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Taiwan research sheds new light on autism treatment

February 05, 2014
Academia Sinica researchers are finding new ways to contribute to the design and development of new drugs to treat autism. (Courtesy of Academia Sinica)

Taipei City-based Academia Sinica researchers recently identified an autism causative gene, T-box brain 1 (TBR1), which might offer new insight into the treatment of autism spectrum disorders.

Led by Hsueh Yi-ping, a research fellow at Academia Sinica’s Institute of Molecular Biology, the team discovered that autism spectrum disorders are caused by abnormal neural development.

Hundreds of mutations have been identified in autistic patients, but it is unclear whether the mutations cause the disorder. In previous studies, TBR1 has been suggested as a hot target for autism. Yet, it is unclear how mutations in TBR1 gene may cause autism, according to Academia Sinica.

Hsueh’s group demonstrated that loss of a copy of TBR1 gene results in the disappearance of the posterior part of anterior commissure, a white matter structure in the brain that links the two amygdalae in the two hemispheres.

The team also found that TBR1 heterozygous mice are characterized by autism-like behaviors, such as reduced social interaction, reduced communication ability, cognitive inflexibility and impaired associated memory. These behavioral defects can be ameliorated by treatment with D-cycloserine.

This study emphasizes the significance of the amygdala in autism and suggests that D-cycloserine might be useful for autism therapies.

Academia Sinica said the findings will help in the design and development of new drugs to treat the disorder in human patients, since it is found by the team that injecting D-cycloserine in the brains or abdomens of the TBR1 mutant mice can significantly improve the social, communication, learning and memory abilities of the mice.

The team’s findings were published last month in top U.S.-based scientific journal Nature Neuroscience. (DF-JSM)

Write to Taiwan Today at ttonline@mofa.gov.tw

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