Attention Deficit Hyperactivity Disorder or ADHD is one of the most common mental disorders that first show during childhood. The disorder is characterized by both hyperactivity and difficulty focusing. With thousands of children and adults being diagnosed with ADHD annually, researchers are scratching their heads to identify why people develop ADHD; what are its secrets? And can it be stopped?
Recently, a joint study by Israeli researchers has begun cracking the code to understand the underlying genetic causes of ADHD better.
What is ADHD?
ADHD, according to the Centers for Disease Control and Prevention, is the most common neurodevelopmental disorder of childhood. It is usually diagnosed during childhood and often lasts into adulthood. Children diagnosed with ADHD may have trouble paying attention, controlling impulsive behaviors, and controlling overactivity.
Although it is perfectly normal to have problems focusing and behaving from time to time, children diagnosed with ADHD do not grow out of these behaviors. Symptoms often continue throughout their lives and may cause difficulty at school, with friends, and more. A child with ADHD may daydream a lot, forget or lose things often, fidget, talk too much, make careless mistakes, take unnecessary risks, have difficulty resisting temptation, have trouble taking turns, and face challenges when getting along with others.
There are three types of ADHD depending on the symptoms exhibited: Predominantly Inattentive Presentation, Predominantly Hyperactive-Impulsive Presentation, or Combined Presentation.
Cracking the Code to ADHD's Genetic Causes
A new study published in the journal Nature Communications, titled "CDH2 mutation affecting N-cadherin function causes attention-deficit hyperactivity disorder in humans and mice," was carried out by a joint team of researchers from Soroka-University Medical Centre and the Ben-Gurion University of the Negev.
Researchers pointed to the gene CDH2. It encodes N-cadherin responsible for helping the activity of brain synapses and their formation. However, a mutation in the gene alters the activity of the brain. In turn, it impacts the molecular pathways and dopamine levels of two brain structures: the ventral midbrain and prefrontal cortex, both of which are involved in ADHD, reports The Jerusalem Post. The discovery was tested via CRISPR to insert the mutation in homologous mouse genes that caused hereditary hyperactivity.
The implications of the joint study could help pave the way for researchers to understand further how the most common neurodevelopmental disorder, ADHD, works and how it can be both treated and managed.
Professor Ohad Birk, the lead author of the study, explains that in addition to the scientific significance of finding a definitive delineation of both novel genetic basis and molecular pathways for ADHD, both the mutated human cells and mouse strain carrying the said mutation serves as an effective model system in discovering novel medications for ADHD patients.
Researchers note that numerous investigations are needed to prove further the interaction and role of the CDH2 gene in developing ADHD. However, they are positive that this is a major stepping stone in finally uncovering the mysteries of ADHD and its development in children.
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