Mice fed faeces from human children with autism developed signs of having the disorder, scientists claim. Rodents given the faecal transplants were less likely to socialise and more likely to develop repetitive behaviour.
Researchers were adamant their research didn’t prove bacteria in the gut caused autism spectrum disorder (ASD).
However, they believe the findings could lead to new treatments for the disorder, such as probiotic drugs.
The study adds further weight to existing suggestions that gut bacteria may play a role in causing the spectrum disorder.
‘This opens the possibility that ASD… may be treated by therapies that target the gut rather than the brain,’ said lead researcher, Dr Sarkis Mazmanian.
Dr Mazmanian, from the California Institute of Technology (Caltech), suggested it could even help other ‘classical neurologic conditions’.
The researchers implanted the stool of children with autism into the stomachs of mice in a laboratory to investigate the gut bacteria theory.
While the gut bacteria – known as the microbiome – triggered autistic symptoms if it came from an autistic child, it had no effect when it came from a healthy child.
‘There are many factors that make autism more complicated in humans than in mice,’ Dr Mazmanian said.
‘In mice, we can model the symptoms of the disorder but not reproduce it.
‘However, this research provides clues into the role that the gut microbiota plays in neural changes that are associated with ASD.
‘It suggests that ASD symptoms may one day be remedied with bacterial metabolites or a probiotic drug.’
- •Mice harboring human autism spectrum disorder, but not typically developing, microbiomes exhibit ASD-like behaviors
- •autism spectrum disorder and typically developing microbiota produce differential metabolome profiles in mice
- •Extensive alternative splicing of risk genes in brains of mice with autism spectrum disorder microbiota
- •BTBR mice treated with 5AV or taurine improved repetitive and social behaviors
READ THE FULL STUDY PUBLISHED IN THE JOURNAL CELL HERE: