Researchers studying immune cells called granulocytes found evidence of weakened cell function in a small study of ten children with autism. In these children, the immune cells were less able to deliver the normal “oxidative burst” of chemicals designed to destroy invading germs. The cells also had signs of stress and dysfunction in the tiny cell powerhouses known as mitochondria.
Drawing a link between autism, mitochondria and immune function, the researchers say their findings suggest a new direction for developing treatments.
The study, from the University of California-Davis, appears today in the journal Pediatrics. It follows up on the team’s earlier research on autism and mitochondrial dysfunction. Both reports involved participants enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The researchers also draw a connection between their new findings and earlier CHARGE studies linking inflammation during pregnancy with increased risk of autism and immune problems in offspring.
Mitochondria and autism
All human cells depend on small but complex structures called mitochondria for the majority of their energy. Mitochondria are especially important for powering energy-demanding cells such as neurons (brain nerve cells).
Certain rare mitochondrial disorders are known to produce behavioral issues and symptoms of autism in some but not all of those affected. Some studies have suggested that milder mitochondrial dysfunction can likewise contribute to the development of autism spectrum disorder (ASD). Still other research indicates that infection and inflammation can worsen mitochondrial disorders.
New biochemical evidence
In their new study, the UC-Davis investigators measured the infection-fighting “oxidative bursts” produced by granulocyte cells. On average, the bursts were three-times lower in the granulocytes of the ten children with autism than in typically developing children.
They also measured free radicals – a sign of stress and dysfunction – inside the mitochondria of these immune cells. On average, the reactive oxygen levels were 1.6 times higher in the mitochondria of the children who had autism than in typically developing children.
In related news, a new study in JAMA Pediatrics tracked another sign of mitochondrial stress and dysfunction – elevated lactate levels – in the brains of individuals with autism. Noninvasive brain imaging showed elevated brain-lactate levels in 13 percent of 75 children and adults with autism compared to just 1 percent of 96 individuals without ASD. The researchers conclude that mitochondrial dysfunction may play a role in producing autism in a subset of individuals with the disorder.