Search Here

Antidepressants may do more than boost moods, new research reveals they can also save people from Alzheimer's disease.

Researchers at the University of Pennsylvania found that Celexa (citalopram), a common selective serotonin reuptake inhibitor (SSRI) halted the growth of amyloid beta plaques, which previous findings suggest might trigger the development of Alzheimer's disease.

Experts say the latest findings are important, as Alzheimer's disease is the sixth leading cause of death in the United States, plaguing at least five million Americans. Official estimates indicate that the number of Alzheimer's patients would triple in the years to come.

Researchers from University of Pennsylvania and Washington University wanted to see how citalopram influenced brain interstitial fluid (ISF) in mice with plaques and the cerebrospinal fluid (CSF) of healthy human subjects.

"Our previous studies have shown an association between anti-depressants and the reduction in amyloid burden in the brain," lead author Yvette Sheline, MD, professor of Psychiatry, Radiology and Neurology and director of the Center for Neuromodulation in Depression and Stress, at Penn's Perelman School of Medicine said in a news release. "Those studies examined a retrospective correlation between the duration of anti-depressant use and amyloid burden shown in PET scans in the brains of elderly volunteers. With this new study we took our research a step further and tested the prospective effect of the SSRI citalopram on the CSF amyloid levels in younger, healthy subjects." Sheline performed the research while at Washington University.

In the latest study, Sheline and her team were able to replicate their previous findings showing that citalopram had significant effects in arresting amyloid beta growth.

Experiments on mouse models revealed the level of amyloid-beta in the ISF decreased in a dose-dependent manner by as much as 25 percent in plaque-bearing mice given citalopram. What's more, the findings show that plaque-bearing mice exposed to two months of citalopram showed no new plaque development, and no growth of existing plaques. In contrast mice in the sugar water "control group" showed a substantial increase in plaque growth and development.

Researchers noted that while citalopram halted growth, the antidepressants had little influence on already existing amyloid plaques.

In another experiment of 23 healthy human participants between the ages of 18 and 50 who were given 60 mg citalopram, roughly equivalent to the dose used in mice, linked the antidepressant to a 38 percent lower A-beta concentration over the 37-hour testing period compared to participants given a placebo. Researchers also found that those in participants in the experimental group showed a drop in newly produced A-beta.

Researchers said the latest findings could pave the road to discovering effective Alzheimer's treatments. They explain that the findings show that even a modest decline in cerebrospinal fluid production can stop or stall symptomatic Alzheimer's disease development.

"While these results are an excellent start at lowering A-beta production, we are a long way from making a statement regarding the ability of SSRIs to prevent the cognitive decline associated with AD," Sheline said. "We are developing a greater understanding of the capabilities of SSRIs, which offer promise for the future as preventive measures, as we continue to uncover the complex mechanisms in the brain that trigger Alzheimer's and dementia."

The findings were published in the latest issue of Science Translational Medicine.