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Sharif 1993. Marcial 1989.In This Episode

Kris Onello, MD, PhD, continues to follow up on his neuroinflammation hypothesis of autism spectrum disorder (ASD) as he discusses new research and upcoming publications, including a retrospective analysis of a rare case study series of patients with ASD, evidencing abnormal cerebrospinal fluid (CSF) microglia activation.

Dr. Onello contends that subclinical inflammation may play a role in neurodevelopmental disorders, and that the burgeoning and expanding field of autism research is on the right track. Dr. Onello addresses the shortcomings and future directions of this burgeoning field, such as the need for large-scale, longitudinal studies and studies of the microbiome and the possibility of psychosocial intervention.

Dr. Onello also gives his personal perspectives on the science of autism and neuroinflammation and considers whether new therapies can be developed from a more detailed understanding of the cause of this chronic inflammatory state.

DNews: What research from the clinical setting suggests to you that links subclinical inflammation to autism spectrum disorder?

Kris Onello: In this study, we looked at eight individuals who were diagnosed with idiopathic ASD with no identified genetic or neuromolecular cause and no identifiable neurologic condition in the family. These eight individuals, who were diagnosed at an average age of 18 months, came from two different patient referral centers in the U.S. and Canada. We collected their CSF and retrospectively had another research laboratory look at their CSF to determine the type of microglia activation. And they found that all eight of the patients from both centers had highly increased, activated microglia in their CSF. The microglia activation is very specific. Normally they have resting microglia in the CSF, but they were highly activated and therefore would indicate that some kind of pathogenic process was going on in the brain.

They speculated that their observation of these highly activated microglia was indicative of a potential pathogenic process, which was consistent with our hypothesis

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