Page ID: 1634

           The number of Autism Spectrum Disorders is on the rise, and the U.S. Centers for Disease Control and Prevention made an announcement in March 2014 that 1 out of every 68 children in the United States is on the Autism Spectrum. In 2002, it was 1 out of every 150 children, which is an increase of almost 47%.

         Some studies suggest that women with certain pro-inflammatory conditions like rheumatoid arthritis and celiac disease are at greater risk for having children with Autism. Inflammation affects the brains of infants with Autism after birth.

Is there a connection?

           In a recent study, researchers studying brains affected by Autism found one common pattern: Widespread activation of brain immune cells that produce inflammation. This is not to say that Autism is caused by inflammation, but more research is needed to see if reducing inflammation might ease Autism symptoms.

extra_large-1464356866-1882-children-with-autism-have-extra-synapses-in-their-brains

(Left) excess synapses in the brain of an Autistic child. (Right) Properly pruned synapses in a developmentally typical child.

(Credit: Guomei Tang/ Mark S. Sonders, Columbia University Medical Center)

The researchers compared gene expression in 72 brains, 47 of which came from children and adults affected by Autism. More specifically, they looked at the gene expression in brain immune cells called microglia. When microglia are activated they destroy microbes and unhealthy cells in the brain, and are associated with brain inflammation that can also damage healthy cells.

In the brains that were not affected by Autism, the researchers found that the microglia were in a largely resting (non inflammatory) state.

Besides fighting infections and clearing away damaged cells, microglia play an important role in pruning away excess brain cell connections- called synapses- during brain development. Synapses allow neurons to communicate with one another through chemical or electrical signaling.

A group of researchers led by David Sulzer at Columbia University Medical Center examined the synapses in the brains of children with autism. Sulzer obtained brains from about two dozen children with autism from ages 2-20 who had died from unrelated causes. Those brains were compared with about two dozen brains from developmentally typical children as a control. While they were looking at the neurons, the children with autism had more synaptic “spines” than the control group. Many of these synapses were damaged and had not been cleared out by autophagy, which is the body’s way of cleaning out imperfect structures.

Continuous Inflammation in Autism

         Long after birth, inflammation is an active player in an Autistic brain. Brain tissue studies of people with Autism frequently show a widespread inflammation. Patterns of elevated brain cytokines have also been observed to be similar to those with autoimmune diseases. Also, inflammatory cytokines in spinal fluid and blood are higher in people with Autism.
         Overactive immune systems respond aggressively to stress, which overloads the body with chemical messengers.  Researchers at Tufts University have proposed that these floods release hormones that activate special cells in the brain, that normally fight infection. Activation of these cells results in inflammation, and over time can cause damage to surrounding cells.
         The rate of seizures in people who have Autism is 10 times higher than in the general population. More data is needed, but preliminary research has suggested that seizures in Autistic people may originate from brain inflammation, and treating inflammation may aid in better seizure control. Long term effects of inflammation in people who have Autism is not known, but early studies in animals suggest that inflammation during development causes cognitive and behavioral changes that mimic Autism.

Cytokines: Cell signalling molecules that help cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma.