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Jun 04, 2014 03:23 PM EDT

Attention deficit hyperactivity disorder may be caused by the miswiring of the brain, according to a recent study.

Neuroscientists at Mayo Clinic in Florida and at Aarhus University in Denmark are shedding light on why neurons in the brain's reward system can be miswired. They believe this could potentially contribute to disorders such as ADHD.

The findings "may increase the understanding of underlying causes of ADHD, potentially facilitating the development of more individualized treatment strategies," researchers said in their study.

For the study, the scientists looked at dopaminergic neurons in mice. These neurons regulate pleasure, motivation, reward, and cognition, and have been implicated in development of ADHD.

While doing this they discovered a receptor system that is "critical, during embryonic development, for correct wiring of the dopaminergic brain area," according to a news release. But they also discovered that after brain maturation, a cut in the same receptor, SorCS2 - which functions as a molecular switch between apparently opposing effects in proBDNF, produces a two-chain receptor that induces cell death following damage to the peripheral nervous system.

ProBDNF is a neuronal growth factor that helps select cells that are most beneficial to the nervous system, while eliminating those that are less favorable in order to create a finely tuned neuronal network. Researchers found that some cells in mice deficient in SorCS2 are unresponsive to proBDNF and have dysfunctional contacts between dopaminergic neurons.

"This miswiring of dopaminergic neurons in mice results in hyperactivity and attention deficits," Anders Nykjaer, senior investigator of the study and a neuroscientist at Mayo Clinic in Florida and at Aarhus University in Denmark, said in a statement. ""A number of studies have reported that ADHD patients commonly exhibit miswiring in this brain area, accompanied by altered dopaminergic function. We may now have an explanation as to why ADHD risk genes have been linked to regulation of neuronal growth."

The findings were recently published in the journal Neuron.

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