These abnormalities were located in the same region of the brain where schizophrenia is believed to develop as well as autism, which further contributed to the belief that ADHD is a neuro-developmental condition. Other studies have suggested that inheriting a DAT1 10 allele causes the brain to produce excess quantities of dopamine transporters, which results in less dopamine signaling between neurons.
Recently Korean scientists have uncovered an adaptor protein called GIT1, linked to ADHD. The study, published in “Nature Medicine” provides further evidence that this behavioral condition has a genetic link. This genetic correlation is not to exclude the possibility of environmental impacts or parenting influencing ADHD; however, it does demonstrate empirical proof that provides the evidence to pursue a discovery of the genes or lack of these genes or modifications of the genes' adaptor proteins with the hopes of ultimately finding a cure for the condition. ADHD seems to be diagnosed more and more and much attention has been given over to this condition in finding its origin with hopes of a better treatment and ultimately a cure some day through medications or genetic engineering.
According to the research one single nucleotide polymorphism or a single variant in the GIT-1 adaptor protein increased the chances 300% that a child may develop ADHD. Additionally, mice that lacked the GIT-1 showed ADHD like symptoms, including hyperactivity and impaired learning and memory.
The team looked at humans and mice. First, they scanned ADHD-associated genes identified in previous genome-wide analyses, specifically focusing on DNA linked to brain function. One potential candidate was GIT-1.
A Comparison of the sequence of the GIT-1 adaptor protein in 192 Korean children with ADHD and a group of 196 age-matched children without the condition found a single nucleotide polymorphism called RS-550818 was more common in children with ADHD than in the control group. Then they genetically engineered mice to lack the GIT-1. Approximately one half of the mice died soon after birth. Surviving mice lacking GIT-1 weighed significantly less than normal mice of the same age (minus 60-70 percent), but otherwise looked normal.
The genetically-modified mice also responded to drugs used to treat human ADHD. This reduced their ADHD-like symptoms back to the normal levels seen in control animals. Read the articles on the genetic link of ADHD and Korean Study
this article is for informational purposes only and not for diagnosing or treating any mental illness
