A common antidepressant could slow the production of a "main ingredient" in brain plaque, which could help stall the progression of Alzheimer's.
Brain plaques are believed to be a contributor to memory problems and condition such as Alzheimer's, a Washington University in St. Louis news release reported.
The antidepressant citalopram proved to stop the growth of plaques in mice. The antidepressant also proved to lower the production of amyloid beta ("the primary ingredient in plaque") by 37 percent in young adults who were mentally healthy.
"Antidepressants appear to be significantly reducing amyloid beta production, and that's exciting," senior author John Cirrito, PhD, assistant professor of neurology at Washington University, said in the news release. "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."
Past research has shown that serotonin (a messenger in the brain) reduces the production of amyloid beta. Antidepressants help keep serotonin circulating throughout the brain.
In mice that had been genetically modified to develop Alzheimer's antidepressants were found to reduce amyloid beta production by about 25 percent after only 24 hours.
In a more recent study researchers gave citalopram to older mice that had already developed brain plaque. The treatment was found to reduce plaque formation by 78 percent.
The researchers also gave a dose of citalopram to 23 human participants between the ages of 18 and 50 who were of good mental health. Spinal fluid samples showed a 37 percent drop in amyloid beta production after the dose was administered.
"We also plan to study older adults who will be treated for two weeks with antidepressants," first author Yvette Sheline, MD, said in the news release. "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."
