a role for neurotransmission and neurodevelopment in attention-deficithyperactivity disorder一个角色在attention-deficithyperactivity神经传递和神经发育障碍.pdfVIP

Minireview A role for neurotransmission and neurodevelopment in attention‑deficit/hyperactivity disorder † Tatiana Roman*, Luis A Rohde and Mara H Hutz* Addresses: *Departamento de Genética, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves, 9500 - Prédio 43323, Sala 115, Caixa postal 15053, CEP 91501-970, Porto Alegre, RS, Brasil. †ADHD Outpatient Program, Serviço de Psiquiatria da Infância e Adolescência, Hospital de Clinicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Instituto Nacional de Psiquiatria do Desenvolvimento, Rua Ramiro Barcelos, 2350, CEP 90035-003, Porto Alegre, RS, Brazil. Correspondence: Mara H Hutz. Email: mara.hutz@ufrgs.br pharmacological evidence, states that abnormal levels of Abstract Attention-deficit/hyperactivity disorder (ADHD) has a moderate dopamine cause ADHD. This led in 1995 to the first to high genetic component, probably due to many genes with association study by Cook et al. [6], who investigated a 40 small effects. Several susceptibility genes have been suggested bp variable number tandem repeat (VNTR) in the 3’ on the basis of hypotheses that catecholaminergic pathways in untranslated region of the dopamine transporter gene the brain are responsible for ADHD. However, many negative (DAT1) in ADHD families. Using the family-based approach association findings have been reported, indicating a limited called ‘haplotype relative risk’, an association with the ten- success for investigations using this approach. The results from genome-wide association studies have suggested that genes repeat allele was detected. In the following year, LaHoste related to general brain functions rather than