Genetic Analysis Offers New Insight into Memory Impairment in Schizophrenia

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Patrick F. Sullivan, M.D., Expert on schizohrenia research
Patrick F. Sullivan, M.D.

Working memory allows us to keep multiple things in mind that we need while performing a task. This kind of temporary repository helps us through all sorts of tasks during the day; deficits in this capacity have been linked to many psychiatric illnesses, including schizophrenia. A new study published in Neuron on February 13th reveals new insights about the biology underlying these deficits.

Researchers, including 2010 NARSAD Distinguished Investigator Grantee, Patrick F. Sullivan, M.D., Distinguished Professor of Genetics at the University of North Carolina School of Medicine, surveyed the genomes of 2,824 healthy people, in early and late life, to identify those places in the DNA related to working memory. They also analyzed the genomes of a large “control” sample of 32,143 people with schizophrenia.

Many different genes were found to be associated with working memory, but the research team found that a subset of genes that are blueprints for molecules called ion channels, and that were related to neuronal “excitability,” were especially linked to working memory across ages and in schizophrenia. (Neuronal excitability determines how well a neuron can sustain electrical activity to regulate behavior and cognition.) Through functional imaging, they were also able to identify the brain regions linked to this subset of genes and to working-memory related activity.

There would be many hurdles to overcome, but scientists suggest that with these new insights, medications may be able to be developed to target these ion channels to improve the working memory impairments of schizophrenia.

Read more about this on the Schizophrenia Research Forum.

Read the abstract for this research.

Article comments

This article is a perfect example of why I will continue to support BHF!

Has the BBRF done any research into the build up of Proline in the brain/ body from mutation of the PRODH gene? Seems figuring out how to get Proline oxidase into the bodies of those with this mutation to replace the missing Proline dehydrogenase would be a completely obvious way to prevent hyperprolinemia and resulting schizophrenia/ Autism. Also, newborn screening seems to be an obvious but completely overlooked preventative step in alleviating schizophrenia and autism before the build up starts to destroy the brain and other body organs.

In addition to the mutations found on Chrom 22 that cause DiGeorge Syndrome and Catch 22 Syndrome responsible for the development of schizophrenia, schizopaffective disorder, bipolar, depression and Autism, replacing the missing Catechol-O-methyl transferase seems to be an obvious way to regulate neurotransmitters that go unchecked due to lack of this enzyme. Why is there no research being done in the area of enzyme replacement for the prevention of neuropsychiatric conditions?

It is so sad how much our loved ones with this disease have to struggle with

I was extremely excited reading this article, and wanted to make a small contribution of my own, however, when I got to the bottom of the article - I forgot what I was going to say :)

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