Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inattentiveness in attention-deficit/hyperactivity disorder.

ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with a long-term impact on functioning, productivity and quality of life of patients. This impact is largely due to the symptoms of inattentiveness. However, despite its impairing role in the lives of ADHD patients, inattentiveness has been studied relatively less frequently than have symptoms of impulsivity/hyperactivity and problems with executive function. This review therefore seeks to integrate the neuropsychological theories and current findings in the research fields of neuropsychology, neurophysiology, and neuroimaging, in an attempt to gain a more complete understanding of the role that inattentiveness plays in ADHD, as well as to suggest directions for future studies. The need for a more comprehensive understanding of inattentiveness and ADHD, which integrates findings from each of the three disciplines mentioned above, is emphasized.

SUBMITTER: Sroubek A

PROVIDER: S-EPMC4440572 | biostudies-other | 2013 Feb

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Attention-deficit hyperactivity disorder.

Project description:Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an evolving construct that has been refined and developed over the past several decades in response to research into its clinical nature and structure. The clinical presentation and course of the disorder have been extensively characterised. Efficacious medication-based treatments are available and widely used, often alongside complementary psychosocial approaches. However, their effectiveness has been questioned because they might not address the broader clinical needs of many individuals with ADHD, especially over the longer term. Non-pharmacological approaches to treatment have proven less effective than previously thought, whereas scientific and clinical studies are starting to fundamentally challenge current conceptions of the causes of ADHD in ways that might have the potential to alter clinical approaches in the future. In view of this, we first provide an account of the diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the eleventh edition of the International Classification of Diseases. Second, we review the progress in our understanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so. Finally, using these discoveries, we explore some of the key challenges to both the current models and the treatment of ADHD, and the ways in which these findings can promote new perspectives.

| S-EPMC7880081 | biostudies-literature

Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

| PRJNA1114309 | ENA

Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

| PRJNA1114310 | ENA

CFTR acts as a potential therapeutic target for attention deficit-hyperactivity disorder

Project description:The occurrence of attention deficit-hyperactivity disorder (ADHD) symptoms in patients with cystic fibrosis (CF) is substantially higher than in the general population, and the cystic fibrosis transmembrane conductance regulator (CFTR) is the pathogenic gene of cystic fibrosis, suggesting the potentially critical role of CFTR in ADHD. Here, we identified three heterozygous missense mutations (p.E217G, p.F316L and p.T1220I) in CFTR, segregating with ADHD in two consanguineous families with 6 affected individuals. Using the zebrafish model, we found that the cftr knockout line displays hyperactive, impulsive-like, and attention deficit-like behaviors, reminiscent of human ADHD patients. Single-cell RNA-seq of 7 dpf larvae identified clusters of neuron cells that were sensitive to cftr, especially, the number of dopaminergic neuron cells decreased in the cftr mutant fish. Bulk RNA-seq and proteomic analysis at the early gastrulation period showed that the expression of nerve system genes was abnormal. Notably, we tried to use CFTR activitors Lumacaftor (VX-809) and Ivacaftor (VX-770) to treat the ADHD zebrafish model (established by per1b mutant), and found enhanced CFTR activity could rescue the ADHD-like behaviors. In brief, we uncover the role of CFTR in ADHD pathogenesis and explore novel diagnoses and therapy for ADHD by targeting CFTR.

2024-12-16 | GSE284214 | GEO

Genetics of attention deficit hyperactivity disorder.

Project description:Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD's high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD's heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD's heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.

| S-EPMC6477889 | biostudies-literature

Linkage analysis of attention deficit hyperactivity disorder.

Project description:Results of behavioral genetic and molecular genetic studies have converged to suggest that both genes contribute to the development of ADHD. Although prior linkage studies have produced intriguing results, their results have been inconsistent, with no clear pattern of results emerging across studies. We genotyped 5,980 SNPs across the genome in 1,187 individuals from families with children diagnosed with ADHD. We then performed two nonparametric linkage analyses on ADHD families: (1) an affected sibling pair linkage analysis on 217 families with 601 siblings diagnosed with ADHD and (2) a variance components linkage analysis using the number of ADHD symptoms as the phenotype on 260 families with 1,100 phenotyped siblings. The affection status linkage analysis had a maximum LOD score of 1.85 on chromosome 8 at 54.2 cM. The maximum LOD score in the variance components linkage analysis was 0.8 on chromosome 8 at 93.4 cM. The absence of regions of significant or suggestive linkage in these data suggest that there are no genes of large effect contributing to the ADHD phenotype.

| S-EPMC4511106 | biostudies-literature

Emotion dysregulation in attention deficit hyperactivity disorder.

Project description:Although it has long been recognized that many individuals with attention deficit hyperactivity disorder (ADHD) also have difficulties with emotion regulation, no consensus has been reached on how to conceptualize this clinically challenging domain. The authors examine the current literature using both quantitative and qualitative methods. Three key findings emerge. First, emotion dysregulation is prevalent in ADHD throughout the lifespan and is a major contributor to impairment. Second, emotion dysregulation in ADHD may arise from deficits in orienting toward, recognizing, and/or allocating attention to emotional stimuli; these deficits implicate dysfunction within a striato-amygdalo-medial prefrontal cortical network. Third, while current treatments for ADHD often also ameliorate emotion dysregulation, a focus on this combination of symptoms reframes clinical questions and could stimulate novel therapeutic approaches. The authors then consider three models to explain the overlap between emotion dysregulation and ADHD: emotion dysregulation and ADHD are correlated but distinct dimensions; emotion dysregulation is a core diagnostic feature of ADHD; and the combination constitutes a nosological entity distinct from both ADHD and emotion dysregulation alone. The differing predictions from each model can guide research on the much-neglected population of patients with ADHD and emotion dysregulation.

| S-EPMC4282137 | biostudies-literature

Molecular genetics of attention deficit hyperactivity disorder.

Project description:Although twin studies demonstrate that ADHD is a highly heritable condition, molecular genetic studies suggest that the genetic architecture of ADHD is complex. The handful of genome-wide linkage and association scans that have been conducted thus far show divergent findings and are, therefore, not conclusive. Similarly, many of the candidate genes reviewed here (ie, DBH, MAOA, SLC6A2, TPH-2, SLC6A4, CHRNA4, GRIN2A) are theoretically compelling from neurobiological systems perspective but available data are sparse and inconsistent. However, candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder, with meta-analyses supportive of a role of the genes coding for DRD4, DRD5, SLC6A3, SNAP-25, and HTR1B in the etiology of ADHD.

| S-EPMC2847260 | biostudies-literature

Effect of methylphenidate on gene expression profiles of Attention Deficit Hyperactivity Disorder patients and unaffected controls.

Project description:Attention deficit hyperactivity disorder (ADHD) is a common psychiatric condition of children with a prevalence of 5-10% worldwide. Up to 30% of adults with a history of childhood ADHD maintain symptoms in later life; these adult ADHD patients are severely impaired in social and professional life due to persistence of ADHD core symptoms like impulsivity, attention deficit and hyperactivity as well as frequently observed co-morbidities like alcohol and drug abuse, major depression, bipolar and personality disorders. Pharmaceutical treatment options include methylphenidate (MPH), which is amongst others an inhibitor of the dopamine transporter and therefore increases dopamine levels in the brain. However, not all ADHD patients are MPH responders with clinical features to distinguish responders and non-responders being not at hand so far. Likewise, neurobiological reasons for drug response are still elusive. Here, we examined the global transcriptional response of MPH on lymphoblastoid cell lines (LCLs) derived from ADHD patients and unaffected controls.

2014-09-05 | E-GEOD-52889 | biostudies-arrayexpress

Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives.

Project description:The role of diet and of food colors in attention-deficit/hyperactivity disorder (ADHD) or its symptoms warrants updated quantitative meta-analysis, in light of recent divergent policy in Europe and the United States.Studies were identified through a literature search using the PubMed, Cochrane Library, and PsycNET databases through February 2011. Twenty-four publications met inclusion criteria for synthetic food colors; 10 additional studies informed analysis of dietary restriction. A random-effects meta-analytic model generated summary effect sizes.Restriction diets reduced ADHD symptoms at an effect of g = 0.29 (95% CI, 0.07-0.53). For food colors, parent reports yielded an effect size of g = 0.18 (95% CI, 0.08-0.24; p = .0007), which decreased to 0.12 (95% CI, 0.01-0.23; p < .05) after adjustment for possible publication bias. The effect was reliable in studies restricted to food color additives (g = 0.21, 95% CI = 0.06-0.36) but did not survive correction for possible publication bias and was not reliable in studies confined to Food and Drug Administration-approved food colors. Teacher/observer reports yielded a nonsignificant effect of 0.07 (95% CI = -0.03 to 0.18; p = .14). However, high-quality studies confined to color additives yielded a reliable effect (g = 0.22, 95% CI = 0.10-0.41, p = .030) that survived correction. In psychometric tests of attention, the summary effect size was 0.27 (95% CI = 0.07-0.47; p = .007) and survived correction. An estimated 8% of children with ADHD may have symptoms related to synthetic food colors.A restriction diet benefits some children with ADHD. Effects of food colors were notable were but susceptible to publication bias or were derived from small, nongeneralizable samples. Renewed investigation of diet and ADHD is warranted.

| S-EPMC4321798 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data