« The Correlation between Traditional Reading Time and Scholarly Success in Youth | Main | First 3D molecular model of the presynaptic terminal »

Autism - A metabolic Disorder?

This summer I am working on a project evaluating a possible connection between Autism Spectrum Disorder (ASD) and neuroinflammation. However, while we work on our project, it is always a good idea to keep an eye out for what others in the field are investigating. It was with this in mind that I sat down to read a new paper by Naviaux et al. that was published in this week's edition of Nature. In the paper Dr. Robert Naviaux and his collaborators set out to test the use of Suramin as a potential drug for relieving autistic symptoms in an animal model, and met some promising results.

The basis of the research that the Naviaux lab performed is that while there is a mixture of factors that can lead to the development of ASD, there is a hypothesized underlying cause of all cases. Specifically Naviaux and his colleagues believe that ASD and other developmental disorders can be acquired when a metabolic response called the cell danger response (CDR) is triggered. However, because this believed foundation of all cases of Autism Spectrum Disorder is metabolic, it should be treatable using the proper metabolic intervention.

To test out their theory, the researchers in the Naviaux lab used the maternal immune activation (MIA) or Poly IC mouse model. In this model a pregnant female mouse is injected with a double stranded segment of polyinosinic:polycytidylic (poly I:C) acid. This injection is used to simulate a viral infection and triggers an immune response which results in the injected mouse's progeny having characteristics associated with ASD and schizophrenia.

When the offspring of the mice were 6.5 months old they gave the mice an injection of either saline, as a control, or Suramin, a drug used as an antipurinergic therapy. They found that while the MIA mice showed ASD-like characteristics pre-injection, the mice injected with a single dose of Suramin had improved social interactions at the same level as mice not from the MIA model. An improvement was even seen five weeks after the Suramin injection, when all of the chemical had washed out of the mice, indicating that the injection of Suramin developed some form of metabolic memory or change that outlasted the drug itself.  

While these results were incredibly promising, there are some limitations of applying the findings of this study to humans. The MIA mouse model is not a perfect model for ASD in humans as it may have a different underlying mechanisms than ASD. Also, chronic use of suramin is associated with toxic side effects making it less likely to be a drug used in human treatment anytime soon.

Regardless of limitations, these results are really exciting for a couple different reasons. First, a single dose of an antipurinergic therapy is capable of reversing the characteristics in the MIA model, meaning that we could possibly find the same results in humans. Also, not only did the drug reverse the characteristics, but the changes incurred by treatment had a lasting effect. It may be naive to hope that we can one day cure autism with a miracle shot, but hopefully we will soon be hearing about the discovery of a drug that has similar effects in humans as the Suramin in MIA .

To read more about the study check out the original paper: “Reversal of autism-like behaviors and metabolism in adult mice with single-dose antipurinergic therapy,” as written by JC Naviaux, MA Schuchbauer, K Li, L Wang, VB Risbrough, SB Powell and RK Naviaux at


~Jack Kent, Summer Research Intern




Reader Comments

There are no comments for this journal entry. To create a new comment, use the form below.

PostPost a New Comment

Enter your information below to add a new comment.

My response is on my own website »
Author Email (optional):
Author URL (optional):
Some HTML allowed: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <code> <em> <i> <strike> <strong>