n the many hypotheses surrounding autism, one posits it is the consequence of abnormal cell communication Science.com reports.

Researchers at the U.C. San Diego recently did a study using a drug from 1916, suramin, which was approved for treating sleeping sickness. The findings inTranslational Psychiatry were that it restored normal cellular signaling in a mouse model of autism, reversing symptoms of the neurological disorder in animals that were the human biological age equivalent of 30 years old. Robert K. Naviaux, MD, PhD, said one of the universal symptoms of autism is metabolic disturbances.

"Cells have a halo of metabolites (small molecules involved in metabolism, the set of chemical processes that maintain life) and nucleotides surrounding them. These create a sort of chemical glow that broadcasts the state of health of the cell." Cells threatened or damaged by microbes, such as viruses or bacteria, or by physical forces or by chemicals, such as pollutants, react defensively, a part of the normal immune response, Naviaux said. Their membranes stiffen. Internal metabolic processes are altered, most notably mitochondria – the cells' critical "power plants. Naviaux and colleagues have focused on a cellular signaling system linked to both mitochondrial function and to the cell's innate immune function. Specifically, they have zeroed in on the role of nucleotides like adenosine triphosphate (ATP) and other signaling mitokines – molecules generated by distressed mitochondria. These mitokines have separate metabolic functions outside of the cell where they bind to and regulate receptors present on every cell of the body.

Nineteen types of so-called purinergic receptors are known to be stimulated by these extracellular nucleotides, and the receptors are known to control a broad range of biological characteristics with relevance to autism, such as impaired language and social skills. In their latest work, Naviaux again tested the effect of suramin, a well-known inhibitor of purinergic signaling that was first synthesized in 1916 and is used to treat trypanosomiasis or African sleeping sickness, a parasitic disease. They found that suramin blocked the extracellular signaling pathway used by ATP and other mitokines in a mouse model of autism spectrum disorder (ASD), ending the cell danger response and related inflammation. Cells subsequently began behaving normally and autism-like behaviors and metabolism in the mice were corrected. However, the biological and behavioral benefits of suramin were not permanent, nor preventive. A single dose remained effective in the mice for about five weeks, and then washed out. Moreover, suramin cannot be taken long-term since it can result in anemia and adrenal gland dysfunction.

"Our work doesn't contradict what others have discovered or done. It's another perspective. Our idea is that this kind of treatment – eliminating a basic, underlying metabolic dysfunction – removes a hurdle that might make other non-drug behavioral and developmental therapies of autism more effective. The discovery that a single dose of medicine can fundamentally reset metabolism for weeks means that newer and safer drugs might not need to be given chronically. Members of this new class of medicines might need to be given only intermittently during sensitive developmental windows to unblock metabolism and permit improved development in response to many kinds of behavioral and occupational therapies, and to natural play."