SCIENTISTS at Edinburgh University have pinpointed a key molecule they think may protect the brain from depression.
They say fresh insights into changes
in the brain linked to depression could pave the way for new treatments, and that their research also sheds light on why a particular category of anti-
depressant drugs – selective sero-
tonin re-uptake inhibitors (SSRIs) – stop working in some people.
The team studied mice bred to have defects in their ability to activate the molecule, known as eIF4E. These animals showed signs of depression, including reduced levels of the
hormone serotonin.
The mice also demonstrated behavioural changes linked to depression, such as lacking interest in food.
Treatment with a commonly prescribed antidepressant called fluoxetine failed to produce a response in the mice, the researchers said. They suggest this means activation of the molecule is required to experience the beneficial effects of fluoxetine.
This could help explain why some patients stop responding to SSRIs, the researchers say. Other studies have shown that eIF4E is involved in regulating protein synthesis in
the brain.
Defects in the molecule have been linked with other neurological
conditions, such as autism and
Fragile X syndrome.
The latest study marks the first time the molecule has been implicated in depression, the Edinburgh team said.
They believe their findings could lead to the development of new medication for depression, which affects around one in four people in the UK each year.
Dr Christos Gkogkas, of the university’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.”
The research, published in the Journal of Neuroscience, was funded by the Wellcome Trust, the Royal Society, the RS Macdonald Charitable Trust and the Patrick Wild Centre.
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