According to recent research, genes are not only the cause of autism in children but there are others too, like zinc deficiency. Though it is a controversial topic and is not understood, scientists have now connected a detailed link between the two.
The research shows that how zinc deficiency can alter connections known as synapses between dendrites and axons of brain cells in early development through complex molecular machinery which have genes that may cause autism.
The findings of the research paper “Shank and Zinc Mediate an AMPA Receptor Subunit Switch in Developing Neurons” are published in Frontiers in Molecular Neuroscience. The study does not say that zinc helps one to prevent autism but gives a push to our thinking about the treatment for these underlying developmental abnormalities.
How is zinc linked to autism related genes?
Dr. Sally Kim, a lead study author of Stanford University School of Medicine, says, “Autism is associated with specific variants of genes involved in the formation, maturation, and stabilization of synapses during early development.”
“Our findings link zinc levels in neurons—via interactions with the proteins encoded by these genes—to the development of autism.”
The team found out that whenever a signal is passed through a synapse, shank2 and shank3 proteins bind themselves to the targeted neuron. Some receptors are found on the surface of the neuron known as AMPAR’s located at the synapse. Shank2 and shank3 proteins not only changes the composition of AMPAR’s but makes the mature changing their function too.
Understanding the mechanism
The research paper talks about a series of experiments in which the researchers studied the mechanism of change in the functioning of the zinc-Shank-mediated AMPAR found in developing synapses.
Dr. Huong Ha, senior author, and a Stanford graduate student says, “In developing rat neurons, we found that Shank 2 and 3 accumulate at synapses in parallel with a switch to mature AMPARs. Adding extra zinc accelerated the switch—but not when we reduced the accumulation of Shank 2 or 3.”
“Furthermore, our study shows mechanistically how Shank2 and 3 work in concert with zinc to regulate AMPAR maturation, a key developmental step.”
In a nutshell, zinc helps in the proper development of developing synapses with the help of Shank proteins. Professor John Huguenard of Stanford University School of Medicine and a co-lead author explains that “This suggests that a lack of zinc during early development might contribute to autism through impaired synaptic maturation and neuronal circuit formation.”
“Understanding the interaction between zinc and Shank proteins could, therefore, lead to diagnostic, treatment and prevention strategies for autism.”
Can a parent protect their child from autism via zinc supplements?
“Currently, there are no controlled studies of autism risk with zinc supplementation in pregnant women or babies, so the jury is still out. We really can’t make any conclusions or recommendations for zinc supplementation at this point, but experimental work on autism models is also published in this Frontiers Research Topic holds promise,” said Craig Garner who is a co-lead author and professor of the German Centre for Neurodegenerative Diseases.
One should keep in his mind that, excess intake of zinc reduces the absorption of copper in the body which eventually increases the risk of anemia and softening of bones. It is not necessary that zinc deficiency in the body is only linked to inadequate intake of zinc but it can also be due to poor absorption in the gut.
Garner concludes, “Nevertheless, our findings offer a novel mechanism for understanding how zinc deficiency—or disrupted handling of zinc in neurons—might contribute to autism.”