Attention+Deficit+Hyperactivity+Disorder
-
Professor Eunjoon Kim Is KAIST's Person of the Year 2014
KAIST announced that it has named Chair Professor Eunjoon Kim of the Department of Biological Sciences as its “Person of the Year 2014.” The award ceremony took place at the auditorium on campus on January 5, 2014.
Established in 2001, the award has been presented to a KAIST faculty member who has made great achievements in research and education, thereby contributing to the advancement of KAIST.
Professor Kim was the first to identify the mechanism of synapse formation between neurons during his post-doctoral program at Harvard Medical School in 1995. The research was published in Nature.
In 2011, Professor Kim discovered that the lack of protein GIT1, a neuronal synapse in the brain, caused ADHD (Attention Deficit Hyperactivity Disorder). He is widely recognized for his work concerning synapse proteins and brain disease related research that set the foundation for future medical developments.
In his award speech, Professor Kim said, “Whenever a research finding concerning a new drug therapy or research is published, I receive many inquiries from the parents of children with ADHD or autism. As a scientist, I would like to focus my research ultimately to help those in pain, rather than just pursuing research excellence or reputation.”
2015.01.06 View 8953 -
Genetic Cause of ADHD (Attention Deficit Hyperactivity Disorder) Found
The cooperative research team consisting research teams under Professor Kim Eun Joon and Professor Kang Chang Won of the department of Biological Sciences discovered that ADHD arises from the deficiency of GIT1 protein in the brain’s neural synapses.
ADHD (Attention Deficit Hyperactivity Disorder) is found in around 5% of children around the world and is a disorder where the child becomes unable to concentrate, show over the top responses, and display impulsive behavior.
The research team found that the difference between children with ADHD and those without it is one base in the GIT1 gene. The difference of a single base causes the underproduction of this protein, and those children with low levels of the protein had a higher probability to develop ADHD.
In addition, further evidence was provided when the research team conducted mice experiments. Those mice with low levels of GIT1 exhibited impulsive and exaggerated reactions like humans with ADHD, had learning disabilities, and produced abnormal brain waves. And upon injecting these mice with cure for ADHD, the symptoms of ADHD disappeared.
The impulsive behavior of ADHD children disappears as the child enters adulthood and a similar pattern was found in mice. A mice with low levels of GIT1 showed impulsive behaviors when 2 months old, but these behaviors disappeared as it got older to around 7 months old (equivalent to 20~30 years old for humans).
Professor Kim Eun Joon commented that there has to be equilibrium between mechanisms that excite the neurons and mechanisms that calm the neurons, but the lack of GIT1 leads to the decrease in the mechanisms that calm the neurons which causes the impulsive behavior of ADHD patients.
In addition, Professor Kang Chang Won commented that the results of the experiment has been receiving rave reviews and is being seen as the new method in the production of the cure for ADHD.
The result of the experiment was published in the online edition of Nature Medicine magazine.
2011.04.30 View 8687 -
The Irish Times: Gene link identified in ADHD, April 18, 2011
The Irish Times wrote an article on the recent research breakthrough made by a KAIST research team to identify a gene that triggers the syndrome of Attention Deficit Hyperactivity Disorder (ADHD) among children. Given the heightened attention to the syndrome across the world, the research result has received a great deal of attention not only from the academia but also from the media and public.
For the article, please visit http://www.irishtimes.com/newspaper/ireland/2011/0418/1224294910305.html. The research paper was appeared online April 17, 2011 in Nature Medicine, which will be printed in its May 2011 issue. For the paper, please click the link of http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2330.html.
2011.04.18 View 8282