New Findings on Brain Inflammation in Autism

Neuroscientists from the University of Maryland have made significant strides in understanding how disorders such as autism and schizophrenia develop in children, potentially paving the way for new treatments. Their research sheds light on a critical aspect of early childhood development and its implications for conditions like autism, often referred to as a “cause of childhood autism.”

Previous studies have linked inflammation in the brain during early childhood to autism and schizophrenia. However, the specific mechanisms behind this connection have remained largely unclear. Now, researchers at Maryland have identified how this inflammation affects human brain cells and their development, providing a potential explanation for this association. Their findings were published in the journal Science Translational Medicine on October 12.

In their study, the research team conducted a post-mortem analysis of brain tissues from 17 children—eight who had died from conditions related to inflammation and nine who had been victims of accidents. The depth of this analysis allowed them to observe the direct effects of inflammation on brain development.

“Inflammation can be induced by many factors,” said Seth Ament, an associate professor in psychiatry at Maryland’s Medicine Institute of Neuroscience Discovery. Ament, along with Margaret McCarthy, serves as a co-lead author of the study. This research highlights the complexity of factors influencing inflammation and its subsequent effects on the developing brain.

“The donors in our sample experienced acute inflammation from causes such as encephalitis and severe asthma attacks. In addition, some donors were identified as having experienced inflammation because their medical records indicated the use of anti-inflammatory drugs,” Ament noted. This variation in causes underscores the multifaceted nature of inflammation and its potential impact on neurodevelopmental outcomes.

Building on previous research, the team focused specifically on the cerebellum, the brain region crucial for movement, balance, motor learning, and speech. Past studies have shown that infants born with abnormalities in this area are at a higher risk of developing neurodevelopmental disorders.

“We looked at the cerebellum because it is one of the first brain regions to begin developing and one of the last to reach its maturity, but it remains understudied,” Ament explained. This focus on the cerebellum allowed the researchers to explore a relatively uncharted territory in the study of childhood autism and related disorders.

Upon examining the cerebellar cells, the team discovered that two specific types of brain cells—Golgi neurons and Purkinje neurons—were particularly susceptible to the damaging effects of inflammation.

“Purkinje and Golgi neurons have critical functions,” Ament stated. “During development, Purkinje neurons form synapses that connect the cerebellum to other brain regions involved in cognition or emotional control, while Golgi neurons coordinate communication between cells within the cerebellum.”

“Disruption of either of these developmental processes could explain how inflammation contributes to conditions like autism spectrum disorders and schizophrenia,” he added. This insight not only enhances our understanding of the relationship between inflammation and neurodevelopmental disorders but also suggests specific targets for potential interventions.

The study marks a significant milestone as the first to demonstrate these effects in humans, supporting findings from previous animal studies while revealing some unexpected outcomes.

“Dr. McCarthy previously found a postnatal critical period in rats during which inflammation blunts the development of Purkinje neurons, so it was very encouraging for us to see similar effects in humans,” Ament said. This correlation between animal and human studies reinforces the validity of their findings and suggests a common pathway that could be exploited for therapeutic purposes.

“By contrast, our findings for Golgi neurons were more unexpected and open up a new line of investigation,” he added. The potential implications of this research could lead to innovative approaches for treating childhood-onset conditions by targeting the underlying inflammation that affects brain development.

This study opens exciting avenues for exploring potential treatments for autism and schizophrenia, particularly as various strategies exist to treat inflammation. However, the critical question remains: will targeting inflammation effectively mitigate its detrimental effects on brain development? More research is necessary to confirm these associations and to understand how best to translate these findings into clinical practice.