High Neonatal Monocyte Chemotactic Protein-1 (MCP-1) Levels May Represent an Early Marker of Autism

Chemokines and brain autism

A study published in the Journal of Neuroinflammation indicates that the chemokine monocyte chemotactic protein-1 (MCP-1) may represent an early marker for ASD.

Immune dysregulation and markers of inflammation have been associated with Autism Spectrum Disorder (ASD).

Yet, most of the prior studies have used specimens taken after clinical diagnosis, and even with the relatively high prevalence, currently there are no definitive predictive or diagnostic markers for ASD.

As discussed in our previous news report, cortisol variation, IL-6 and TNF-α were recently suggested as potential biomarkers for ASD.

In the Journal of Neuroinflammation study Ousseny Zerbo and colleagues from Kaiser Permanente Northern California and the University of California at Davis, CA measured cytokine and chemokine concentrations in archived neonatal blood specimens maintained by the California Department of Public Health, and from the Early Markers for Autism (EMA) population-based, nested case-control study. Newborn blood specimens were obtained by the heel-stick method, usually within 24 to 48 hours of birth.

The researchers found elevated levels of MCP-1 and decreased levels of RANTES in the newborn blood of children subsequently diagnosed with ASD.

This appears to be substantiated by a recent study using amniotic fluid and reporting elevated levels of MCP-1 for children who were later diagnosed with autism.

Interestingly, MCP-1 has been implicated in neuroinflammation related to diseases characterized by neuronal degeneration. In addition, it appears to contribute to brain development and heterologous desensitization, and to influence neurotransmitter systems and pathways such as opioids, cannabinoids, etc.

Thus, if replicated in future studies, these observations may indicate that cytokine/chemokine profiling and immune system’s assessment in the first few days of life may help in the early identification of particular neurodevelopmental trajectories.

Source: J Neuroinflammation, 2014, 11:113. doi: 10.1186/1742-2094-11-113.
Read more: jneuroinflammation.com