New research carried out by the Columbia University Medical Center has discovered new links between the onset of schizophrenia and genetic factors.
The research was published in Nature Genetics and discussed how fresh mutations in DNA occur in around 50% of all subjects with schizophrenia. In the study patients with no previous family history of schizophrenia were studied to ensure that the genetic relationship could not be one passed on by parents.
40 Genes With Genetic Mutations
The scientists discovered 40 different genes which had signs of genetic mutations and this in their opinion could go a long to explain why there are so many cases of schizophrenia around the world.
It is thought that around 1 in every 100 people will develop schizophrenia at some point in their lives, and although many of these will recover, many will remain schizophrenic for the rest of their lives.
Genetics has always played a role in schizophrenia. 10% of all schizophrenics have a parent with the condition. However, by eliminating those with a parent with schizophrenia from the study the results do suggest that it is the DNA mutations that are leading to the development of schizophrenia in some people.
225 People Studied
In total 225 people were studied, some of which had schizophrenia. Professor Bin Xu who was part of the research team explained that the indentification of mutated genes provided an amazing breakthrough in not only genetic science but also the understanding of schizophrenia.
However, if schizophrenia is caused by genetic mutations affecting a wide range of genes it is hard to see how an effective cure could ever be produced. Unless it becomes possible to vaccinate against late onset genetic mutation there seems little chance at the moment of preventing or treating schizophrenia in the future.
“Exome sequencing supports a de novo mutational paradigm for schizophrenia” by Bin Xu, J Louw Roos, Phillip Dexheimer, Braden Boone, Brooks Plummer, Shawn Levy, Joseph A Gogos & Maria Karayiorgou. Published in Nature Genetics (2011) doi:10.1038/ng.902. 07 August 2011.