The research identifies brain abnormalities and what causes them. This better understanding of the abnormalities will lead to improved treatment and preventative approaches that stop the problems developing.

Led by Professor Gavin Reynolds, Professor of Neuroscience the group is studying human post mortem brain tissue to understand the nerve cell changes resulting in the symptoms of schizophrenia.

According to Professor Reynolds: Schizophrenia remains a huge mystery to us still; we understand very little of what causes it, while the treatments available are not very effective. We have found that the changes in a gene (Neuregulin) which increases the liability of contracting schizophrenia also causes nerve cell changes in the brain.

The genetic risk factors are inherited from parents as common variations in our genes. Having these risk factors has only a small effect on whether someone develops schizophrenia.

Backed by the Stanley Medical Research Institute, Professor Reynolds said: It has been recognised that Queen ™s has experience and expertise in the study of post mortem brain tissue and how we identify the problems in the brain that cause schizophrenia.

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However, when the RNA nucleotide repeats are expressed, they stimulate a signal that is normally present in embryonic tissues and not in adults. Specifically, the protein kinase C pathway is reactivated resulting in the addition of the phosphate molecules to CUGBP1. With the addition of the phosphate molecules, CUGBP1 levels increase to those observed in the embryonic period.

This affects alternative splicing, said Cooper. It changes the splicing from an adult pattern to an embryonic pattern. Adult tissues express embryonic proteins, and that's why people get sick.

Another RNA-binding protein called muscleblind like 1 (MBNL1) is also involved in the disease. It binds genetic material in the nucleus of the cell, trapping the RNA there and preventing it from transporting the RNA messages into the cell's cytoplasm. MBNL also becomes trapped with the RNA rendering it unable to function.

In addition to gaining a better understanding of what causes this disease, we have learned that both CUGBP1 and MBNL1 regulate splicing of many genes during normal muscle development, said Cooper.

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