27/02/2018 11:15 GMT

Long-Term Depression Could Be Causing The Same Damage As Alzheimer’s

The brain is displaying the same warning markers.

People with long-term depression might actually be experiencing the same debilitating process in the brain as those with Alzheimer’s disease

A new study has shown that having depression for more than a decade causes cerebral deterioration (by killing neurons) that exactly mirrors what happens with dementia patients. 

This is an important turning point in the potential treatment of depression as it has never previously been classed as a degenerative brain disease.

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The study, published in the Lancet Psychiatry journal, found leaving depression untreated for years on end causes increased inflammation in the brain.

This inflammation is a known risk factor for neurodegeneration. Lead author Dr Jeff Meyer explained: “Greater inflammation in the brain is a common response with degenerative brain diseases as they progress, such as with Alzheimer’s disease and Parkinson’s disease.”

But now they have been able to show that depression has the same effect. Meyer added: “Progressive neurodegeneration itself occurs in major depressive disorder”.

The study looked at PET (positron emission tomography) brain scans of 50 depressed patients, 50% of whom had suffered from the condition for more than ten years.

Images were also taken from a control group of 30 people who had never had depression.

Comparing the resulting scans, levels of translocator proteins [TSPO], which are a marker of inflammation, were measured. They found that those with long-lasting untreated depression were found to have 30% more TSPO than those who had experienced depression for shorter periods. 

The findings suggest that different stages of depression should be treated in different ways, Meyer said.

MIND says that approximately every 3.3 people in 100 in the UK experience depression in any given week. And currently depression is treated using the same approach irrespective of how long the patient has been ill.