Researchers have discovered a brain cell malfunction in schizophrenia as DNA stays too tightly wound in certain brain cells of schizophrenic subjects.

Findings in a study by the Scripps Research Institute suggest that drugs already in development for other diseases might eventually offer hope as a treatment for schizophrenia and related conditions in the elderly.

The study shows that the deficit is especially pronounced in younger people.

Study authors said treatment might be most effective early on at minimizing or even reversing symptoms of schizophrenia, a potentially devastating mental disorder associated with hallucinations, delusions, and emotional difficulties, among other problems. 

“We’re excited by the findings and there’s a tie to other drug development work, which could mean a faster track to clinical trials to exploit what we’ve found,” said Scripps Research Associate Professor Elizabeth Thomas, a neuroscientist who led the study that was published in Nature journal, Translational Psychiatry.

Thomas explained that while there is a range of such so-called epigenetic effects that change the way DNA functions without changing a person’s DNA code, there is one critical area of epigenetic research is tied to histones, structural proteins that DNA has to wrap around.

“There’s so much DNA in each cell of your body that it could never fit in your cells unless it was tightly and efficiently packed,” said Thomas.

While there is no single right or wrong configuration as the histone-DNA complexes, known as chromatin, are constantly relaxing and condensing to expose different genes, the balance can still shift in ways that can cause or exacerbate disease.

As Thomas was studying the roles of histone acetylation in Huntington’s disease she began to wonder whether similar mechanisms of gene regulation might also be important in schizophrenia.

“It occurred to me that we see the same gene alterations, so I thought, ‘Hey, let’s just try it,’” she said.

Working with lead author Bin Tang, a postdoctoral fellow in her lab, and Brian Dean, an Australian colleague at the University of Melbourne, Thomas obtained post-mortem brain samples from schizophrenic and healthy brains held at medical ”Brain Banks” in the United States and Australia, the authors explained.

The researchers found that compared to a healthy brain, the brain samples from subjects with schizophrenia showed lower levels of acetylation in certain histone portions that would block gene expression.

Another critical finding was that in younger subjects with schizophrenia, the problem was much more pronounced.

The researchers are suggested that if they can reliably show that acetylation is a cause of the problem, they can look for ways to open the closed guide pages and hopefully cure or improve the condition in patients.