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1 fundamental cognitive functions determining intellectual abilities, such as the broadly defined exec
2 e process involved in another determinant of intellectual abilities, the working memory, measured by
4 tially accounts for life-span transitions in intellectual ability, memory, and susceptibility to beha
5 ional complexity and engagement in cognitive-intellectual activities, are frequently considered indic
8 National Institutes of Health and associated Intellectual and Developmental Disabilities Research Cen
12 rboxylate transporter 8 (MCT8) causes severe intellectual and motor disability and high serum tri-iod
14 s have a crucial impact on the course of the intellectual battle between the two historically competi
15 miologic studies of the Flynn effect is that intellectual capacity gains due to education plateau in
16 nd without help, or if they had insufficient intellectual capacity to understand questions and follow
18 tron transfer (EET) stimulates a plethora of intellectual concepts leading to potential applications
20 individuals have global developmental and/or intellectual delay, all had seizures, two had polymicrog
22 senting heterozygous dominant de novo autism-intellectual disabilities (ID) causing mutations is acti
24 autism spectrum disorders (ASDs), and other intellectual disabilities (IDs), which are therefore cla
26 es including Autism Spectrum Disorder (ASD), intellectual disabilities and Phelan-McDermid syndrome.
27 certained autism spectrum disorder (ASD) and intellectual disabilities from records of additional sup
30 X syndrome (FXS), a common form of inherited intellectual disabilities with a high risk for ASDs.
31 orders, including autism spectrum disorders, intellectual disabilities, and schizophrenia, are linked
36 ght also underlie developmental delay and/or intellectual disability (DD and/or ID) disease phenotype
37 thylases KDM5A, KDM5B, or KDM5C are found in intellectual disability (ID) and autism spectrum disorde
38 with neurodevelopmental diseases, including intellectual disability (ID) and autism spectrum disorde
39 pe subunits have recently been implicated in intellectual disability (ID) and developmental delay (DD
40 y identified in nine individuals with severe intellectual disability (ID) and disruptive behavior.
42 RIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abno
43 icase DDX3X account for 1%-3% of unexplained intellectual disability (ID) cases in females and are as
44 e contribution of de novo variants in severe intellectual disability (ID) has been extensively studie
48 efficacy for ADHD in children with comorbid intellectual disability (ID) or borderline intellectual
49 ree affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD)
50 families with multigenerational nonsyndromic intellectual disability (ID) segregating with a recurren
51 r rates of global developmental delay (GDD), intellectual disability (ID), and motor delay in individ
52 ociated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ).
53 ficantly different in their association with intellectual disability (ID), consistent with the existe
55 -q13.3 locus with a common facial phenotype, intellectual disability (ID), distinctive behavioral fea
56 e facial features with gingival enlargement, intellectual disability (ID), hypertrichosis, and hypopl
57 neurodevelopmental disorder characterized by intellectual disability (ID), motor and speech delay, au
64 iduals, with male-to-female ratios of 2:1 in intellectual disability and 4:1 in autism spectrum disor
65 al phenotypic overlap, including features of intellectual disability and abnormal growth, underscorin
67 ral brain disorders, including the inherited intellectual disability and autism spectrum disorder, fr
68 iquitinating enzyme previously implicated in intellectual disability and autism spectrum disorder.
69 aptic disorder, and a disease model for both intellectual disability and autism spectrum disorder.
70 in individuals with Pitt-Hopkins syndrome-an intellectual disability and autism spectrum disorder.
71 the fourth mutation, A1622D, causing severe intellectual disability and autism without epilepsy, we
72 ontrast, the R1620L mutation associated with intellectual disability and autism-but not epilepsy-redu
73 hared and specific biological information of intellectual disability and CHD by conducting systems bi
75 ts in RALA were also described as a cause of intellectual disability and developmental delay, indicat
76 ntribute to this proposed monogenic cause of intellectual disability and epilepsy remain unresolved.
77 four children from independent families with intellectual disability and epilepsy, revealing bi-allel
80 were recently reported to be associated with intellectual disability and epilepsy; the functional eff
81 enriched for syndromic causes of autism and intellectual disability and for genes that in later deve
82 on of trisomy 21, we have learned much about intellectual disability and genetic risk factors for con
83 individuals had developmental delays and/or intellectual disability and impairments in speech and la
84 yndrome is the most common form of inherited intellectual disability and is caused by a deficiency of
86 alencephaly, a subgroup with higher rates of intellectual disability and larger cerebral volumes, may
87 yseal dysplasia, sensorineural hearing loss, intellectual disability and Leber congenital amaurosis (
88 is case-control study, we used data from the Intellectual Disability and Mental Health: Assessing the
89 t variants in KDM4B are associated with GDD/ intellectual disability and neuroanatomical defects.
90 elative short stature and variable degree of intellectual disability and neurological features as the
91 rological phenotype, with high prevalence of intellectual disability and optic nerve atrophy/hypoplas
93 lepsy, cerebral palsy, feeding difficulties, intellectual disability and other neurological and behav
94 d NETO genes in individuals with Scz, ASD or intellectual disability and population controls; perform
95 ofound hypotonia and muscle weakness, severe intellectual disability and progressive cerebellar atrop
97 culminating in a recognizable syndrome with intellectual disability and signature brain and congenit
99 est that SHANK3 deficiency may predispose to intellectual disability and socio-communicative impairme
101 e (FXS) is the most common form of inherited intellectual disability and the leading monogenetic caus
102 yndrome (FXS) is the leading known inherited intellectual disability and the most common genetic caus
103 cause of a neurodevelopmental disorder with intellectual disability and variable brain anomalies.
104 ilies with the common phenotypic features of intellectual disability and/or global developmental dela
105 eafness, onychodystrophy, osteodystrophy and intellectual disability are associated with a spectrum o
107 genetic variations found in individuals with intellectual disability are the causes for the phenotype
109 rphisms, short stature, developmental delay, intellectual disability as well as cardiac hypertrophy.
110 e, Dravet syndrome and infantile spasms with intellectual disability as well as relatively mild epile
111 icantly enriched in patients with autism and intellectual disability compared to healthy controls and
112 ther genes carrying rare mutations linked to intellectual disability contribute to ADHD risk through
113 that are associated with human cancer or the intellectual disability disorder Sifrim-Hitz-Weiss syndr
119 in a diagnostic gene panel of 396 autosomal intellectual disability genes were tested for associatio
120 tified 28 rare or novel CNVs associated with intellectual disability in 22 additional obese subjects
121 to the OGT catalytic domain lead to X-linked intellectual disability in boys, but it is not clear if
124 in the SYNGAP1 gene have been shown to cause intellectual disability in humans and have been linked t
128 phenotype of thrombocytopenia accompanied by intellectual disability in patients with a de novo heter
129 d significant speech delay (50% non-verbal); intellectual disability in the moderate to severe range;
130 e role of genetic variation in both genes in intellectual disability may be through different mechani
132 had motor and language developmental delay, intellectual disability often associated with early-onse
133 th autism spectrum disorder (autism) without intellectual disability often have normal structural lan
134 n patients with autism spectrum disorder and intellectual disability or developmental disorders to sh
137 se Nicolaides-Baraitser syndrome (NCBRS), an intellectual disability syndrome associated with delayed
138 nyder-Robinson syndrome (SRS) is an X-linked intellectual disability syndrome caused by a loss-of-fun
140 ions) in 4,789 (0.6%) children, with ASD and intellectual disability the most common combination.
142 disability (present in 84%) ranged from mild intellectual disability to severe global disability; mov
143 equencing on 1696 patients with epilepsy and intellectual disability using a gene panel with 480 epil
144 rt of children with autism spectrum disorder/intellectual disability versus healthy controls revealed
145 d clinically recognizable syndromic forms of intellectual disability with contrasting craniofacial dy
146 characterized by global developmental delay, intellectual disability with language deficit, autistic
147 features, especially midface hypoplasia, and intellectual disability with severe expressive language
148 causing intermediate or severe epilepsy, or intellectual disability without epilepsy, respectively)
150 fication factors (site, age at baseline, and intellectual disability), with an additional prespecifie
151 ith de novo heterozygous mutations displayed intellectual disability, ambulation deficits, severe lan
152 disorder (CDD) is characterized by epilepsy, intellectual disability, and autistic features, and CDKL
154 a few individuals with developmental delay, intellectual disability, and brain malformations have mi
159 ral sclerosis, Huntington disease, dementia, intellectual disability, and other brain diseases from 1
160 associated with cancer-related pathologies, intellectual disability, and schizophrenia are increasin
162 al phalanges with small finger and toenails, intellectual disability, and seizures; this condition ov
163 ons, seizures, global developmental delay or intellectual disability, and severe sleep disturbance.
165 e epilepsy, autism spectrum disorder, and/or intellectual disability, as well as other systemic manif
166 ntal symptoms including developmental delay, intellectual disability, ataxia, axial hypotonia, cerebr
167 such as developmental delay, mild-to-severe intellectual disability, ataxia, epilepsy, and behaviora
168 le to neurodevelopmental disorders including intellectual disability, autism spectrum disorder, and a
169 phenotypes that include developmental delay, intellectual disability, autism spectrum disorder, and b
170 The most common features in our cohort were intellectual disability, autism spectrum disorder, seizu
171 nked to neurodevelopmental disorders such as intellectual disability, autism, and schizophrenia.
172 ts (CNVs) have been robustly associated with intellectual disability, autism, and schizophrenia.
173 with neurodevelopmental disorders, including intellectual disability, autism, schizophrenia, and bipo
174 clinical features, including mild to severe intellectual disability, autism, severe speech and motor
175 n inborn error of metabolism presenting with intellectual disability, behavioral disturbances and epi
176 autistic behavior, language impairment, and intellectual disability, but feeding difficulties and ga
177 isk factors for autism spectrum disorder and intellectual disability, but it has not been reported if
178 , and wide mouth, developmental delay and/or intellectual disability, corpus callosum agenesis or hyp
179 m of clinical features including ichthyosis, intellectual disability, decreased fertility, and short
180 VTs or indices, in clinical populations with intellectual disability, degenerative brain disease, bra
181 ected individuals include variable levels of intellectual disability, delayed speech and motor milest
182 ion variants in DYRK1A exhibit microcephaly, intellectual disability, developmental delay and/or cong
183 ts are the cause of a recessive disease with intellectual disability, developmental delay, and short
184 er characterized with a spectrum of central (intellectual disability, developmental delay, motor impa
185 guineous families with probands that exhibit intellectual disability, developmental delay, short stat
186 fox1, an RNA binding protein associated with intellectual disability, epilepsy and autism, increases
187 lapping, syndromic forms of NDDs with severe intellectual disability, epilepsy and microcephaly.
188 eurodevelopmental disorders that manifest as intellectual disability, epilepsy, autism, or schizophre
190 IFA (cleft lip, cataract, tooth abnormality, intellectual disability, facial dysmorphism, attention-d
191 individuals with developmental delay and/or intellectual disability, facial dysmorphisms, and congen
192 erozygous mutations have been shown to cause intellectual disability, growth deficiency, and dysmorph
193 phenotype consisting of developmental delay, intellectual disability, growth retardation, microcephal
194 ation of 15q11.2-13.1) cases associated with intellectual disability, highlight RNA-editing dysregula
195 ndrome (FXS) is characteristically displayed intellectual disability, hyperactivity, anxiety, and abn
196 lobal motor development delay, speech delay, intellectual disability, hypotonia and a history of seiz
197 ls include global developmental delay and/or intellectual disability, hypotonia, cerebellar ataxia, c
198 ndividuals present with developmental delay, intellectual disability, hypotonia, feeding difficulties
199 and Rett syndrome (RTT) are associated with intellectual disability, infantile spasms and seizures.
201 Syndrome (FXS), a common inheritable form of intellectual disability, is known to alter neocortical c
202 ile X syndrome (FXS), an X-chromosome linked intellectual disability, is the leading monogenetic caus
203 neurodevelopmental disorder characterized by intellectual disability, lack of speech, ataxia, EEG abn
204 s in PAK1 in four unrelated individuals with intellectual disability, macrocephaly and seizures.
205 variants in PAK1 lead to moderate-to-severe intellectual disability, macrocephaly caused by the pres
206 symptoms included neurodevelopmental delay, intellectual disability, macrocephaly, and psychiatric d
207 ly recognizable by the combined phenotype of intellectual disability, macrothrombocytopenia, camptoda
208 ith Takenouchi-Kosaki syndrome revealed that intellectual disability, macrothrombocytopenia, camptoda
209 B1 as a genetic etiology in individuals with intellectual disability, microcephaly, and epilepsy.
210 s have a speech delay, and most present with intellectual disability, motor delay, behavioral issues,
211 nts, who present with a clinical spectrum of intellectual disability, motor delay, speech delay, seiz
212 obal developmental delay, severe to profound intellectual disability, muscle weakness and abnormal to
213 for de novo mutations underlying autism and intellectual disability, mutations in the ADNP gene are
214 esenting with an X-linked syndrome involving intellectual disability, proportionate short stature, mi
216 isk of neuropsychiatric disorders, including intellectual disability, schizophrenia, attention-defici
217 developmental disorder characterized by mild intellectual disability, seizures, behavioral abnormalit
218 xtrapolate the core phenotype, consisting of intellectual disability, short stature, microcephaly, li
219 viduals presenting with microcephaly, severe intellectual disability, simplification of cerebral gyra
220 comprising global developmental delay and/or intellectual disability, subtle facial dysmorphisms, beh
221 f neurological disorders, such as autism and intellectual disability, that are characterized by dendr
222 attention deficit hyperactivity disorder and intellectual disability, to later life, such as dementia
223 terized by global developmental delay and/or intellectual disability, variable axon pathfinding defec
224 me (FXS), the most common cause of inherited intellectual disability, yet it is unknown how FMRP func
257 missense variants associated with autism and intellectual disability.SIGNIFICANCE STATEMENT Here, we
258 neurodevelopmental condition associated with intellectual disability/developmental delay, autism spec
259 les from mothers of children with autism and intellectual disability; (2) an inflammatory cytokine mi
260 uals with autism spectrum disorder (ASD) and intellectual disability; however, its clinical significa
261 ns and exhibiting developmental delay and/or intellectual disability; the individuals are from 17 unr
262 tein 2 (MeCP2), is one of the most prevalent intellectual disorders without effective therapies.
263 for plastic changes in response to lifetime intellectual enrichment and potentially also a higher re
264 ng the imaging markers, and early to midlife intellectual enrichment to predict longitudinal cognitiv
271 he proper practice of activities that foster intellectual growth, such as journal clubs, lab meetings
272 Fragile X syndrome (FXS) is an inherited intellectual impairment that results from the loss of fr
274 etraparesis, severe generalized dystonia and intellectual impairment, sharing a unique brain malforma
276 ce statement must disclose all financial and intellectual interests related to health care from the p
277 and motor delay, and variable expression of intellectual or learning disability are common clinical
279 ins of allergen immunotherapy share the same intellectual paradigm, and subsequent innovations in vac
281 also serve as a good strategy for developing intellectual properties which will be critical for produ
282 nancial data, due to regulatory limitations, intellectual property and privacy control, still hinder
287 ly valuable PET radiopharmaceuticals without intellectual property residing in regulatory limbo, with
291 ctious disease epidemiology has undergone an intellectual rebirth in recent years amid increasing rec
292 icant investment of financial, physical, and intellectual resources that catalyze impressive scientif
294 rovides the strongest evidence to date of an intellectual sparing advantage with PRT in the treatment
298 nowledge, this is the first study to compare intellectual trajectories between pediatric patients tre
299 sequences of excessive physical training and intellectual work into a single neuro-computational mech