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
Hans W. M. Moises

TL;DR
This study uses an evolutionary approach to analyze human genome data, proposing that decreased cerebral protein-synthesis rate causes schizophrenia and that increasing it could be a therapeutic mechanism.
Contribution
It introduces a novel hypothesis linking protein-synthesis rate to schizophrenia etiology and suggests new prevention and treatment strategies based on this link.
Findings
CPSR deficiency may underlie schizophrenia susceptibility
Antipsychotic effects may involve increasing CPSR
Genetic and environmental factors influence CPSR levels
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…
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Taxonomy
TopicsGenetic Associations and Epidemiology · Genetics and Neurodevelopmental Disorders · Bioinformatics and Genomic Networks
