Neonatal chemokine markers predict subsequent diagnosis of autism spectrum disorder and delayed development.

Scientists tested blood from newborn babies to see if they could predict which children would later be diagnosed with autism. They looked at immune system chemicals in the blood and found two that were different in babies who later developed autism. One chemical (CTACK) was lower in babies who got autism diagnoses, while another (MPIF-1) was higher. This suggests that immune system differences might be present from birth in children who develop autism.

This study analyzed blood spots from 398 newborns to examine whether immune system markers at birth could predict later autism diagnosis. Researchers compared children who developed autism spectrum disorder (ASD), developmental delays (DD), or typical development. They found that two specific chemokine proteins - CTACK and MPIF-1 - showed different patterns in children who later received an ASD diagnosis. Higher CTACK levels were associated with reduced odds of ASD, while higher MPIF-1 levels were associated with increased ASD odds compared to children with developmental delays.

The findings suggest immune system differences may be detectable at birth in children who later develop autism.

Results suggest potential for developing early biomarker panels to identify autism risk at birth. However, clinical application requires replication in larger studies and validation across diverse populations before implementation. The distinct chemokine profiles may inform understanding of autism's biological origins.

Single study design limits generalizability. The study does not specify methodology details or control for potential confounding factors. Sample characteristics and study design are not fully described, making it difficult to assess the robustness of findings.

Immune dysregulation has been found to be related to a diagnosis of autism spectrum disorder (ASD). However, investigations in very early childhood examining immunological abnormalities such as altered neonatal cytokine/chemokine profiles in association with an aberrant developmental trajectory, are sparse. We assessed neonatal blood spots from 398 children, including 171 with ASD, which were subdivided according to severity (121 severe, 50 mild/moderate) and cognitive/adaptive levels (144 low-functioning, 27 typical to high-functioning). The remainder were 69 children with developmental delay (DD), and 158 with typical development (TD), who served as controls in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study.

Exploratory analysis suggested that, in comparisons with TD and DD, CTACK (CCL27) and MPIF-1 (CCL23), respectively, were independently associated with ASD. Higher neonatal levels of CTACK were associated with decreased odds of ASD compared to TD (odds ratio [OR] = 0.40, 95% confidence interval [Cl] 0.21, 0.77), whereas higher levels of MPIF-1 were associated with increased odds of ASD (OR = 2.38, 95% Cl 1.42, 3.98) compared to DD but not to TD. MPIF-1 was positively associated with better scores in several developmental domains. Dysregulation of chemokine levels in early life can impede normal immune and neurobehavioral development, which can lead to diagnosis of ASD or DD.

This study collectively suggests that certain peripheral chemokines at birth are associated with ASD progression during childhood and that children with ASD and DD have distinct neonatal chemokine profiles that can differentiate their diagnoses.