Researchers at the University of Edinburgh pinpointed a key molecule that may protect the brain from depression. Fresh insights into changes in the brain linked to depression could pave the way for new therapies.

 

The study also sheds light on why a certain category of antidepressant drugs stops working in some people.

The team studied mice that were bred to have defects in their ability to activate this molecule, called eIF4E.

These animals showed signs of depression, including reduced levels of the hormone serotonin, which is a hallmark of the condition.

The mice also showed behavioral changes related to depression, such as disinterest in food.

Treatment with a commonly prescribed antidepressant called fluoxetine failed to produce a response in the mice.

This suggests that activation of eIF4E is required for the beneficial anti-depressant effects of fluoxetine, which belongs to the category of drugs called selective serotonin reuptake inhibitors (SSRIs).

Researchers say this could help explain why some patients stop responding to SSRIs.

Previous studies have shown that eIF4E plays a key role in regulating protein synthesis in the brain.

Defects in eIF4E have been associated with other neurological conditions, including autism and Fragile X syndrome. This is the first time the molecule has been implicated in depression.

Experts say the latest findings could help develop new medications for depression, which affects about one in four people in the UK each year.

Dr Christos Gkogkas, a Chancellor's Fellow in the University of Edinburgh's Centre for Discovery Brain Sciences, said, "Our study reveals that altered protein synthesis through eIF4E is a key cellular process in the brain that can go awry in depression. Importantly it may explain why some people with depression become resistant to treatment with SSRIs. This knowledge can help us design a new generation of antidepressants."