Endocrine Abstracts

JOINT201

Background: Children with obesity exhibit subtle neurocognitive deficits, the mechanism of which remains unknown. α-synuclein plays a fundamental role in neurodegeneration. Moreover, its role in glucose and lipids metabolism is emerging.

Objectives: This study aims to assess whether α-synuclein is correlated with the degree of neurodegeneration in children with obesity in comparison to healthy controls and correlate it to various neurocognitive and metabolic parameters.

Subjects/Methods: Forty children with obesity and 40 matched-healthy controls were assessed for anthropometric measurements and blood-pressure. Cognitive evaluation was performed using Stanford–Binet scale and Barkley Deficits in Executive Functioning (EF) Scale-Children and Adolescents. α-synuclein, fasting lipids and glucose were measured with calculation of the homeostatic model of insulin-resistance.

Results: Children with obesity had significantly higher α-synuclein (P < 0.001) and total EF percentile (P = 0.001) than controls. α-synuclein was negatively correlated to total IQ (P = 0.001), and positively correlated with total EF percentile (P = 0.001) and EF symptom count percentile (P < 0.001) in children with obesity. Multivariate-regression revealed that α-synuclein was independently related to diastolic blood-pressure percentile (P = 0.013), waist/hip ratio SDS (P = 0.007), total EF percentile (P = 0.033) and EF symptom count percentile (P < 0.001) in children with obesity.

Conclusion: α-synuclein could have a mechanistic role in neurocognitive deficit among children with obesity.

Keywords Alpha-synuclein, obese children, neurodegeneration.