Scientists reverse autism-like condition in laboratory mice

Researchers successfully reverse experimentally induced autism spectrum disorders-like symptoms in mice, even in adult mice, and shed new light on a possible underlying mechanism for why the condition occurs.

by John Tyburski

Copyright © Daily Digest News, KPR Media, LLC. All rights reserved.

First published at Daily Digest News on June 18, 2014

Approximately one to two percent of children born in the U.S. are diagnosed with autism spectrum disorders (ASDs), a collection of conditions involving a number of physical, cognitive, and social impairments. Despite extensive study, the causes of ASDs are not fully understood, and no known cures exist. Recent research published Tuesday in the journal Translational Psychiatry indicates that ASDs may be reversible or at least possibly managed better.

A team of researchers at the University of California, San Diego (UCSD), led by Dr. Robert Naviaux, professor of medicine and co-director of the Mitochondrial and Metabolic Disease Center at UCSD, set out to test whether treating the underlying metabolic disorders that accompany ASDs produces improvement in ASDs symptoms. Past work in children with ASDs has shown temporary improvements in most following high fever. Although the symptoms returned as the fevers subsided, the observations suggested that ASD impairments are reversible.

The UCSD researchers induced mice to be born with ASD-like symptoms by exposing pregnant females to simulated viral infections. The mouse pups are born with ASD-like symptoms that are thought to be the result of activation of cell danger response (CDR), a metabolic response to threat (such as simulated viral infection during gestation).

Then the researchers inhibited the CDR response with a drug called suramin, a drug that attacks purine pathways and has been around for treating African sleeping sickness for nearly 100 years. The result of blocking CDR function with suramin was a restoration of normal behavior in the mice with ASD-like symptoms.

“Cells behave like countries at war,” said Naviaux. “When a threat begins, they harden their borders. They don’t trust their neighbors. But without constant communication with the outside, cells begin to function differently.”

“In the case of neurons, it might be by making fewer or too many connections,” continued Naviaux. “One way to look at this related to autism is this: when cells stop talking to each other, children stop talking.”

The researchers stressed caution in interpreting these results with mice in the context of human applications. Regardless, a small phase one trial to assess suramin in treating children with ASDs is planned for this year.