Attention-deficit/hyperactivity disorder (ADHD) is a common psychiatric disorder in which different genetic and environmental susceptibility factors are involved. Several lines of evidence support the view that at least 30% of ADHD patients diagnosed in childhood continue to suffer the disorder during adulthood and that genetic risk factors may play an essential role in the persistence of the disorder throughout lifespan. Genetic, biochemical and pharmacological studies support the idea that the serotonin system participates in the etiology of ADHD. Based on these data, we aimed to analyze single nucleotide polymorphisms across 19 genes involved in the serotoninergic neurotransmission in a clinical sample of 451 ADHD patients (188 adults and 263 children) and 400 controls using a population-based association study. Several significant associations were found after correcting for multiple testing: (1) the DDC gene was strongly associated with both adulthood (P = 0.00053; odds ratio (OR) = 2.17) and childhood ADHD (P = 0.0017; OR = 1.90); (2) the MAOB gene was found specifically associated in the adult ADHD sample (P = 0.0029; OR = 1.90) and (3) the 5HT2A gene showed evidence of association only with the combined ADHD subtype both in adults (P = 0.0036; OR = 1.63) and children (P = 0.0084; OR = 1.49). Our data support the contribution of the serotoninergic system in the genetic predisposition to ADHD, identifying common childhood and adulthood ADHD susceptibility factors, associations that are specific to ADHD subtypes and one variant potentially involved in the continuity of the disorder throughout lifespan.

A continued improvement of symptoms is expectable until 12 weeks in treatment-naïve ADHD patients treated with atomoxetine as first-line medication. Chief limitations are the small, national sample size and the absence of data beyond the 12-week time-point.

A mismatch negativity event-related potential protocol was administered to dyslexic children and their respective controls to test whether a specific auditory deficit concerning phonetic processing or a lower level auditory processing deficit was present in developmental dyslexia. Three different contrast conditions were explored, including nonphonological sounds, contrasted in pitch and duration, and phonemes. Mismatch negativity amplitudes differed significantly between groups in the duration condition, whereas no differences were found in the frequency and phoneme conditions. Moreover, the dyslexic children had delayed mismatch negativity latencies in the three contrast conditions. Our results suggest a deficit in low-level auditory discrimination in dyslexic children, in particular when detecting stimulus duration, and support the rapid auditory processing theory of dyslexia.

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