may underlie the pathophysiology of ADHD. Finding inflammatory genes (IL16 and ADAMTS2) is somewhat surprising, although inflammation is already known to be involved in different psychiatric disorders, like major depression and Alzheimer’s disease (Anisman 2009; Bazar et al. 2006; Garcia-Bueno et al. 2008; Serretti et al. 2007). The analysis of age of onset of ADHD revealed a number of environmentally regulated genes (Lasky-Su et al. 2008a), which may suggest a particularly important influence of the environment in this aspect of the disorder. However, all of these biological hypotheses must be tempered by the limited knowledge of the genetic architecture of ADHD at this point. Currently, we do not have sufficient information to draw strong conclusions about the relative impact of the biological pathways and genetic influences, aside from likely knowing that the genetic effects are modest in size.
