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Abstract
Background
The Voltage Dependent Anion Channel (VDAC) is involved in control of autism. Treatments, including coenzyme Q, have had some success on autism control.
Data sources
Correlation of porin redox activity and expression of autism is based on extensive literature, especially studies of antibodies, identification of cytosolic nicotinamide adenine dinucleotide reduced (NADH) dehydrogenase activity in the VDAC, and evidence for extreme sensitivity of the dehydrogenase to a mercurial. Evidence for a coenzyme Q requirement came from extraction and analog inhibition of NADH ferricyanide reductase in the erythrocyte plasma membrane, done in 1994, and reinterpreted when it was identified in VDAC in 2004. The effects of ubiquinol (the QH2 – reduced form of coenzyme Q) in children with autism were studied.
Results
A new role for coenzyme Q in the porin channels has implications on autism. Ubiquinol, the more active form of coenzyme Q, produces favorable response in children with autism. Agents which affected electron transport in porin show parallel effects in autism.
Conclusion
We propose a hypothesis that autism is controlled by a coenzyme Q-dependent redox system in the porin channels; this conclusion is based on the effects of agents that positively or negatively affect electron transport and the symptoms of autism. The full understanding of the mechanism of their control needs to be established.
Acknowledgments
This paper was supported by the Grant Ministry of Education of Slovakia, VEGA 1/0614/12, FLC 1992 support. The authors would like to acknowledge the Folkers Foundation. The authors would also like to acknowledge Professor Anthony W Linnane (Centre of Molecular Biology and Medicine, Melbourne, VIC, Australia) for reviewing the manuscript.
Disclosure
The authors report no conflicts of interest in this work. Work was done between 1990–1992 and 2012–2013 and has not been previously published, with one exception – in 1992 Sun et al published extraction studies.