According to new research from Washington University School of Medicine in St. Louis and the University of Pennsylvania, a commonly prescribed antidepressant may be able to reduce production of amyloid beta, the main harmful ingredient in Alzheimer's brain plaques—both in mice and in people.
Levels of amyloid beta rise in the brains of patients with Alzheimer's, causing it to clump together into plaques. Plaques are also present in people with cognitively normal brains, although at much lower levels. Alzheimer's brain plaques are closely related to memory problems and other cognitive impairments. Health experts believe that stopping plaque buildup may slow down mental decline as well.
This study found that regular consumption of a common antidepressant stopped plaque growth in a mouse model of Alzheimer's disease. Not only that, but in young, cognitively healthy adults, a single antidepressant dose lowered production of amyloid beta, the primary harmful ingredient in Alzheimer's brain plaques, by 37 percent.
Although these findings are encouraging, the study authors say it is still too early to recommend taking antidepressants to slow Alzheimer's disease development. While antidepressants are generally safe, they still have certain risks and side effects; and there is still much work to do to show that the risks are worth the benefits.
Earlier research has shown that serotonin, a chemical messenger in the brain, reduces amyloid beta production. Since most antidepressants keep serotonin circulating in the brain, researchers had earlier tested several antidepressants in young mice genetically altered to develop Alzheimer's disease as they aged. In these mice, which had not yet developed brain plaques, antidepressants were shown to reduce amyloid beta production by an average of 25 percent after 24 hours.
For this new study, the research team gave the antidepressant to older mice with brain plaques and tracked the growth of Alzheimer's-like plaques in the mice for 28 days. They saw that growth of existing plaques stopped, while formation of new plaques was reduced by 78 percent.
In a second experiment, the scientists gave a single antidepressant dose to 23 people aged 18-50 years who were not cognitively impaired or depressed. Samples of spinal fluid taken from these participants over the next 24 hours showed a 37 percent drop in amyloid beta production.
Following on from these successful results, researchers are now trying to understand the molecular mechanisms by which serotonin affects amyloid beta production, both in mice and in older adults, treated for longer periods with antidepressants.