A popular antidepressant may reduce the spread of Alzheimer’s disease, thanks to a decrease in the primary ingredient used in plaque production, a new study finds.

The antidepressant citalopram has been found to significantly cut the levels of Alzheimer’s disease in mice, and in young adults the drug reduced levels of amyloid beta, a protein found in the brain that forms into destructive plaques in too-high concentrations. It’s this protein scientists believe catalyzes the gradual, crushing slide into Alzheimer’s.

"Antidepressants appear to be significantly reducing amyloid beta production, and that's exciting," said senior author Dr. John Cirrito, assistant professor of neurology at Washington University, in a statement. Cirrito made clear, however, that his team’s research is still very much in its infancy. Testing antidepressants on humans can yield tremendous ill side-effects, and the risks aren’t worth it, he argues. “There is still much more work to do."

Alzheimer’s disease afflicts as many as five million Americans, according to the Centers for Disease Control and Prevention. Characterized by severe declines in memory, language, and reasoning skills, the disease is the leading cause of dementia in older adults. Scientists have yet to pin a cause to Alzheimer’s. Current theories speculate that some mix of genetics, social, and environmental factors are at play. And the latest study upholds prior research, which suggests a link between serotonin levels, which stir feelings of pleasure, and the prevention of Alzheimer’s.

A natural limitation to this kind of research is time. Scientists must carry out multi-decade studies in order to gauge how well a drug works. And even then, isolating the drug’s effects compared to a placebo or other environmental influences can be difficult. The best science can do is look at the success in mouse models, which carry a shorter time burden (because mice don’t live as long as humans), and hope to observe similar results in human models.

In their current study, researchers gave citalopram to older mice with brain plaques. For the next 28 days, they then used a technique called two-photon imaging to track the growth of these plaques. When the researchers interrupted the growth with doses of the antidepressant, the plaques stopped growing. Even better, new plaques quit forming by 78 percent.

In a follow-up experiment, they tested citalopram on adults between the ages of 18 and 50 — another limiting factor, as Alzheimer’s disease appears most often after age 60. These subjects were neither cognitively impaired nor depressed. After they received doses of the antidepressant, spinal fluid tests over the next 24 hours showed a drop in amyloid beta protein by 37 percent. Up next are older adults, according to lead author Dr. Yvette Sheline — and somewhere down the line, a blanket drug that could halt Alzheimer’s 15 years before it begins.

"If we see a drop in levels of amyloid beta in their spinal fluid after two weeks,” she said of the follow-up research, “then we will know that this beneficial reduction in amyloid beta is sustainable."

 

Source: Sheline Y, West T, Yarasheski K, et al. An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice. Science Translational Medicine. 2014.