Plasma clusterin levels in autism spectrum disorder: bridging biomarkers to social and cognitive dysfunctions

Autism Spectrum Disorder (ASD) is a set of complex neurodevelopmental disorders that affect social, communication, and behavioral development, as well as other associated areas such as sensory processing. Extensive research evidence suggests that clusterin (CLU) exerts essential physiological processes in the human body, including neuroprotection, neuroinflammation, cellular arrest, chemoresistance, and apoptosis, that are considered hallmarks in the pathophysiology of autism spectrum disorder (ASD). The contributing role of CLU in neurodegenerative disorders has been widely accepted. However, its role in neurodevelopmental disorders like ASD remains largely unexplored. Therefore, we aimed to investigate the potential role of plasma CLU as a biomarker for ASD and its relationship with ASD severity and social impairment. Plasma CLU level was measured in 38 children with ASD (aged 3–12 years) compared to 40 age and sex-matched healthy controls (aged 3–13 years), using enzyme-linked immunosorbent assay (ELISA). The childhood autism rating scale (CARS) and Social Responsiveness Scale (SRS) were used to assess the severity of ASD and social impairment, respectively. Spearman’s correlations (r) between CLU, CARS, SRS, and age were calculated by SPSS. Our results indicated that the plasma CLU levels in the ASD group were significantly higher [(median (IQR), 13.61 (8.25)] than in controls [11.75 (7.08)], p=0.041. Furthermore, children with severe autism and impaired social interactions exhibited a significantly higher plasma CLU level [14.08 (13.55)] compared to the mild to moderate subgroup [9.29 (4.80)], p=0.01. However, there was no significant correlation between CLU and severity scores (CARS, SRS) and age of ASD subjects (p>0.05). This study shows that plasma CLU levels could be implicated in the pathophysiology of ASD and may serve as a potential biomarker for ASD. Furthermore, our results suggest that CLU may be associated with the severity of social behavior impairments. However, there was no correlation between CLU and the severity of the disease. More studies with large populations are required to confirm the role of CLU in ASD.

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Journal
BMC Pediatrics
Published
2026-01-30
DOI
https://doi.org/10.1186/s12887-026-06530-1
Primary Topic
Clusterin in disease pathology
Type
article
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article

Plasma clusterin levels in autism spectrum disorder: bridging biomarkers to social and cognitive dysfunctions

Nadra Elyass Elamin, Laila Yousif Al-Ayadhi, Durria Ahmed Abdulmaged, Dost Muhammad Halepoto et al.
BMC Pediatrics
Clusterin in disease pathology
article

Plasma clusterin levels in autism spectrum disorder: bridging biomarkers to social and cognitive dysfunctions

Nadra Elyass Elamin, Laila Yousif Al-Ayadhi, Durria Ahmed Abdulmaged, Dost Muhammad Halepoto, Farah Al-Ghamdi, Hend Al-Ghamdi
article en

Abstract

Autism Spectrum Disorder (ASD) is a set of complex neurodevelopmental disorders that affect social, communication, and behavioral development, as well as other associated areas such as sensory processing. Extensive research evidence suggests that clusterin (CLU) exerts essential physiological processes in the human body, including neuroprotection, neuroinflammation, cellular arrest, chemoresistance, and apoptosis, that are considered hallmarks in the pathophysiology of autism spectrum disorder (ASD). The contributing role of CLU in neurodegenerative disorders has been widely accepted. However, its role in neurodevelopmental disorders like ASD remains largely unexplored. Therefore, we aimed to investigate the potential role of plasma CLU as a biomarker for ASD and its relationship with ASD severity and social impairment. Plasma CLU level was measured in 38 children with ASD (aged 3–12 years) compared to 40 age and sex-matched healthy controls (aged 3–13 years), using enzyme-linked immunosorbent assay (ELISA). The childhood autism rating scale (CARS) and Social Responsiveness Scale (SRS) were used to assess the severity of ASD and social impairment, respectively. Spearman’s correlations (r) between CLU, CARS, SRS, and age were calculated by SPSS. Our results indicated that the plasma CLU levels in the ASD group were significantly higher [(median (IQR), 13.61 (8.25)] than in controls [11.75 (7.08)], p=0.041. Furthermore, children with severe autism and impaired social interactions exhibited a significantly higher plasma CLU level [14.08 (13.55)] compared to the mild to moderate subgroup [9.29 (4.80)], p=0.01. However, there was no significant correlation between CLU and severity scores (CARS, SRS) and age of ASD subjects (p>0.05). This study shows that plasma CLU levels could be implicated in the pathophysiology of ASD and may serve as a potential biomarker for ASD. Furthermore, our results suggest that CLU may be associated with the severity of social behavior impairments. However, there was no correlation between CLU and the severity of the disease. More studies with large populations are required to confirm the role of CLU in ASD.

BMC PediatricsVol. 26(1)
Riyadh Armed Forces Hospital (SA), King Saud University (SA), Saudi Center for Organ Transplantation (SA)
Openalex Percentile: Top 73%
Clusterin in disease pathology
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