An Academia Sinica study linking low zinc concentrations often detected in autistic people to genetic defects in two proteins suggests that autism-like behavior could be greatly ameliorated by boosting the transmission of zinc to the brain with the help of an antibiotic.
Academia Sinica research fellow and project leader Hsueh Yi-ping (薛一蘋) said her team obtained the results after performing an experiment on mice, which she said are sociable animals and therefore perfect test subjects.
Scientists compared the interactions of test mice by placing the subjects in a box, mice that had been unchanged, mice with their Tbr1 and Shank2 proteins “knocked off” and another “stranger” mouse.
They found that unchanged mice engaged in high-level interaction with the “stranger” mouse, while mice with Tbr1 and Shank2 deficiencies interacted very little.
Hsueh’s team had previously determined that Tbr1 is a contributing factor of autism, while a team led by South Korean scientist and project coleader Eunjoon Kim discovered that Shank2 is also implicated in the condition.
Both deficiencies hamper the transmission of zinc ions to the NMDAR (N-methyl-D-aspartate) receptor, impairing function.
About 30 percent of children with autism suffer from zinc deficiency.
The researchers used clioquinol, an antibiotic used to increase zinc absorption, on the mice displaying autistic behavior and found that they began behaving in a way almost identical to that of the unchanged mice as both the level of activity and interaction with the “stranger” mouse increased, Hsueh said.
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http://epiphanyasd.blogspot.ca/2015/06/ ... k-ca2.html