Brain’s sensory processor may prompt memory problems in autism

Silencing several autism- or schizophrenia-linked genes in the thalami of mice increases neuronal excitability there and leads to memory problems reminiscent of those seen in people with these conditions, a new study shows. A drug that reverses the hyperexcitability boosts the animals’ recall, suggesting an avenue for future therapies, researchers say.

“It’s exciting to see how different genetic changes can converge onto the same circuits in the brain, and even onto the same physiological mechanism,” says Audrey Brumback, assistant professor of neurology and pediatrics at the University of Texas at Austin, who was not involved in the research. “We’re really then getting toward the final common pathway that could be a target for treatment.”

Mice lacking the high-confidence autism-linked gene PTCHD1 in the thalamic reticular nucleus, a subregion of the thalamus, are hyperactive and have attention deficits, according to a 2015 study. In the new work, the same team eliminated PTCHD1 expression and the expression of four other genes linked to either autism or schizophrenia in a different subregion, the anterodorsal thalamus.

In all five models, the engineered mice performed poorly on tests of long-term and working memory. These memory problems could contribute to learning difficulties in people with autism or schizophrenia, the researchers say. In three of the five models, the memory problems seemed to be due to increased excitability of thalamic neurons.

“It is now very clear that for every phenotype or symptom that you have, there’s a particular circuit responsible,” says lead investigator Guoping Feng, Poitras Professor of Neuroscience at the Massachusetts Institute of Technology in Cambridge. The work was published in June in Neuron.



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