Serum Brain-derived neurotrophic factor levels in Chinese children with autism spectrum disorders: A pilot study.
Brain-derived neurotrophic factor (BDNF) plays a critical role in the pathogenesis of Autism spectrum disorders (ASD).
The purpose of this study was to investigate the potential role of BDNF in Chinese children with ASD.
Sixty patients (48 male, 12 female) diagnosed with ASD and 60 healthy sex and age control subjects were assessed for serum BDNF content at admission. BDNF were assayed with enzyme-linked immunosorbent assay methods, and severity of ASD was evaluated with the Childhood Autism Rating Scale (CARS) Score.
The results indicated that the median serum BDNF levels were significantly (P<0.0001) higher in children with ASD as compared to normal cases [17.6(IQR: 13.7-21.4) ng/ml and 11.5(9.6-13.8) ng/ml, respectively].
Based on the Receiver operating characteristic (ROC) curve, the optimal cut-off value of serum BDNF levels as an indicator for auxiliary diagnosis of autism was projected to be 15.0ng/ml.
Further, we found that an increased risk of ASD was associated with BDNF levels >15.0ng/ml (adjusted OR 10.4, 95% CI: 4.39-29.32) after adjusting for above possible confounders.
Our study demonstrated that serum BDNF levels were associated with ASD, and higher levels could be considered as an independent risk factor of ASD.
Copyright © 2014. Published by Elsevier Ltd.
Further Readings of Interest
The effects of enriched environment on BDNF expression in the mouse cerebellum depending on the length of exposure.
Área de Psicobiología, Universidad Jaume I, Castellon de la Plana, España.
Environmental enrichment (EE) has been proposed as a factor that improves neuronal connectivity and brain plasticity.
The induction of molecular mechanisms that takes place in the cortex, nucleus accumbens and hippocampus resulting from exposure to EE has been attributed partly to the role of neurotrophins as brain-derived neurotrophic factor (BDNF). Recent data directly implicate this neurotrophin in the modulation of plasticity changes in the cerebellum produced by living under environmental enrichment.
In the present study, we aimed to assess the effects of different lengths of exposure to EE on cerebellar BDNF expression and western blotting analysis.
On the whole, the present data has shown that BDNF increased under EE.
However, changes in expression as a result of extending the duration of EE were only seen in Purkinje neurons. In Purkinje neurons, long-term exposure was required in order to fully express this neurotrophin.
These data support BDNF as one of the long-term plasticity mechanisms induced by environment, suggesting that cerebellar plasticity can be stimulated as a response to challenges generated by environment.
Our findings could have functional implications for various neurodegenerative disorders such as spinocerebellar ataxias, autism, schizophrenia and certain prion encephalopathies, most of them pathologies which have demonstrated to be characterized by alterations in Purkinje neurons and to show a partial recovery by exposure to EE.