Biochemical and genetic analyses of childhood attention deficit/hyperactivity disorder

Abstract

Attention deficit/hyperactivity disorder (ADHD) in children is a neurobehavioral disorder characterized by inattention, hyperactivity, and/or impulsivity. The biochemical abnormalities and genetic factors play significant roles in the etiology of ADHD. These symptoms affect the behavior performance and social relationships of children in school and at home. Recently, many studies about biochemical abnormalities in ADHD have been published. Several research groups have also suggested the genetic contribution to ADHD, and attempted to identify susceptibility and candidate genes for this disorder through the genetic linkage and association studies. To date, these studies have reported substantial evidence implicating several genes (dopaminergic: DRD4, DAT1, DRD5, COMT; noradrenergic: DBH, ADRA2A; serotonergic: 5-HTT, HTR1B, HTR2A; cholinergic: CHRNA4, and central nervous system development pathway: SNAP25, BDNF) in the etiology of ADHD. Understanding the biochemistry and genetics of ADHD will allow us to provide a useful addition with other treatment procedures for ADHD.

Arsenic in groundwater and its health risk assessment in drinking water of Mailsi, Punjab, Pakistan

“…The results showed that residents of the area had a toxic risk index in order of Mailsi>Sargana ( Nguyen et al 2009;Caylak 2012) and is much higher than other studies done in different areas of Pakistan (0.00-5.56×10 −7 mg/kg/day (Muhammad and Khan 2010). The ADD range is larger in Mailsi area as compared to Sargana area.…”

Short-term oral atrazine exposure alters the plasma metabolome of male C57BL/6 mice and disrupts α-linolenate, tryptophan, tyrosine and other major metabolic pathways

“…Clinical plasma metabolomic analyses show that linoleic acid and α-linolenic acid metabolic pathways are disrupted in patients with amnestic mild cognitive impairment and with Alzheimer's disease (Wang et al 2014). Epidemiological studies also demonstrate that imbalance in PUFAs is associated with increased risk of several neurodevelopmental disorders, including attention-deficit/hyperactivity disorder and autism (Caylak 2012;Lyall et al 2013). In line with these studies, we reported that short-term ATR exposure (≥125 mg/kg) decreased the number of dopamine neurons in the substantia nigra pars compacta and ventral tegmental area in juvenile mice (Coban and Filipov 2007).…”

Dopamine’s Actions in Primate Prefrontal Cortex: Challenges for Treating Cognitive Disorders

“…Genetic studies indicate that ADHD is highly heritable but is a polygenetic disorder with thousands of genes likely implicated, all with small effect size (Elia et al, 2012;Akutagava-Martins et al, 2013). Candidate gene studies have shown a small linkage with the DArelated genes DR5 and the DA transporter DAT1, as well as the catecholamine-related genes DRD4 and catechol-O-methyltransferase and the NE-related genes DBH and ADRA2A (Caylak, 2012). However, it is likely that most genes implicated in ADHD have other roles, e.g., involvement in PFC development and function independent of DA.…”

“…Postmortem studies show that DA fibers are reduced in the dlPFC of patients with schizophrenia, but only from layer VI and not from more superficial layers (Akil et al, 1999). PET imaging findings also show evidence that D1/5R are increased in the dlPFC early in the illness in unmedicated patients (Abi-Dargham et al, 2002, 2012, possibly as compensation for reduced DA release (Slifstein et al, 2015). Dihydrexidine (now referred to as DAR-0100A) is currently being tested in schizotypal patients who have cognitive deficits that are qualitatively similar to patients with schizophrenia.…”