An analysis of attention deficit hyperactivity disorder adhd
They are not defined based on etiological sources, or any biologically identified markers.
A primary aim of the study is to correlate genetic and biological markers for diagnosis and prognosis of ADHD identified through the use of state of the art genomics, which includes enome-wide association studies, linkage analysis, whole genome and exome sequencing, and targeted gene capture in cosmopolitan and isolated populations.
Affected children are at increased risk for poor educational achievement, low income, underemployment, legal difficulties, and impaired social relationships.
Twins studies showed that monozygotic twin pairs have much higher concordance rates for ADHD than dizygotic twin pairs Faraone et al.
This review article will examine existing studies that focused on understanding the etiology, clinical profile, trajectories, neurocognitive impairments, and neurobiological and pathological mechanisms of ADHD.
Adults with ADHD may start relationships impulsively, display sensation-seeking behavior, and be short-tempered. Moreover, existing studies also observed the involvement of the fronto-striatal circuit in working memory impairment and delay aversion in ADHD Castellanos et al.
Intermediate phenotypes were suggested to play a role in mediating the associations between clinical phenotypes and genes in mental disorders Gottesman and Gould,
What gene causes adhd
However, such statement could not be applied on other environmental risk factors, such as perinatal complications or lead exposure. The NIH Research Domain Criteria RDoC represents a new research framework for investigating ADHD by integrating multi-level information from genomics and circuits to behavior and self-reports to explore basic dimensions of functioning that span the full range of human behavior from normal to abnormal. Existing research suggests that genetic variants, and pre- and peri-natal risk factors relate to the manifestation of ADHD symptoms, and appear to be associated with various neurodevelopmental and psychiatric outcomes Bonvicini et al. Multiple factors, such as psychiatric and behavioral comorbidities, symptom severity levels, and inter-individual variability in the amount of dopamine released by neurons, may contribute to the treatment response heterogeneity in ADHD. It is still debatable about whether adult ADHD is defined as a childhood-onset neurodevelopmental disorder or not Moffitt et al. Intermediate phenotypes were suggested to play a role in mediating the associations between clinical phenotypes and genes in mental disorders Gottesman and Gould, In addition, none of these theoretical models completely address the heterogeneity of ADHD. Working memory processing allows for temporary storage, maintenance, and manipulation of sensory and cognitive information, and provides an interface between perception, attention, memory, and action, and is crucial for higher order cognitive processes Baddeley, DRD4 has been reported to significantly interact with high stress level during pregnancy and some chemical toxins, e. These models included: 1 cognitive and motivational impairment models Tannock et al. Moreover, existing studies also observed the involvement of the fronto-striatal circuit in working memory impairment and delay aversion in ADHD Castellanos et al. Despite evidence of a strong genetic contribution to ADHD, the inconsistent findings from genetic association studies may result from the relatively small effect sizes, with each gene only accounting for a small proportion of the overall ADHD risk Gizer et al. Genes and environment do not work independently of each other Nigg et al. A recent longitudinal study found that 2. Exposures to other toxins in prenatal and postnatal life have also been considered as increasing the risk of ADHD Thapar et al.
based on 39 review