In people with autism, neural communications are disrupted due to genetic mutations inherent in the disease. If previous studies had already shown the important role of zinc in the development of the disease, it is not the first time that a real improvement in cellular communication has been observed. A feat achieved in mice in a study relayed by The Journal of Neuroscience.
It was by studying the regulation of expression of the Shank3 gene, involved in autism and schizophrenia, that the New Zealand researchers came to this conclusion. In fact, Shank3 codes for a protein involved in synaptic plasticity, otherwise the ability of neurons to transmit messages. However, by binding to SHANK3, zinc regulates its expression. Better, the researchers were able to show that genes directly involved in TED are very sensitive to zinc.
“Autism is associated with genetic changes that lead to behavioral changes,” says Johanna Montgomery, associate professor in the Department of Physiology at the University of Auckland and author of the study. “It starts in the cells and expresses itself at the behavioral level. We are looking for ways to reverse these cellular deficits caused by changes in brain cells associated with autism,” explains Johanna Montgomery.
However, the conclusions of this study reveal that zinc seems to reverse this process by facilitating neuronal exchanges at the level of the Shank3 gene.
Diet and environmental factors such as zinc consumption could alter the signaling system of this protein and reduce its ability to regulate nerve cell function in the brain.
The next step of this study is to analyze the impact of dietary zinc supplements on autistic people.
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