Taiwan: Two
research teams have discovered that increases in zinc reduce
social defects in two mouse models of autism. The research was published
in Nature Communications on May 18, 2015. Drs. Kim’s and Hsueh’s laboratories demonstrated that administration of
the clinical drug clioquinol increases zinc in a certain part of mouse
brains resulting in the noticeable improvement of social defects in the
two types of mice. Using established autism mouse models (Shank2-/- and
Tbr1+/- mice), members of the two laboratories demonstrated that
mobilization of zinc from presynaptic termini to the postsynaptic sites
of neurons induced by clioquinol enhances postsynaptic protein kinase
activity and thus rescues the activation of NMDAR, one of the major
excitatory ion channels in the central nervous system. This finding
explains the role of zinc in neuronal activation and provides a
potential therapy for autism spectrum disorders (ASDs).
ASDs are one of most common neurodevelopmental disorders. Both genetic
and environmental factors are involved in the etiology of ASDs. Zinc
deficiency is frequently associated with ASDs, but the mechanism
underlying the role of zinc deficiency in ASDs is unclear. According to
research published in the journal Scientific Reports in 2011, an
examination of the hair of 1,967 children with autistic disorders (1,553
males and 414 females) showed that almost 30% had low zinc
concentrations. In this work, Dr. Kim’s lab carried out the Shank2 study and Dr. Hsueh’s lab analyzed the effect of Cq on Tbr1 mutant mice, which was conducted by Dr. Tzyy-Nan Huang. The study of Tbr1 mutant mice was supported by the Frontier Research Grant of the Ministry of Science and Technology to Dr. Hsueh. Dr. Huang is supported by the Postdoctoral Fellowship of Academia Sinica.
The full article entitled “Trans-synaptic
Zinc mobilization improves social interaction in two mouse models of
autism through NMDAR activation” is available at Nature Communications
website at: http://www.nature.com/ncomms/2015/150518/ncomms8168/full/ncomms8168.html