction in disorders such as schizophrenia and dyslexia, diseases in which sex differences in incidence
145 In contrast, children with developmental dyslexia exhibited impairment in their ability to modify
146 For every stimulus type, individuals with dyslexia exhibited significantly diminished neural adapt
147 mulus repetition in adults and children with dyslexia for a wide variety of stimuli, spoken words, wr
148 paired reading development, individuals with dyslexia frequently exhibit behavioral deficits in perce
149 ional neuroimaging studies, individuals with dyslexia frequently exhibit both hypoactivation, often i
150 ognitive neuroscience measures could prevent dyslexia from occurring in the majority of children who
151 within the reading system; in developmental dyslexia, functional imaging is being used to identify t
153 demonstrate that suppression of a candidate-dyslexia gene causes deficits on tasks of rapid stimulus
154 ng Kiaa0319 RNAi and suggests that different dyslexia genes may cause different deficits in the speec
157 of known reading regions (seeds) among three dyslexia groups characterized by (a) no remediation (cur
158 rontal gyrus was significantly weaker in all dyslexia groups, irrespective of remediation status/lite
159 ur results contribute to the hypothesis that dyslexia has a developmental neurobiological basis by li
161 r to depend upon magnocellular pathways, and dyslexia has been associated with deficits in this pathw
162 he perception of rapidly presented sounds in dyslexia has been interpreted as evidence of a prolonged
164 k involved in reading and its dysfunction in dyslexia has been well studied, it is unknown whether dy
168 use of reading difficulties in developmental dyslexia; however, existing evidence also implicates deg
169 sess three leading theories of developmental dyslexia: (i) the phonological theory, (ii) the magnocel
170 typically developing readers, children with dyslexia improved their reading of novel words presented
171 ss gray matter volume (GMV) in developmental dyslexia in bilateral temporoparietal and left occipitot
173 vestigated the functional anatomy of surface dyslexia in SD using functional magnetic resonance imagi
174 ted by neuropsychological studies of surface dyslexia in semantic dementia and the connectionist tria
175 t of a focal cortical thickness reduction in dyslexia in the subregion of ventral occipitotemporal co
176 meliorate clinical conditions (e.g., autism, dyslexia) in which multisensory temporal function may be
177 of a QTL influencing multiple components of dyslexia, in particular the reading of irregular words (
178 ave identified several candidate regions for dyslexia, including one on chromosome 3 segregating in a
180 8p QTL is probably a general risk factor for dyslexia, influencing several reading-related processes.
182 nce was examined to test the hypothesis that dyslexia involves a deficit in a specific visual pathway
183 behavioral plasticity in adult developmental dyslexia involves two distinct neural mechanisms, each o
197 the altered cerebral structural symmetry in dyslexia is associated with abnormal development of cell
198 d normal readers to test the hypothesis that dyslexia is associated with an abnormality in the magnoc
199 ortex, much in the same way as developmental dyslexia is associated with hypoactivation of this area.
201 has been well studied, it is unknown whether dyslexia is caused by structural abnormalities in the re
206 blem in studying children with developmental dyslexia is how to separate inefficiency in learning on
207 uroimaging tests reviewed here indicate that dyslexia is indeed associated with cerebellar impairment
209 support a conclusion that the impairment in dyslexia is phonologic in nature and that these brain ac
212 has suggested that a fundamental deficit in dyslexia is the inability to process sensory input that
215 ilities (such as IQ, language impairment and dyslexia) is expected to provide new insights into the b
219 eflected functional atypicalities related to dyslexia itself, independent of current reading ability,
220 The reported neuroanatomical differences in dyslexia may be causal to the reading problems, followin
223 n children with dyslexia (n = 25) or without dyslexia (n = 20) to discover whether initial behavioral
224 ngitudinal study over 2.5 y in children with dyslexia (n = 25) or without dyslexia (n = 20) to discov
225 AA0319, have been previously associated with dyslexia, neuronal migration, and ciliary function.
228 identified a risk haplotype associated with dyslexia on chromosome 6p22.2 which spans the TTRAP gene
229 ral connectivity are related to the cause of dyslexia or if they are consequences of reading difficul
230 tnessed an explosion in our understanding of dyslexia (or specific reading disability), the most comm
231 four genes thus far linked to developmental dyslexia participate in brain development, and abnormali
232 tigates cortical signatures of developmental dyslexia, particularly from the perspective of behaviora
233 of variance); dark adaptation improved in 5 dyslexia patients after supplementation with a docosahex
234 g different reading experiences, rather than dyslexia per se, whereas the neuroanatomical precursors
236 a specific genotype, rather than the entire dyslexia population, contributing to the large variabili
239 olymorphisms (SNPs) that was associated with dyslexia (reading disability) in two independent samples
241 eptual distortions experienced by those with dyslexia reflect a disturbance in the basic mechanisms s
242 In contrast, areas of hypoactivation in dyslexia reflected functional atypicalities related to d
247 results indicate that the GMV differences in dyslexia reported here and in prior studies are in large
252 eviously identified as enhancing the risk of dyslexia showed a reduced left-hemispheric asymmetry of
254 nomalous expression of cerebral asymmetry in dyslexia similar to that of the planum temporale, which
255 ved across children with evidence of classic dyslexia, specific comprehension deficit, and language l
257 regions in men with persistent developmental dyslexia, suggesting that the anatomical disconnection o
260 p quantitative-trait loci (QTLs) influencing dyslexia susceptibility have targeted specific chromosom
261 l cooperative associations may be present in dyslexia that are indicative of poor perceptual integrat
262 ith an increasingly sophisticated account of dyslexia that does not single out either phonological, o
263 n as a core neurophysiological difference in dyslexia that may underlie impaired reading development.
265 ical mechanism leading to the development of dyslexia: the risk haplotype on chromosome 6p22.2 down-r
266 enge is to find ways that allow a child with dyslexia to read more words in less time, because readin
269 We studied the neural mechanisms underlying dyslexia using a simple frequency-discrimination task.
270 discrimination in children with and without dyslexia, using magnocellular and parvocellular visual s
275 r reading skills in adults and children with dyslexia were associated with greater repetition-induced
276 d may also have bearing on disorders such as dyslexia, which show sexual dimorphisms, and in which fu
277 sent data support the phonological theory of dyslexia, while acknowledging the presence of additional
278 g task and in young adults with a history of dyslexia who are well compensated for their disorder.
279 mining iFC can reveal cortical signatures of dyslexia with particular promise for monitoring neural c
280 zophrenia patients met criteria for acquired dyslexia, with 50% reading below eighth grade level desp
281 tential to reconcile influential theories of dyslexia within a predictive coding framework of brain f
282 cal processing predicted which children with dyslexia would improve reading skills 2.5 y later with >
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