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Increased ADHD risk in children in terms of hazard ratios (HRs) and 95% confidence intervals (CIs) was associated with prenatal exposure to paternal autoimmune diseases, including Sjögren’s syndrome (HR: 8.
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Larger sample sizes and functional studies are warranted to explore the clinical utility of FAAH genotyping as a possible marker for increased ADHD risk in children.
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Adhd Risk sentence examples within Increase Adhd Risk
In the other direction, there was weak evidence that smoking initiation increases ADHD risk, but follow-up analyses suggested a high probability of horizontal pleiotropy.
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In the other direction, there was weak evidence that smoking initiation increases ADHD risk, but follow‐up analyses suggested a high probability of horizontal pleiotropy.
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Adhd Risk sentence examples within Polygenic Adhd Risk
Here, we investigate genetic overlap between polygenic ADHD risk and multiple literacy-related and/or language-related abilities (LRAs), as assessed in UK children (N ≤ 5919), accounting for genetically predictable educational attainment (EA).
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Here, we aim to study the association between polygenic ADHD risk and language abilities in the general population.
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Adhd Risk sentence examples within adhd risk gene
Adhd Risk sentence examples within adhd risk factor
Environmental ADHD risk factors including toxic, nutritional factors and stressful life events lead to changes in DNA methylation and in histone modification levels.
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These data suggest that microglial inflammasome activation and pyroptosis are essential for normal brain development and that genetic and pharmacological disruptions in this pathway may represent new ADHD risk factors.
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Adhd Risk sentence examples within adhd risk locus
Adhd Risk sentence examples within adhd risk prediction
First, we expand upon the results from the aforementioned GWAS by incorporating additional samples of non-European ancestry to advance locus discovery, improve fine-mapping of the identified loci, and evaluate transferability of ADHD risk prediction across ancestries.
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We expand upon this result by incorporating additional samples of non-European ancestry in order to advance genome-wide variant discovery, improve fine-mapping, and evaluate transferability of ADHD risk prediction across ancestries.
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However, there was insufficient evidence for the association between antibiotic intake after birth and ADHD risk.
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Quantifying early health services use among children later diagnosed with ADHD could help us understand the early life impact of the disorder and uncover health care utilization patterns associated with higher ADHD risk.
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5-methoxytryptophol (5-MTX), a neuroendocrine molecule which also has antioxidant and immunomodulatory properties, was inversely associated with acetaminophen and ADHD risk.
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If confirmed, these findings support previous evidence that maternal ASD or neuroticism may be possible targets for intervention to help break the chain of the intergenerational transmission of ADHD risk.
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Simultaneously decreasing all constituents of common-detect OPE-phthalate mixture, specifically DPHP, DNBP, and 6 phthalate metabolites, by a quartile resulted in an ADHD risk ratio of 0.
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Increased ADHD risk in children in terms of hazard ratios (HRs) and 95% confidence intervals (CIs) was associated with prenatal exposure to paternal autoimmune diseases, including Sjögren’s syndrome (HR: 8.
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In analyses of the polygenic architecture, we found higher polygenic score (PGS) of ADHD risk variants in persistent ADHD (mean PGS=0.
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Interestingly, a causal effect from cannabis use to ADHD risk was also observed for the first time.
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We used genetic variants from alcohol metabolising genes (alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)) as proxies for fetal alcohol exposure to investigate their association with offspring ADHD risk around age 7-8.
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While genetic factors contribute to ASD and ADHD risk, the environmental contribution to ASD and ADHD has been recognized as having potentially equal importance, which raises the hope for early prevention and intervention.
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Dose–response analysis for parental age and ADHD risk was performed.
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We investigated associations between maternal prenatal smoking, alcohol and caffeine consumption with childhood ADHD risk accounting for shared familial factors.
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Although ADHD is highly heritable, environmental factors also appear to contribute to ADHD risk.
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We derived ADHD-PRS and identified 25 ADHD risk-factors in Danish national registers.
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The study of ADHD risk genes such as ADGRL3 requires the gene to be first identified using human studies.
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The authors investigated the overlap between common genetic variation associated with ADHD risk and these brain volume measures to identify underlying biological processes contributing to the disorder.
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Two environmental exposures independently associated with dopaminergic dysfunction and ADHD risk include exposure to deltamethrin, a pyrethroid insecticide, and chronic stress.
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As a potential ADHD risk gene, KCNJ6, therefore, may contribute to the endophenotypic variation of the disorder.
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CONCLUSIONS
Infant anger reactivity exerts a direct effect on later ADHD from infancy, suggesting anger reactivity as a very early indicator of ADHD risk.
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Leveraging this enrichment, we identified 19 novel ADHD risk loci and 40 novel BD risk loci at condFDR <0.
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This suggests that the common ASD risk gene variants have a stronger association to behavioral regulation aspects of executive dysfunction than ADHD risk or INT variants in a clinical sample with ASD symptoms.
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In the other direction, there was weak evidence that smoking initiation increases ADHD risk, but follow-up analyses suggested a high probability of horizontal pleiotropy.
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Likewise, ADHD risk-increasing alleles (Pthr<0.
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Environmental ADHD risk factors including toxic, nutritional factors and stressful life events lead to changes in DNA methylation and in histone modification levels.
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OBJECTIVE
To assess the interaction between maternal attention-deficit/hyperactivity disorder (ADHD) history and young parental age on child's ADHD risk.
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Here, we investigate genetic overlap between polygenic ADHD risk and multiple literacy-related and/or language-related abilities (LRAs), as assessed in UK children (N ≤ 5919), accounting for genetically predictable educational attainment (EA).
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This study was performed to evaluate the association of MTHFR polymorphisms with ADHD risk in Iranian children.
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Conclusions We combine ADHD risk gene identification in an individual family with genetic association testing in a large case–control data set and functional validation in a model system, together providing an important illustration of an integrative approach suggesting that FBXO25 contributes to key features of ADHD and comorbid neuropsychiatric disorders.
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Larger sample sizes and functional studies are warranted to explore the clinical utility of FAAH genotyping as a possible marker for increased ADHD risk in children.
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In this way, we were recently able to show ADHD risk loci to influence intracranial volume.
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Results A total of 15 175 later-born siblings were classified by familial risk status based on the older child’s diagnostic status: ADHD risk (n = 730; male [51.
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ADHD risk was increased among offspring born to asthmatic mothers (hazard ratio (HR) 1.
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These data suggest that microglial inflammasome activation and pyroptosis are essential for normal brain development and that genetic and pharmacological disruptions in this pathway may represent new ADHD risk factors.
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Finally, SLC1A3 rs1049522 showed significant association with ADHD risk in two stages with CA genotype vs AA genotype, odds ratio (OR) = 0.
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Results The meta-analysis of the highly heterogeneous case-control studies did not find significant association between maternal diabetes and ADHD risk (OR: 1.
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OBJECTIVE
To assess the interaction between maternal attention-deficit/hyperactivity disorder (ADHD) history and young parental age on child's ADHD risk.
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, six or more inattentive and/or hyperactive-impulsive symptoms), with an interest in the age at which ADHD risk first emerged.
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This study aimed to identify novel ADHD genes by investigating whether genes carrying rare mutations linked to ID contribute to ADHD risk through common genetic variants.
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In a sibling-stratified Cox regression, intrapartum cesarean was associated with increased ADHD risk, but other exposures were not.
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We conducted a population-based cohort study to examine the association between antibiotic use in the first year of life and ADHD risk.
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ADHD risk alleles correlated with increased expression (and decreased methylation) of ARTN and PIDD1 and with a decreased expression (and increased methylation) of C2orf82.
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Here, we aim to study the association between polygenic ADHD risk and language abilities in the general population.
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The aim of the study is to assess the impact of CNVs on ASD /ADHD risk in multiplex families.
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Results When association analysis was done between ADHD children without ASD and samples of normal control and pseudo-control, the T allele of rs7106631 of SHANK2 significantly decreased the ADHD risk (p=0.
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We show that different combinations of the same ASD and ADHD risk-increasing alleles can simultaneously re-capture known ASD-related positive and ADHD-related negative associations with EA.
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Since both ADHD risk and brain volumes are highly heritable, we hypothesized that both traits are genetically linked by shared common variant architecture.
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First, we expand upon the results from the aforementioned GWAS by incorporating additional samples of non-European ancestry to advance locus discovery, improve fine-mapping of the identified loci, and evaluate transferability of ADHD risk prediction across ancestries.
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In the other direction, there was weak evidence that smoking initiation increases ADHD risk, but follow‐up analyses suggested a high probability of horizontal pleiotropy.
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Discussion We are aiming to provide a biological link between ADHD risk factors (NET16 and MSDP), cortical thickness and behavioural/clinical outcomes.
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We will present results from analyses of the impact of ultra-rare deleterious variation on ADHD risk based on the full sample of ADHD cases and controls.
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We therefore hypothesized that several ADHD risk genes related to dopamine might also be predictive of reduced ELE.
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The results of this study provide additional evidence for an increased genetic burden of ADHD risk in females diagnosed with ADHD and their relatives, although it would appear that common genetic variants may not play a substantial role.
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Additionally, the polygenic risk score (PRS) based on ADHD risk SNPs was found to be particularly elevated in individuals diagnosed with both ADHD and CD compared to those who only had ADHD.
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We expand upon this result by incorporating additional samples of non-European ancestry in order to advance genome-wide variant discovery, improve fine-mapping, and evaluate transferability of ADHD risk prediction across ancestries.
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