A commonly used medication could hold the key to treating or preventing Alzheimer’s disease.
New research published in the journal Science Translational Medicine reveals that the frequently prescribed antidepressant citalopram, also known as Celexa, could play a role in halting the progression of the brain-wasting disease.
Antidepressants like citalopram offer hope by targeting the brain’s amyloid beta proteins, which seem to be responsible for triggering the plaque build-up associated with the decline of memory and cognitive function in Alzheimer’s patients.
“The way the Alzheimer’s field is going is [we are] trying to find the initial insult in Alzheimer’s disease,” study author John Cirrito, assistant professor of neurology at the Washington University School of Medicine, told FoxNews.com. “We think it is the build-up of this amyloid beta peptide, and once it builds up, a lot of things go wrong.”
Amyloid beta proteins are produced by normal brain activity, but in Alzheimer’s patients, levels of this protein increase abnormally, clumping together to form plaques.
Previous research has shown that serotonin, a brain chemical thought to influence mood, seems to reduce amyloid beta production in the brain. In fact, an earlier study demonstrated that people with a history of antidepressant use had less amyloid plaques in their brains than those who never used antidepressants.
A popular type of antidepressant known as selective serotonin reuptake inhibitors (SSRIs) can influence serotonin levels, so the researchers were interested in testing its effects on mice and human models. Using mice genetically engineered to develop Alzheimer’s disease, the researchers discovered that the SSRI citalopram was able to completely stop the growth of brain plaques in the study group.
“SSRIs, by lowering a-beta levels 25 percent, were able to completely block that [plaque] growth,” Cirrito said. “The plaques never got smaller, and we couldn’t reverse the plaque [that was already there], but we could prevent it from growing.”
The researchers also tested citalopram in a group of cognitively healthy young adults. They discovered that after receiving a single dose of the antidepressant, the participants saw a 37 percent reduction of amyloid beta levels in their cerebrospinal fluid.
Currently, Cirrito said amyloid beta has no “known function” in the human body, and decreasing levels of the protein in humans doesn’t seem to have any ill effects on health. However, he noted that much research needs to be done before SSRIs can be proven effective at treating or preventing Alzheimer’s in humans.
“The SSRIs in this study were all given to healthy young people not at risk for Alzheimer’s,” Cirrito said. “We don’t know if the same thing will happen in people older, and not at risk for Alzheimer’s, and have no idea if it affects cognition,” Cirrito said.
Furthermore, he cautioned people against preemptively taking SSRIs in hopes of fending off or treating Alzheimer’s disease.
“There are certainly side effects [of SSRIs] that if they don’t need to be taken, it’s not a good idea to be on them until we know they can have an effect on Alzheimer’s, it’s premature to take them as a preventative measure,” Cirrito noted. “We’ve cured a mouse of a lot of different diseases, including Alzheimer’s disease many times, and those things haven’t panned out in people yet.”
Next, Cirrito and his team hope to move forward to study how SSRIs act on the brain to lower amyloid beta levels – and to continue to study the effects of SSRIs on different human populations.
“On the human side, we’re doing a similar study to what we just completed but in people [who are] older and at risk for Alzheimer’s, to see if we can affect a-beta in those people or not,” Cirrito said. “If not, then the utility of this for people with Alzheimer’s would go down dramatically.”