Antidepressant Found to Slow One of the Main Causes of Alzheimer's Disease

The Washington University School of Medicine in St. Louis and the University of Pennsylvania conducted a study that found, both in mice and people, an antidepressant prevents a plaque buildup that typically leads to Alzheimer's.

The antidepressant used in the study is called Citalopram, otherwise known as its commercial name, Celexa. Knowing that serotonin signaling suppresses the generation of amyloid-β (Aβ), which has shown to cause Alzheimer's disease, the researchers conducted the study with Celexa because it is a selective serotonin reuptake inhibitor.

A lack of amyloid-β (Aβ) results in the growth of amyloid plaques, which clumps together in the brain and is thought to short-circuit the wiring of neurons, ultimately resulting in Alzheimer's. Celexa was found to reduce the concentration of amyloid plaques by 38% in human volunteers who did not have any forms of dementia. A 78% decrease was witnessed in the older mice who were bred to develop an animal version of Alzheimer's.

The study, "An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice," was published on Wednesday in the journal Science Translational Medicine. The researchers believe that this antidepressant can provide a cheap and convenient way to prevent Alzheimer's disease or other forms of dementia in patients who are at risk.

"We had predicted the results, but they were very exciting," said lead author Dr. Yvette Sheline of the University of Pennsylvania, in this BBC News article. "I am eager to get on to the next study, where we will look at whether the effect can be sustained."

The 23 human participants were aged 18 to 50 were given the antidepressant and had spinal fluid extracted from their bodies to document the production of amyloid-beta. In their next study, the researchers want to use older adults and treat them with the antidepressants over a two-week period to see if this treatment is sustainable and effective. The drug's effect on older mice proved effective, which is promising for the future human trial.