Diet and drug alleviate symptoms in autism rat models

Two studies in autism rat models suggest that a high-fat, low-carbohydrate diet and an unapproved drug for dementia may improve some symptoms of the disorder, according to unpublished results presented Sunday at the 2013 Society for Neuroscience annual meeting in San Diego.

By Laura Geggel
12 November 2013 | 3 min read

This article is more than five years old.

Neuroscience—and science in general—is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.

Two studies in autism rat models suggest that a high-fat, low-carbohydrate diet and an unapproved drug for dementia may improve some symptoms of the disorder, according to unpublished results presented Sunday at the 2013 Society for Neuroscience annual meeting in San Diego.

In both studies, the researchers made rat models of autism using valproic acid (VPA), an epilepsy drug. Exposure to VPA in utero is linked to an increased risk of autism

In the diet study, the researchers fed VPA-exposed rats a ketogenic diet, which contains high levels of fat and low levels of carbohydrate. A study published earlier this year found that mice belonging to the asocial BTBR strain are more sociable after eating ketogenic food, which forces the body to run on fat, rather than on sugar.  The diet has also been shown to alleviate epileptic seizures1.

In this study, the researchers fed VPA-exposed rats and saline-exposed controls either a ketogenic diet or a regular diet for 10 to 14 days after weaning. They found that the VPA-exposed rats fed a ketogenic diet showed a 20 percent increase in their weight over this time. In contrast, the VPA-exposed rats fed a normal diet doubled their weight.

By 33 to 38 days of life, the VPA-exposed rats fed a ketogenic diet were more playful, attacking each other more than those that ate regular food, the researchers found. “When they start to play, they usually do the nape or back attack,” says Younghee Ahn, research associate of neuroscience in Jong Rho’s lab at Alberta Children’s Hospital, who presented the work.

However, both groups of rats responded similarly to a recurring loud sound, suggesting that the diet does not improve the rats’ difficulty with filtering out repeated stimuli.

Another study presented at the conference looked at Cerebrolysin, an unapproved medication that is being considered as a treatment for dementia2. VPA-exposed rats received Cerebrolysin from days 5 to 21 of their life.

VPA-exposed pups typically show a small delay in when they first open their eyes. Cerebrolysin abolishes this delay. The drug also corrects the rats’ crooked tails. What’s more, these mice approach other rats more often and spend more time interacting with them than do rats that do not get the drug.

However, Cerebrolysin does not alleviate the hyperactivity seen in VPA-exposed rats, or their inability to habituate to their environment. 

More work is needed to learn to parse these effects of the drug, says Maria Elena Bringas-Tobón, a graduate student of behavioral neuroscience in Gonzalo Flores’ lab at Instituto de Fisiología in Puebla, Mexico, who presented the study.

For more reports from the 2013 Society for Neuroscience annual meeting, please click here.

References:

1: Neal E.G. et al. Lancet Neurol. 7, 500-506 (2008) PubMed

2: Chen N. et. al. Cochrane Database Syst. Rev. 1 (2013) PubMed

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