ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD): BEHAVIORAL AND GENETIC ASPECTS

Abstract

Attention Deficit Hyperactivity Disorder (ADHD) occurs during neurodevelopment, being more common in childhood and adolescence, but can last until adulthood. It is usually associated with symptoms involving family and school problems, negative psychological outcomes with increased risk for personality disorders, and psychotics. Indistinctly, they may present symptoms of inattention, while in others there is a predominance of impulsiveness and restlessness. The diagnosis is usually made in childhood, and it is difficult to validate before the age of five because it presents signs that are still nonspecific. There is a tendency for hyperactivity and compulsiveness to decrease in adolescence, although inattention persists. Language and learning problems are considered as common comorbidities for ADHD at this stage. In adults, the difficulty in diagnosis is recurrent due to the non-recognition of the problem, often due to the confusion of symptoms with personality failure due to emotional complaints. ADHD is considered a multifactorial and heterogeneous disorder, with hereditary and environmental contributions that interfere with neurodevelopment. There are strong indications of genetic contribution of this condition, between 70 – 80% heritability. Molecular studies of association of candidate genes and meta-analysis indicate the participation of the dopamine receptor genes (D4 and D5), in addition to the COMT gene, which encodes the enzyme catechol-O-methyltransferase, responsible for the degradation of catecholamines. Epigenetic patterns of methylation of dopaminergic, serotonergic, neurotrophic, and nerve growth factor receptor genes seem to be associated with different symptoms and severity of ADHD. The diagnosis is strictly clinical, based on the behavioral symptoms of inattention, impulsivity, and hyperactivity.