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Updated: Jan 31, 2026

Testing Sensory and Multisensory Function in Children with Autism Spectrum Disorder
Published on: April 22, 2015
Correlation Between A Disintegrin and Metalloproteinase (ADAM) Family Proteins (8, 10, 17, 22) and Link with
Dost Muhammad Halepoto1, Laila Al-Ayadhi1,2, Abdulrahman Alhowikan2
1Autism Research and Treatment Center, Al-Amodi Autism Research Chair, Department of Physiology, Faculty of Medicine, King Saud University, P.O. Box 2925, Riyadh 11461, Saudi Arabia.
None:
Background: Autism spectrum disorder (ASD) is a condition related to neurodevelopment, typically identified by impaired social interactions and repetitive stereotypical behaviors. The etiology of ASD is not well known, but neuroplasticity has been suggested to play a pathological role. A disintegrin and metalloproteinases (ADAMs) are multifunctional transmembrane proteins that are important for development, communication, and plasticity in the nervous system. This study aimed to determine the correlations among ADAM proteins (ADAM-8, 10, 17, and 22) in children with ASD and to discuss their potential roles as molecular contributors to processes underlying neuroplasticity. Methods: The Spearman correlation coefficient (r) between plasma levels of ADAM 8, 10, 17, and 22 in children with ASD (n = 40) was obtained using the Statistical Package for the Social Sciences software, SPSS. Results: A significant correlation was obtained between plasma levels of the ADAM 8 and ADAM-17 (r = 0.523, p ≤ 0.001); ADAM 8 and ADAM 22 (r = 0.576, p ≤ 0.001); and ADAM 17 and ADAM 22 (r = 0.489, p ≤ 0.001). However, no significant correlation between ADAM 10 and ADAM 8 (r = -0.147, p = 0.372); ADAM-17 (r = -0.143, p = 0.378), and ADAM-22 (r = -0.066, p = 0.684), was obtained. Conclusions: This study provides the first evidence of associations among circulating ADAM proteins (ADAM-8, ADAM-17, and ADAM-22) in children with ASD, suggesting their potential molecular involvement in pathways related to neuroplasticity. Further studies with larger cohorts and direct neuroplasticity measures are needed to clarify these relationships and their relevance to ASD pathophysiology.
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