A widely-used antidepressant can reduce levels of a brain-clogging protein linked to Alzheimer’s disease, research has shown.

Scientists say it is too early to recommend the drug to Alzheimer’s patients, but the build-up of “plaque” deposits in the brain is closely associated with declining memory and other symptoms of the disease.

In healthy adults aged 18 to 50, a single dose of the antidepressant citalopram lowered production of the plaque protein amyloid beta by 37 per cent.

The drug, marketed in the UK as Cipramil, also had a dramatic effect on elderly mice, halting the growth of existing plaques and reducing the formation of new deposits by 78 per cent.

Lead scientist John Cirrito, from Washington University School of Medicine in the US, said: “Antidepressants appear to be significantly reducing amyloid beta production, and that’s exciting. But while antidepressants generally are well tolerated, they have risks and side effects.

“Until we can more definitively prove that these drugs help slow or stop Alzheimer’s in humans, the risks aren’t worth it. There is still much more work to do.”

Amyloid beta is a waste product of normal brain activity. But its levels rise in the brains of Alzheimer’s patients, causing it to clump together in plaques.

Earlier research by Cirrito’s team showed that serotonin, a brain messenger chemical, reduces amyloid beta production.

Serotonin is also linked to mood, and many antidepressants work by keeping the neurotransmitter circulating in the brain.

The scientists, whose research appears in the journal Science Translational Medicine, are now investigating how serotonin affects amyloid beta production in mice at the molecular level.

Co-author Yvette Sheline, from the University of Pennsylvania, US, said: “We also plan to study older adults who will be treated for two weeks with antidepressants.

“If we see a drop in levels of amyloid beta in their spinal fluid after two weeks, then we will know that this beneficial reduction in amyloid beta is sustainable.”