Early-life treatment stops autism-like symptoms developing in mice

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Alexas_Fotos on pixabay
Alexas_Fotos on pixabay

Blocking an overactive protein during the first five weeks of life prevents autism-like symptoms from developing in mice, according to international researchers. The team conducted their study on mice genetically engineered to have a condition similar to Tuberous Sclerosis Complex (TSC), a neurodevelopmental disorder with high rates of autism. They administered a drug called rapamycin which inhibits the production of a protein that is overproduced in people and animals with TSC. After four weeks of treatment and four weeks without treatment, the mice displayed normal social behaviour and normal activity in their brains, resembling mice without TSC. The researchers say their results suggest administering a treatment during critical periods in development might prevent autism symptoms from ever manifesting. In humans, TSC is often diagnosed in utero, providing an opportunity to administer a preventative during this crucial time, they add.

Media release

From: Society for Neuroscience

Early Life Treatment Prevents Autism Symptoms From Developing in Mice 

Identifying the window of development could reveal ideal time to intervene in autism 

Timing is key when treating developmental disorders. Blocking an overactive protein during the first five weeks of life prevents autism symptoms from ever developing in mice, according to new research published in JNeurosci.

The brain develops capabilities, like language, during specific spans of time called critical periods. The symptoms of disorders like autism arise during a set critical period; administering a targeted intervention only during the critical period could prevent the disorder from ever taking shape without the burden of a life-long treatment.

Gibson et al. compared intervention timing in a genetic mouse model of Tuberous Sclerosis Complex (TSC), a neurodevelopmental disorder with high rates of autism spectrum disorder. The research team administered the drug rapamycin to inhibit production of mTOR, a protein that is overproduced in people and animals with TSC. After four weeks of treatment and four weeks without treatment, the mice displayed normal social behavior and normal activity in cerebellum neurons, resembling the control mice without TSC. These results indicate administering a treatment during critical periods in development could prevent autism symptoms from ever manifesting. In humans, TSC is often diagnosed in utero, providing an opportunity to administer a preventative during this crucial time.

Journal/
conference:
JNeurosci
Research:Paper
Organisation/s: University of Texas Southwestern Medical Center, USA
Funder: J.M.G. acknowledges support from National Heart, Lung, and Blood Institute (1T32HL139438- 28 01A1). P.T.T. acknowledges support from the National Institute of Neurologic Disorders and 29 Stroke of the NIH (K08 NS083733) and National Institute of Mental Health of the NIH (R01 30 MH116882).
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