The Metabolic Insight into Autism Spectrum Disorder: Evaluating Adiponectin's Impact on Severity and Therapy
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Abstract
Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition with a complex interplay of genetic and environmental factors. Recent research has suggested a significant link between metabolic alterations and ASD pathology, particularly focusing on adiponectin, a hormone related to glucose regulation and fatty acid breakdown. Anomalies in adiponectin levels have been associated with cognitive impairment and the severity of ASD.
Objective: This study aims to evaluate the potential of the ADIPOQ gene as a biomarker for dementia in individuals with ASD, exploring its correlation with cognitive decline and metabolic dysregulation.
Methods: A total of 108 EDTA blood samples from ASD patients and 32 from healthy controls were collected after obtaining written informed consent. The inclusion criteria included individuals aged over 40 with Type II Diabetes Mellitus and confirmed cases of diabetes and dementia. Exclusion criteria comprised the absence of clinical history, refusal of consent, and secondary autism. Adiponectin levels were quantified using ELISA, and cognitive function was assessed via MMSE scores over a six-month follow-up period. Data analysis was conducted using GraphPad Prism 9.0 with ANOVA for statistical significance.
Results: The study found a significant decrease in adiponectin levels among ASD patients (5.17±1.04 µg/mL) compared to healthy controls (11.37±4.14 µg/mL, p=0.014). MMSE scores were notably lower in the ASD group (10.26±2.56) than in controls (23.1±3.12, p=0.006). A marked underexpression of ADIPOQ gene (fold change of 4.9) was observed in patients with dementia.
Conclusion: The ADIPOQ gene shows potential as a biomarker for the early detection of dementia in ASD, offering avenues for personalized medical interventions and preventative healthcare measures. Recognizing its role could lead to improved therapeutic strategies and a reduction in the healthcare burden due to neurodegenerative diseases associated with ASD.
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