Scientists discover that a gene for autism is present in the brain of a monkey

New research has found that a key component of the brain’s ability to recognize social cues has been inherited from the mother.

A study published in The Lancet Diabetes & Endocrinology showed that the gene for a gene called MT1, which is part of a group of genes that encode the protein kinase B, was found in the brains of a number of laboratory monkeys, including a baby that was born with a brain disorder called dystonic autism.

The gene was found to be absent in a mouse model of the disorder, suggesting it may play a role in its development.

The study was led by Dr. Michael Schuster of the Max Planck Institute for Evolutionary Anthropology in Germany.

In the mouse model, the gene was identified in a part of the central nervous system known as the amygdala, the region of the human brain that is the site of a range of social and emotional responses.

Dr. Schuster said the findings were “important because the amygdala is responsible for controlling social interactions in the mouse.”

In the human animal model, however, the researchers found the gene in a region of brain called the prefrontal cortex, a region thought to be involved in regulating social cognition and social behavior.

In humans, the amygdala also plays a role as a neural reward center.

“The amygdala is a complex system that integrates multiple systems, and it appears to be important for social cognition, social interaction, emotion regulation and social communication,” said Dr. John P. Voss, a neuroscientist at the University of California, San Diego, and lead author of the study.

Dr Voss and his colleagues began their research with a series of experiments to identify the brain structure and function of dystonics, a genetic disorder that affects approximately one in every three people in the United States.

In one experiment, they placed dystonically-affected babies in a maze and watched them navigate it by pointing their fingers and making eye contact.

The babies did not show any behavioral differences from normal controls, but when they reached a different part of their maze, they began to react differently to the maze.

“These findings suggest that dystonia might be a kind of behavioral phenotype, and we want to investigate whether dystonians have an autism-like phenotype,” Dr. Vos said.

The researchers then looked for the same gene in the offspring of dystons and mice.

“We found that MT1 is expressed in the adult brain of dystrophy-affected mice, but not in normal mice, and in dystonice-affected individuals we found no MT1 expression in the prefrontal lobe,” Dr Vos explained.

In a second experiment, the dystonic babies were given an emotional cue and then told they could either tell the baby to stop touching her or go back to the original task.

In both cases, MT1 was absent.

“It’s important to note that in both experiments, dystones and controls did not differ in their response to this cue,” Dr Schuster explained.

“In the dystoned animals, MT2 is also absent.

This suggests that MT2 does not play a causal role in dystony behavior, but rather may be a specific form of MT1 that mediates dystonian social interaction.”

The scientists found that dystonics had an average brain size of 1.9 centimeters in the cortex and 3.5 centimeters in hippocampus, the regions involved in processing social signals.

The dyston-affected monkeys had an estimated brain size 3.6 centimeters, or 2.5 inches, in cortex and 6.4 centimeters in hippocampal volume, which suggests that the dystrophasic animals had a brain that was bigger than normal, Dr Schusters said.

“Dystonia is one of the most common neurodevelopmental disorders, affecting 1 in every 100,000 children,” Dr Kajita S. Gomes, an evolutionary anthropologist at the California Institute of Technology, said in a statement.

“A large number of studies have shown that dystic brains are larger than normal.

This study provides new evidence that the genetic background of dystic behavior in dystrottans could contribute to its development.”

In addition to Dr. Gombs, Dr. P. J. Vass and Dr Schauer, other co-authors of the paper include Dr. Rana M. K. Singh of the Massachusetts Institute of Health, Dr Lidia S. V. Salgado of the University College London, and Dr. Daniel M. Lippmann of the Institute of Molecular Genetics in Zurich, Switzerland.

The research was funded by the National Institutes of Health and the Swiss National Science Foundation.

The Times will update this story when more information becomes available.

The Associated Press contributed to this report.