Research at two U.S. universities has shown that a common antidepressant could cut the production of an important ingredient linked to the brain plaques associated with Alzheimer’s disease.
Work by scientists from St. Louis’s Washington University School of Medicine and the University of Pennsylvania supported studies using mouse subjects and a number of antidepressants, ScienceDaily reports. Findings regarding mouse and human subjects appeared in the journal Science Translational Medicine.
Alzheimer’s disease is the most common form of dementia. More than 5 million Americans have the disorder, and someone new develops it every 67 seconds, according to the Alzheimer’s Association. It’s the sixth-leading cause of U.S. deaths.
The researchers discovered that a commonly prescribed antidepressant halted the growth of brain plaques in a mouse model of the disease. Experts have shown that these plaques are tied to memory issues and other types of Alzheimer’s cognitive problems. They theorize that halting the buildup of these plaques could stop the cognitive decline caused by the illness.
MedlinePlus indicates that the antidepressant, citalopram, is part of a class of drugs called selective serotonin reuptake inhibitors (SSRIs). SSRIs increase a patient’s amount of serotonin, substances the brain naturally produces to maintain mental balance. The drug is also sometimes used to treat eating disorders, panic disorder, social phobias, and alcoholism.
Among healthy young adults, just one dose of citalopram cut the production of amlyoid beta, the main ingredient found in brain plaques, by 37 percent. However, the researchers caution that despite initially positive results, it’s too early to conclude that individuals should take antidepressants to try to halt Alzheimer’s disease.
Most patients tolerate antidepressants well. However, senior author John Cirrito, Ph.D., of Washington University, cites risks and side effects associated with these medications. He sees the recent research as an initial step toward slowing the disease.
The scientists knew from earlier research that serotonin cuts the manufacture of amyloid beta. Since many antidepressants work by circulating serotonin in the brain, they wondered whether these drugs could block a rise of amyloid beta levels and slow the disease.
In 2011, they tested various antidepressants on young mice altered to develop Alzheimer’s but without any brain plaques. The drugs cut amyloid beta production by about 25 percent after just 24 hours.
More recent work involved giving citalopram to older mouse subjects that had brain plaques. After 28 days, the production of new plaques had fallen by 78 percent.
The researchers then administered one dose of citalopram to 23 human subjects between 18 and 50. These individuals were not depressed or cognitively impaired. Over a 24-hour period, spinal fluid samples showed a drop of 37 percent in amyloid beta production.
Plans for additional research include uncovering the details of how serotonin affects the manufacture of amyloid beta in mice and studying older adults treated with antidepressants for two weeks.
Vonda J. Sines has published thousands or print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.