A commonly prescribed antidepressant stops the growth of brain plaques in a mouse model of Alzheimer's disease, a new research has claimed.
Researchers at Washington University School of Medicine in St Louis and the University of Pennsylvania found that the antidepressant citalopram can reduce production of the main ingredient in Alzheimer's brain plaques.
In young adults who were cognitively healthy, a single dose of the antidepressant lowered by 37 per cent the production of amyloid beta, the primary ingredient in plaques.
Although the findings are encouraging, the scientists cautioned that it would be premature for people to take antidepressants solely to slow the development of Alzheimer's disease.
"Antidepressants appear to be significantly reducing amyloid beta production, and that's exciting," said senior author John Cirrito, assistant professor of neurology at Washington University.
"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," he said.
Amyloid beta is a protein produced by normal brain activity. Levels of this protein rise in the brains of patients with Alzheimer's, causing it to clump together into plaques. Plaques also are sometimes present in cognitively normal brains.
Cirrito's earlier research had shown that serotonin, a chemical messenger in the brain, reduces amyloid beta production.
Most antidepressants keep serotonin circulating in the brain, so this led Cirrito and first author Yvette Sheline to wonder whether the drugs block the increase of amyloid beta levels and slow the progression of Alzheimer's.
The team gave citalopram to older mice with brain plaques. Using a technique called two-photon imaging, researchers tracked the growth of Alzheimer's-like plaques in the mice for 28 days.
Giving the mice the antidepressant stopped the growth of existing plaques and reduced the formation of new plaques by 78 per cent.
In a second experiment, the scientists gave a single dose of citalopram to 23 people ages 18 to 50 who were not cognitively impaired or depressed. Samples of spinal fluid taken from the participants over the next 24 hours showed a 37 per cent drop in amyloid beta production.
"We also plan to study older adults who will be treated for two weeks with antidepressants," said Sheline, who is now at the University of Pennsylvannia.
"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," Sheline said.
The findings are published in the journal Science Translational Medicine.
