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Evidence for a relation between plasma membrane coenzyme Q and autism
Frederick L Crane1, Hans Low, Iris L Sun
1Department of Biological Sciences, Purdue University, W. Lafayette, Indiana, USA. flccoq10@aol.com
Frontiers in Bioscience (Elite Edition)
|June 11, 2013
Summary
Voltage Dependent Anion Channel (VDAC) may play a role in autism development. Increased antibodies to VDAC in autistic children inhibit its functions, suggesting a novel link between VDAC activity and autism pathogenesis.
Area of Science:
- Biochemistry
- Cell Biology
- Neuroscience
Background:
- Voltage Dependent Anion Channel (VDAC) facilitates transport across cell membranes.
- VDAC also functions as a transmembrane NADH dehydrogenase.
- Autism is associated with increased antibodies targeting VDAC proteins.
Purpose of the Study:
- Investigate the potential role of VDAC function in autism development.
- Explore the coenzyme Q requirement for VDAC's dehydrogenase activity in erythrocyte membranes.
Main Methods:
- Analysis of VDAC antibody levels in autistic children.
- Assessment of VDAC transport and dehydrogenase activities.
- Investigation of coenzyme Q requirement for erythrocyte membrane dehydrogenase.
Main Results:
- Autistic children exhibit elevated antibodies against VDAC.
- Antibody binding inhibits both VDAC transport and NADH dehydrogenase activities.
- Erythrocyte membrane dehydrogenase activity requires coenzyme Q, suggesting a novel VDAC function.
Conclusions:
- VDAC's function may be implicated in the pathogenesis of autism.
- Coenzyme Q is essential for VDAC's dehydrogenase activity in erythrocyte membranes.
- This finding offers a new perspective on VDAC's role in cellular metabolism and disease.
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Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by persistent deficits in social communication and interaction alongside restrictive and repetitive behaviors or interests. ASD is sometimes accompanied by intellectual impairment.
These core symptoms manifest differently among individuals, ranging from mild to severe. The disorder's complexity extends beyond its clinical presentation, encompassing a diverse range of biological, cognitive, and sociocultural influences.
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