Human Genome data analyzed by an evolutionary method suggests a decrease in cerebral protein-synthesis rate as cause of schizophrenia and an increase as antipsychotic mechanism
Abstract
The Human Genome Project (HGP) provides researchers with the data of nearly all human genes and the challenge to use this information for elucidating the etiology of common disorders. A secondary Darwinian method was applied to HGP and other research data to approximate and possibly unravel the etiology of schizophrenia. The results indicate that genetic and epigenetic variants of genes involved in signal transduction, transcription and translation - converging at the protein-synthesis rate (PSR) as common final pathway - might be responsible for the genetic susceptibility to schizophrenia. Environmental (e.g. viruses)and/or genetic factors can lead to cerebral PSR (CPSR) deficiency. The CPSR hypothesis of schizophrenia and antipsychotic mechanism explains 96% of the major facts of schizophrenia, reveals links between previously unrelated facts, integrates many hypotheses, and implies that schizophrenia should be easily preventable and treatable, partly by immunization against neurotrophic viruses and partly by the development of new drugs which selectively increase CPSR. Part of the manuscript has been published in a modified form as "The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia" in BMC Psychiatry available online at http://www.biomedcentral.com/1471-244X/2/8/
Cite
@article{arxiv.cond-mat/0110189,
title = {Human Genome data analyzed by an evolutionary method suggests a decrease in cerebral protein-synthesis rate as cause of schizophrenia and an increase as antipsychotic mechanism},
author = {Hans W. M. Moises},
journal= {arXiv preprint arXiv:cond-mat/0110189},
year = {2015}
}
Comments
This paper has been withdrawn by the author because it was largely based on a significant association of our schizophrenia sample with the genetic marker D8S1777. According to the available gene maps of the early Human Genome Project in 2000, the EIF4EBP1 gene was within range of that locus, but later versions of the HGP showed that the NRG1 gene actually mapped to this locus