The Brain

Neurobiological Origin of Attention Deficit Disorder Discovered

April 11, 2014 | by Lisa Winter

Photo credit: ArtM

Neurobehavioral disorders like attention deficit disorder (ADD) can have a wide range of symptoms and affect people differently, meaning they are not a black and white diagnosis like cancer or an infectious disease. For a host of reasons, including better access to doctors and a decreased stigma about seeking help for mental health, diagnoses have been increasing. This has left many critics claiming that it doesn’t exist and is merely an excuse for laziness or poor behavior, while many doctors and diagnosed adults insist that the symptoms are real; the disorder itself is just poorly understood.

However, the way that ADD is understood and treated could be about to change considerably. A large collaborative study led by Michael Reber of the University of Strasbourg has confirmed the biological origin of the disorder. The results were published in an open-access format in the journal Brain Structure & Function.

The superior colliculus is found in the midbrain and has many sensory- and motor-related functions. The researchers introduced a population of mice to a genetic mutation which doubled the connections between the retina and superior colliculus, creating visual hyperstimulation. Those with the mutation also had a superior colliculus with a buildup of the neurotransmitter noradrenaline, which is “fight or flight” molecule that increases heart rate and prepares the body to react to a stimulus. 

ADD has a multitude of symptoms, including impulsiveness, inattention, anxiety, and hyperactivity. Traditionally, these symptoms have been controlled with a combination of therapy, psychostimulants, and training to work around symptoms. While medication has been shown to greatly reduce symptoms, they come with a list of side effects, including nervousness, loss of appetite, dry mouth, and others.

This work differs from other studies regarding ADD which primarily focus on dopamine synthesis and transmission. The mice with a genetically-altered superior colliculus did not have any defects in dopamine production or pathways, yet exhibited all classic symptoms of ADD. This adds to the physiological complexity of the disorder.

The researchers will continue along this line of study in an effort to better understand the role of the excess noradrenaline. This widened approach to understanding the neurobiological causes of ADD could eventually revolutionize how the disorder is diagnosed and treated. New medications could be developed to target the problem at its root with fewer side effects.

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