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The Evolution of Suramin for Autism

The wonders of modern medicine have led to a greater understanding of how our bodies function from the cellular level and how these manifest in the physical. In turn, this has lead to the evolution of suramin for autism as well as other drugs for neurological conditions.

The Evolution of Suramin for Autism

Several drugs have been developed over recent years and, through them, medicinal chemistry has improved. One treatment that has remained in circulation for many decades is suramin. It has been in existence since around 1922 and was initially developed to treat African sleeping sickness, but later its mechanism was found to be effective in the treatment of several other conditions—including autism spectrum disorder (ASD). 

To understand the mechanism behind suramin and why scientists believe it could be a potential treatment for autism, we need to break down the biological science behind it. But first, let’s explore what suramin is. 

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What is suramin?

Suramin is a drug that was initially designed to treat African sleeping sickness aka human African trypanosomiasis (HAT) — a disease caused by infection with the parasite Trypanosoma brucei from the tsetse fly. The tsetse parasitic fly is only found in Sub-Saharan Africa and symptoms of infection by the tsetse fly include sleeping disorder, among several others—hence its name.

Suramin was developed around 1922 when HAT was a prominent disease. In treating African sleeping sickness, suramin is only administered during the first stage of infection when the parasitic infection has not reached the central nervous system (because suramin cannot cross the blood-brain barrier). 

Suramin has been used to treat various conditions such as viral diseases, parasitic diseases, cancer, snakebite, and up until recently researchers have been studying whether suramin can be used to treat autism symptoms. 

Let’s take a look at the biological science behind suramin and its link to autism, but first we need to look at some more general definitions.

Some definitions

I’d like to take a quick look at some definitions before breaking down the biological science behind autism and suramin, as I understand some terms may be foreign to readers.  

Nucleotide

  • A nucleotide is the basic building block of nucleic acids

The purinergic signaling pathway

  • Comes from the word “purine” 
  • The purinergic system consists of purine nucleotides such as ATP among others
  • The pathway is a process that occurs outside the cell (extracellular) mediated by purine molecules i.e. ATP and other molecules 
  • It activates purinergic receptors in the cell or neighboring cells

ATP

  • If you’re now wondering what ATP is, it’s an abbreviation for adenosine triphosphate
  • It is a high energy molecule that plays a role within the cell (intracellular) and outside the cell 
  • There are extracellular enzymes outside the cell that help to regulate the amount of ATP available for signaling as well as support ATP’s extracellular actions 

The biological science behind suramin

The mitochondria is the “powerhouse of the cell” and this organelle regulates the cell danger response, aka CDR, thanks to its ability to monitor and respond to the physical, chemical and microbial conditions within and around the cell. 

The cell danger response (CDR) is a metabolic response that protects cells and the host from environmental threat, injury or harm. It is so impactful that, although it occurs at the cellular level, it can also impact areas such as “human thought and behavior, child development, physical fitness and resilience, fertility, and the susceptibility to disease”.

Different types of threats can cause a variety of problems, some of which people believe might contribute to the development of conditions such as autism. 


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Why is that? It boils down to the belief of some that, other than genetic influences, ASD is possibly caused by metabolic dysfunction or impaired communication between the cells in the brain or the immune system. It is possible that these incidences are caused by abnormal CDR regulation.

When a threat is spotted, the CDR protects the cell by hardening its membrane and prevents interaction with anything in its surrounding until the threat subsides. If this process is not regulated properly, and the CDR fails to perform, this can permanently impact how the cell responds in its environment—and can lead to chronic diseases. When this happens during child development, some researchers believe it could cause autism and other childhood disorders.  

Where does suramin fit?

If CDR behaves abnormally, the cell is in constant “fight mode” therefore, it continues to act as though it is in danger—even when the threat has subsided. During this process, the purinergic signaling pathway is activated, and a purinergic nucleotide called ATP, produced by cellular mitochondria is released continuously. In this instance, ATP acts as a siren or danger signal.

Suramin is then used to stop the binding of extracellular (outside the cell) ATP as well as other molecules to purinergic receptors. By doing this, it stops the “siren” and tells the cell that the danger is over and returns to normal functioning. 

Suramin is not yet approved as a treatment option but it could potentially improve neurodevelopment, growth and healing. 

Clinical trial evidence of suramin and autism

Naviaux, et al. (2017) conducted a trial that studied the impact of a single dose of suramin in children with autism and compared their result to a group of children who received the placebo drug (Saline). 

In this trial, 10 male children with ASD were grouped into five pairs, ages 5–14 years. Randomly, suramin and saline (in the placebo group) was administered intravenously (inside the vein) at a low dosage.

The trial results showed that one intravenous dose of suramin improved the score of language, social interaction, and reduced reactive or repetitive behaviors. The five children who received the placebo did not demonstrate these results.

Side effects of suramin

Due to the high dosage of suramin administered for the treatment of African sleeping disorder, some of the side effects include diarrhea and nausea. Whereas this study found that, at a low dosage, the children who were administered the suramin infusion did not observe any side effects besides a mild passing skin rash.

Conclusion

Suramin is a decades-old drug. It’s a marvel that this drug is still viable to today, so much so that scientists have looked into whether it can be used to treat other conditions, including autism. 

It is crucial to highlight that suramin is not an approved treatment for symptoms of autism; its efficacy in treating ASD relies on the biological function of the drug in relation to the cellular processes observed in individuals on the autism spectrum. More research needs to be conducted at a larger scale.

We should also note that safe administration of suramin requires accurate dosage, monitoring of toxicity and a trained professional. Parents are advised to consult with their medical doctors before considering any kind of medical treatments for their autistic little ones.

References

Naviaux R. K. (2014). Metabolic features of the cell danger response. Mitochondrion, 16, 7–17. https://doi.org/10.1016/j.mito.2013.08.006 

Naviaux R. K. (2020). Perspective: Cell danger response Biology-The new science that connects environmental health with mitochondria and the rising tide of chronic illness. Mitochondrion, 51, 40–45. https://doi.org/10.1016/j.mito.2019.12.005 

Naviaux, R. K., Curtis, B., Li, K., Naviaux, J. C., Bright, A. T., Reiner, G. E., Westerfield, M., Goh, S., Alaynick, W. A., Wang, L., Capparelli, E. V., Adams, C., Sun, J., Jain, S., He, F., Arellano, D. A., Mash, L. E., Chukoskie, L., Lincoln, A., & Townsend, J. (2017). Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial. Annals of clinical and translational neurology, 4(7), 491–505. https://doi.org/10.1002/acn3.424

Wiedemar, N., Hauser, D. A., & Mäser, P. (2020). 100 Years of Suramin. Antimicrobial agents and chemotherapy, 64(3), e01168-19. https://doi.org/10.1128/AAC.01168-19

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