Cellular changes in the brain caused by genetic mutations that occur in autism can be reversed by zinc, according to research at the University of Auckland. International studies have found that normally there are high levels of zinc in the brain, and brain cells are regulated by zinc, but that zinc deficiency is prevalent in autistic children. Research using animal models has shown that when a mother is given a low zinc diet, the offspring will be more likely to display autistic associated behaviours.
Research has focussed on the protein Shank3, which is localized at synapses in the brain and is associated with neuro-developmental disorders such as autism and schizophrenia. Human patients with genetic changes in Shank3 show profound communication and behavioural deficits. In this study, we show that Shank3 is a key component of a zinc-sensitive signalling system that regulates how brain cells communicate. Intriguingly, autism-associated changes in the Shank3 gene impair brain cell communication. These genetic changes in Shank3 do not alter its ability to respond to zinc. As a result, we have shown that zinc can increase brain cell communication that was previously weakened by autism-associated changes in Shank3.
Disruption of how zinc is regulated in the body may not only impair how synapses work in the brain, but may lead to cognitive and behavioural abnormalities seen in patients with psychiatric disorders. Together with our results, the data suggests that environmental/dietary factors such as changes in zinc levels could alter this protein’s signalling system and reduce its ability to regulate the nerve cell function in the brain.
A new study published in the online journal, Public Library of Science One (PLOS One) found that Vitamin B12 levels in the brain are significantly decreased in the elderly and are much lower in individuals with autism or schizophrenia, as compared to their peers at similar ages. For example, children with autism under the age of 10 were found to have three times lower brain B12 levels, which is similar to levels for generally healthy adults in their 50s, indicating a premature decrease.
These are particularly significant findings because the differences we found in brain B12 with aging, autism and schizophrenia are not seen in the blood, which is where B12 levels are usually measured. The large deficits of brain B12 from individuals with autism and schizophrenia could help explain why patients suffering from these disorders experience neurological and neuropsychiatric symptoms.