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Study confirms zinc deficiencies’ link to early development of autism


Researchers have confirmed a link between zinc deficiency and the develpment of autism in a study of brain cells’ connections from rats’ hippocampal neurons

A link between zinc deficiency and the development of autism has been confirmed in a study of brain cells’ connections from rats’ hippocampal neurons.



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Although researchers said their findings don’t show how to prevent autism, they help explain developmental abnormalities and could lead to eventual treatment. The findings were published Friday in the journal Frontiers.


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“Autism is associated with specific variants of genes involved in the formation, maturation and stabilization of synapses during early development,” study senior author Dr. Sally Kim, of Stanford University School of Medicine, said in a Frontiers press release. “Our findings link zinc levels in neurons — via interactions with the proteins encoded by these genes — to the development of autism.”

Autism develops as a neurological and developmental disorder that is prevalent in 1 in 59 children, the Centers for Disease Control and Preventionfound in tracking 11 communities across the country.

The exact cause of autism is not known, but theories include heredity, genetics and medical problems, according to Autism Society. Researchers have been investigating pregnancy or delivery problems, as well as environmental factors that include viral infections, metabolic imbalances and exposure to chemicals.

Zinc deficiency has been studied.

When a signal is transferred via a connection, zinc enters the target neuron where it can bind two such proteins: Shank2 and Shank3. In turn, they cause changes in the composition and function — or “maturation” of adjacent signal receptors, called “AMPARs.”

Experiments on the mechanism of zinc-Shank-mediated AMPAR maturation in developing synapses were performed by the Stanford scientists.

“In developing rat neurons, we found that Shank 2 and 3 accumulate at synapses in parallel with a switch to mature AMPARs,” said lead author Dr. Huong Ha, a former Stanford graduate student. “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.”

Understanding the interaction between zinc and Shank proteins “could therefore lead to diagnostic, treatment and prevention strategies for autism,” said co-senior author Dr. John Huguenard, also of Stanford University School of Medicine.

No controlled studies of autism risk with zinc supplementation in pregnant women or babies have been studied.

“So the jury is still out. We really can’t make any conclusions or recommendations for zinc supplementation at this point, but experimental work in autism models … holds promise,” said co-senior author Dr. Craig Garner of the German Center for Neurodegenerative Diseases.’

A zinc deficiency does not necessarily imply a dietary deficiency and instead could result from problems with absorption in the gut, according to the researchers.

Too much zinc reduces the amount of copper the body can absorb and can lead to anemia and weakening of the bones.

“Nevertheless, our findings offer a novel mechanism for understanding how zinc deficiency — or disrupted handling of zinc in neurons — might contribute to autism,” Garner said.



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