Key to Schizophrenia May Lie Outside Our Genes

One of the greatest hurdles facing schizophrenia researchers, especially those concentrating on the disease's genetic factors, is that there is not one simple on/off genetic switch within our DNA. Rather, predisposition for the disease rests as much on genes' effects on their surrounding cellular structures and vice versa as on the actual DNA code itself.

It is what geneticists call an epigenetic disease, a label it shares with other devastating illnesses such as Huntington's disease, Parkinson's disease, and drug addiction, among others. Now, researchers at Scripps Research Institute say that adding schizophrenia to that list opens up new possibilities for novel treatments.

In the case of schizophrenia, problems arise in structures called histones. These histones are proteins around which DNA must be tightly wrapped for it to fit within each cell at all. In healthy cells, the histones are able to expand and contract slightly, a process called acetylation. If histones stop undergoing acetylation, however, they lose the ability to expand and literally strangle the underlying DNA, cutting off certain genes and crippling the DNA's normal functions.

In the past, neuroscientists believed that all traces of acetylation dissipate at the time of death, and because observing the brain cells directly requires a patient to be deceased, it was thought there was no way to directly observe chemical differences in the histones of those with schizophrenia and healthy individuals.

So the Scripps researchers developed a new chemical technique which has allowed them to run post-mortem analyses on donated brains. They found radically decreased evidence of acetylation in certain histones associated with mental effects. By modulating the degree of acetylation in these genes, treatments would, in effect, give those genes room to breathe.

Besides highlighting the importance of early detection (it seems younger brains are more susceptible to decreased acetylation), the study offers hope of a new treatment—drugs to stimulate the production of chromatin, a key catalyst in the acetylation process. The team at Scripps now plans to focus their efforts on chromatin-boosting drugs already in development.

Source: Translational Psychiatry

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