The results of a recent study on the causes of autism may have opened a path to a possible treatment for the disease.
This line of research began a decade ago when a group of scientists from the California Institute of Technology (Caltech) in Pasadena, conducted a pioneering study on the relationship between certain irregularities in the immune system and neurodevelopmental disorders such as autism. Since then, the postmortem analysis of brains, and studies of people living with autism and several epidemiological studies has supported the link between certain immune system disorders and autism spectrum disorders.
However, what has remained unanswered is whether the immune changes are a cause in the development of autism or are simply a symptom of disorders of this assembly.
Recently, the results of a new study conducted in the Caltech suggest that specific changes in a hyperactive immune system itself can contribute to promoting behaviors in mice as typical human autism, and in some cases this may be related to activation which undergoes a fetus in the womb.
“We had long suspected that the immune system is involved in the development of autism spectrum disorders,” says Paul Patterson, of the research team and professor of biological sciences at Caltech.
The first step in the study was to establish a mouse model that it relates behaviors typical of autism with immune changes. Several large epidemiological studies, including one that includes a medical history tracking of every person born in Denmark between 1980 and 2005, have shown a correlation between viral infection during the first trimester of pregnancy and an increased risk of autism spectrum disorders in the child.
Patterson’s team, Elaine Hsiao and Sarkis Mazmanian found that the children of the affected mice exhibit major behavioral symptoms associated with classic autism spectrum disorders (roughly, repetitive or stereotyped behaviors, decreased social interaction, and problems communication). In mice, this result in compulsive behaviors such as burying marbles placed in their cage, self grooming excessive, the preference to spend time alone or with a toy rather than interacting with a new mouse, or a less frequent ultrasonic vocalization or alterations in comparison with what is typical in normal mice.
Next, the researchers characterized the immune system of the children of mothers who had been infected, and found that they show various changes in their immune system. Some of these changes, the same as those seen in individuals with autism include decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Another important finding of the study, as outlined Hsiao, is that these anomalies were present in both the young and the young adult mothers with said viral infection, indicating that a prenatal problem of this nature can have long-term health and development of children.
Once the mouse model, the group was able to test whether the immune problems of children exercised promote behavioral effects associated with autism. In the most revealing test of this hypothesis, the researchers were able to correct many of the autistic-like behavior, making the children affected bone marrow transplantation from typical mice. Normal stem cells in the bone marrow transplant not only immune deficiencies settle on of recipient animals, but changed their autistic-like behaviors.
Researchers clarify that, given that the work was done in mice, it is unwise to extrapolate the results to human autism, and therefore cannot actually consider that a bone marrow transplant is a suitable treatment for autism. Moreover, still has to check if it was the mother cell aggregation or bone marrow transplantation in corrected himself what autistic behavior in mice.
However, Patterson believes the results suggest that immune irregularities detected in children may be an important target on which to act in order to achieve significantly mitigate the major behaviors associated with autism spectrum disorders. Correcting these immune problems, it may be possible to solve, if only partially, some developmental delays typically seen in autism.