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1 afflicts human female oocytes (e.g., giving Down syndrome).
2 s contributing to intellectual disability in Down syndrome.
3 c strategy for treating cognitive defects in Down syndrome.
4 lectual disability is a prominent feature of Down syndrome.
5 ell-positive subjects was seen in those with Down syndrome.
6 e neonatal brains of Ts65Dn mice, a model of Down syndrome.
7 ave a higher risk of fathering children with Down syndrome.
8 evated interferon signaling is a hallmark of Down syndrome.
9 nd, as we show, for the Tc1 mouse models for Down syndrome.
10 mRNA levels within the human brain underlie Down Syndrome.
11 genesis of HSA21-related disorders including Down Syndrome.
12 s might be central to the pathophysiology of Down syndrome.
13 DYRK1Ais a major candidate gene in Down syndrome.
14 smal fitness, manifest in conditions such as Down syndrome.
15 y loss and several genetic disorders such as Down syndrome.
16 severe mental retardation in females, after Down syndrome.
17 on show an unfounded bias against those with Down syndrome.
18 n VI microfibrils, an outcome accentuated by Down syndrome.
19 ntribute to distinct cognitive phenotypes in Down syndrome.
20 oid population, this has not been studied in down syndrome.
21 ogical alterations found in individuals with Down syndrome.
22 deficits in the peripheral nervous system in Down syndrome.
23 stic neurological disorder in the context of Down syndrome.
24 e dentate gyrus of the Ts65Dn mouse model of Down syndrome.
25 research has tended to focus on dementia in Down syndrome.
26 ass-switch recombination in 17 children with Down syndrome.
27 ve symptoms in children and adolescents with Down syndrome.
28 espiratory tract infections of patients with Down syndrome.
29 xtual learning, in the Ts65Dn mouse model of Down syndrome.
30 ve diseases, including Alzheimer disease and Down syndrome.
31 d in tonsils from 4 additional children with Down syndrome.
32 and synaptic phenotypes in a mouse model of Down syndrome.
33 prove cognitive function in individuals with Down syndrome.
34 megakaryocytic abnormalities that accompany Down syndrome.
35 tions to support primary care of adults with Down syndrome.
36 fic cytokine patterns among individuals with Down syndrome.
37 file across the lifespan of individuals with Down syndrome.
38 prevalence and earlier onset in adults with Down syndrome.
39 th existing guidance for individuals without Down syndrome.
40 mer's disease in a population of adults with Down syndrome.
41 interleukin-8 levels compared to males with Down syndrome.
42 re the leading cause of death in adults with Down syndrome.
43 nterleukin-10 were observed in children with Down syndrome (1-10 years; Down syndrome n = 5, controls
44 ambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with pro
47 nflammatory phenotype across the lifespan in Down syndrome, a knowledge that is relevant for the disc
51 son/Outcome (PICO) questions for adults with Down syndrome addressing multiple clinical areas includi
52 OR, 1.31; 95% CI, 1.17-1.47; P < 0.001), and Down syndrome (adjusted OR, 6.22; 95% CI, 2.08-18.66; P
54 oning in 63 adults (31 male, 32 female) with Down syndrome aged 30-53 years who did not exhibit sympt
56 ulations of 40 children and adolescents with Down syndrome and 51 controls were quantified, and pheno
58 ne supplementation (MCS) in a mouse model of Down syndrome and Alzheimer's disease, the Ts65Dn mouse
64 frontal cortex from foetuses to adults with Down syndrome and control subjects (16 gestational weeks
65 rget for Alzheimer's disease, especially for Down syndrome and EGCG which inhibits Dyrk1A may have po
66 rrent healthcare issues for adolescents with Down syndrome and intellectual disabilities, including b
67 with cognitive deficits in individuals with Down syndrome and may enable discovery of the underlying
68 trum disorder trait, nutritional deficiency, Down syndrome and Non-specific neurodevelopmental delay
69 teen children (aged 10 months-14 years) with Down syndrome and nystagmus, and a control group of 93 a
70 r disease and is associated with dementia in Down syndrome and poor neurological outcome after trauma
71 in understanding of other disorders such as Down syndrome and Rett syndrome, for example, are also r
73 e significantly more likely to be male, have Down syndrome, and have higher MRD levels on day 19 and
74 tential drug target for Alzheimer's disease, Down syndrome, and TBC1D24-associated epilepsy, while al
79 lasma NFL values changed in individuals with Down syndrome as early as the third decade of life, and
80 g and adaptive behaviour in adolescents with Down syndrome, as it has not been studied before in this
81 mary cultures and hippocampus of adults with Down syndrome, as well as the effects of sex on cytokine
84 tal cortex of children and young adults with Down syndrome before the development of full-blown Alzhe
86 synaptic plasticity and a major candidate of Down syndrome brain alterations and cognitive deficits.
87 orted that Dyrk1A, which is overexpressed in Down syndrome brains, regulates alternative splicing of
88 n neoplasms are uncommon among patients with Down syndrome, but organ-specific autoimmune diseases ar
89 21 (HSA21) cause intellectual disability and Down Syndrome, but our understanding of the HSA21 geneti
90 ssed Alzheimer's disease in individuals with Down syndrome, but the natural history of biomarker chan
91 rnia [n = 6,176], gastroschisis [n = 4,845], Down syndrome by presence of CHD [n = 22,317], and triso
93 lymphocyte subpopulations, individuals with Down syndrome can mount effector T-cell responses with s
94 Our findings indicate that many adults with Down syndrome can tolerate amyloid-beta deposition witho
96 ene X box binding protein-1 (Xbp1), (ii) the Down Syndrome Cell Adhesion Molecule (Dscam) gene and ii
101 d use a gain-of-function mouse allele of the Down syndrome cell adhesion molecule (Dscam) to compleme
102 nce of deleted in colorectal cancer (DCC) or Down syndrome cell adhesion molecule (DSCAM), and expres
107 /intellectual disability/mental retardation, Down syndrome, cerebral palsy, autism spectrum disorder)
108 fold reduction in the probability to have a Down syndrome child between a 20 and 30 years old Down s
110 rotein-beta, were found in young adults with Down syndrome compared to euploid cases (13-25 years, Do
113 examines the functional interactions between Down syndrome critical region 1 (DSCR1) and amyloid-prec
115 ibroblast growth factor-inducible 14 (Fn14), Down syndrome critical region 1 (Dscr1) and Nuclear rece
117 . demonstrate that the calcineurin regulator Down syndrome critical region 1 protein modulates both b
118 us introns from the human beta-globin, mouse Down syndrome critical region 1, or hagfish coagulation
119 rectifying potassium channel and maps to the Down syndrome critical region between DIRK1A and DSCR4.
121 based experiments suggest that the so-called Down syndrome critical region of human chromosome 21 is
122 on-regulated kinase 1 A (DYRK1A) maps to the Down syndrome critical region; copy number increase of t
123 s in the transchromosomic Tc1 mouse model of Down syndrome, demonstrating that ultrastructural abnorm
124 cultures from second trimester foetuses with Down syndrome (Down syndrome n = 7, controls n = 7).
126 ipper motif) mediates rab5 overactivation in Down syndrome (DS) and AD, which is caused by elevated l
127 ical correlates of genetic disorders such as Down syndrome (DS) and autism spectrum disorders (ASDs).
129 xpression and pathways common to humans with Down syndrome (DS) and mouse models we can discover nove
133 in anatomy in children and young adults with Down syndrome (DS) are limited, with no diffusion tensor
134 tal heart defect present in individuals with Down syndrome (DS) at a > 2000-fold increased prevalence
142 eta precursor protein gene on chromosome 21, Down syndrome (DS) individuals develop high levels of Ab
161 We show here that axonal GCs of human fetal Down syndrome (DS) neurons (and of a DS mouse model) ove
163 ctive sleep apnea (OSA) has been reported in Down syndrome (DS) owing to the coexistence of multiple
164 ukemia (AMKL) is more frequently observed in Down syndrome (DS) patients, in whom it is often precede
165 allate (EGCG) is a candidate therapeutic for Down syndrome (DS) phenotypes based on in vitro inhibiti
171 1, which is a phenotype long associated with Down syndrome (DS) that can also cause familial Alzheime
174 ses skeletal alterations in individuals with Down syndrome (DS), but the causative trisomic gene and
182 preleukemic disorder unique to neonates with Down syndrome (DS), may transform to childhood acute mye
184 vioral deficits in the Ts65Dn mouse model of Down syndrome (DS), translation to human clinical trials
187 ative diseases, Alzheimer's disease (AD) and Down syndrome (DS), using DNA methylation datasets from
198 course of both Alzheimer's disease (AD) and Down syndrome (DS); however, it is not clear how dysfunc
199 k of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of w
200 cute megakaryocytic leukemia associated with Down syndrome (DS-AMKL), where they occur in over half o
201 e United States, which is more than that for Down syndrome, fetal alcohol syndrome, and neural tube d
204 fication analyses revealed that females with Down syndrome had increased interleukin-6 and interleuki
205 Alzheimer's disease in individuals with Down syndrome has a long preclinical phase in which biom
207 date, investigations of neural anomalies in Down syndrome have focused on the central nervous system
209 attention-deficit hyperactivity disorder and Down syndrome have potential links to abnormal cerebella
211 is showcased by exploring multimorbidity in Down syndrome (ICD-10 code Q90) and hypertension (ICD-10
212 lcineurin phosphatase that is triplicated in Down syndrome, impairs neurotrophic support of sympathet
213 More than half of infants and children with Down syndrome in Cairo had ophthalmic abnormalities; myo
217 nt AD linked to PSEN1 mutations, in demented Down syndrome individuals and in sporadic AD subjects co
222 of the basis for intellectual impairment in Down syndrome is hindered by the large number of genes d
225 reased DYRK1A gene dosage, such as occurs in Down syndrome, is known to affect neural progenitor cell
226 e implicated in autism spectrum disorder and Down syndrome, is required presynaptically for normal sy
227 signaling effector candidates including the Down syndrome kinase Dyrk1a, STAT3, USP21, and SH2D2A.
228 nt Alzheimer's disease and the prevalence of Down syndrome make this population a suitable target for
231 le therapeutic target in myeloid leukemia of Down syndrome (ML-DS) and chronic myeloid leukemia (CML)
234 ildren with myeloid leukemia associated with Down syndrome (ML-DS) have superior outcome compared wit
235 s in visual and olfactory sensory systems in Down syndrome model mice, which provide insight into def
237 Importantly, restoring DSCR1 level in a Down syndrome mouse model effectively rescued adult neur
239 lder adults with Down syndrome (39-68 years, Down syndrome n = 22, controls n = 16) displayed reduced
240 in children with Down syndrome (1-10 years; Down syndrome n = 5, controls n = 10) and higher levels
243 comprehensive screening of a large cohort of Down syndrome neonates for the transient abnormal myelop
244 nderstanding of how human trisomy 21 effects Down syndrome neurobiology, and the translational potent
246 ors also contribute to visual acuity loss in Down syndrome, nystagmus alone could account for most of
247 that were used for this study, and in human Down syndrome, older females have significantly lower pr
249 ineteen (12%) individuals had a diagnosis of Down syndrome or other developmental disorder, while 84
252 ortant Hedgehog (Hh) pathway, but cells from Down syndrome patients paradoxically display reduced Hh
254 es and cerebral amyloid angiopathy of AD and Down syndrome patients, colocalizing with general Abeta
258 lence increased with age in individuals with Down syndrome, reaching 90-100% in the seventh decade of
259 -centre cross-sectional study of adults with Down syndrome recruited through a population-based healt
262 Munc18-1 is a proposed substrate for the Down Syndrome-related kinase dual-specificity tyrosine p
264 study how immunodeficiency in patients with Down syndrome results from immunologic defects in the B-
266 We used clinical data sets (United Kingdom Down syndrome screening data from Glasgow (1991-2003), E
269 collagen vascular disease, aortic aneurysm, Down syndrome, sleep apnea, depression, hyperlipidemia,
270 rom the Biomarkers of Alzheimer's Disease in Down Syndrome study (n = 138, 50 +/- 7 years, 39% women)
271 nd autoimmune disorders are more frequent in Down syndrome, suggesting abnormality of adaptive immuni
273 Although it is clear that trisomy 21 causes Down syndrome, the molecular events acting downstream of
274 que clinical comorbidities among adults with Down syndrome, there are no clinical guidelines for the
275 also located within the critical region for Down syndrome; therefore, understanding the role of DYRK
277 es women who receive a prenatal diagnosis of Down syndrome to receive positive information about the
279 multiple forms of AD.SIGNIFICANCE STATEMENT Down syndrome (trisomy 21) (DS) is a neurodevelopmental
280 urin-NFAT, candidates in the pathogenesis of Down syndrome (trisomy 21)-associated transient myelopro
282 disorders, such as Parkinson's, autism, and Down syndrome, understanding mechanisms modulating Synap
283 pseudotumor cerebri syndrome group included Down syndrome, vitamin A derivatives, and growth hormone
284 Cognitive impairment in participants with Down syndrome was classified with the Cambridge Cognitiv
289 s were significantly higher in subjects with Down syndrome, whereas their inhibitory receptor express
290 ement of care and follow-up for infants with down syndrome who are born even late preterm or early te
291 nificant differences between the adults with Down syndrome who had elevated neocortical Pittsburgh co
292 males and 56 females; aged 6-18 years) with Down syndrome who were born at or after 35 weeks gestati
293 Moreover, our sample included adults with Down syndrome who were most 'resistant' to the effects o
294 ia, diaphragmatic hernia, gastroschisis, and Down syndrome with an associated CHD has significantly i
295 que because it is the first reported case of Down syndrome with morning glory optic disc anomaly in l
296 r is frequently reported in individuals with Down syndrome, with considerable variation in the expres
298 analysis of previously reported 30 births in Down syndrome women shows a similar tendency with an alm
299 tion Medical Care Guidelines for Adults with Down Syndrome Workgroup (n = 13) developed 10 Population
300 ely to contribute to cognitive disability in Down syndrome, yet the neural network basis of this path