Why is the study being done?

 

Psychosis, such as occurs in schizophrenia and related disorders, affects over 1 in 100 of the population. Symptoms can be distressing and can cause long-term illness. It usually starts in the late teens and twenties and symptoms commonly come on quite slowly.

The aim of this research is to follow up recent clues about what happens in the brain that leads to psychosis. Recent research suggests that brain cells, which communicate with each other using two related chemical messengers called glutamate and GABA, start communicating abnormally. In some people this may be because a form of mild inflammation takes place. In others, the GABA and glutamate problems could be due to what genes they inherited. We want to find out whether problems with GABA and glutamate communication is common in early psychosis and whether this settles down or changes in those who have had the illness for some years. Another question is whether GABA and glutamate problems are usually due to a mixture of inflammation and genes, or whether it’s usually just one of them.

When we know the answers, we will be better able to think about slowing or stopping the development of psychosis with completely new treatments for the early stages.

We will:

• Measure genes and inflammation in blood samples
• Measure brain cell communication using a technique called magnetoencephalography (MEG)
• Measuring GABA and glutamate in brain using magnetic resonance spectroscopy (MRS)
• Measure inflammation in the brain using positron emission tomography (PET)

We will compare these measures in people with early psychosis or who have had symptoms for a number of years and people with no history of psychosis

For more information on taking part in the study see: Taking part