Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by hyperactivity, inattention, and impulsive behaviors and has significant societal impact. ADHD is recognized as a heterogeneous disease, and genetic and/or environmental factors underlying pathogenesis remain largely unknown. There is an obvious need to increase knowledge on molecular signaling and brain pathways underlying disease development, and genetic mouse models are key to this goal. In this issue of EMBO Molecular Medicine, D'Andrea et al (2015) combine state-of-the-art genetic and behavioral approaches in the mouse to demonstrate an essential role for PI3Kγ and cAMP homeostasis in ADHD-related behaviors, through signaling mechanisms operating at the level of the locus coeruleus, the main source of noradrenaline in the brain. Furthermore, the study posits PI3Kγ knockout mice as a novel tool of high interest for modeling ADHD endophenotypes.
Highlights
Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by hyperactivity, inattention, and impulsive behaviors and has significant societal impact
Attention-deficit/hyperactivity disorder is one of the most common childhood disorders, affecting around 7% of children in the world (Thomas et al, 2015) and this disorder often persists through adolescence and into adulthood
A main hypothesis, centered on monoamine neurotransmission, supposes that the complex interactions between dopamine, noradrenaline, and serotonin neurotransmitter systems are deregulated, and human studies have associated ADHD diagnosis with genes belonging to monoamine receptors and transporters (Kebir & Joober, 2011)
Summary
Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by hyperactivity, inattention, and impulsive behaviors and has significant societal impact. Several genetically modified mouse lines have provided clues on genes and pathways involved in the development of ADHD-related behaviors, and these studies have been reviewed recently (Leo & Gainetdinov, 2013). Dopamine transporter (DAT) knockout (KO) mice represent one of the earliest genetic mouse models for ADHD and recapitulate several ADHD-like symptoms, including spontaneous hyperactivity (Gainetdinov & Caron, 2001), impaired learning and memory, and increased impulsivity (Yamashita et al, 2013).
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