Study finds that antidepressants might slow the development of Alzheimer's Disease
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Study finds that antidepressants might slow the development of Alzheimer's Disease


A antidepressant that is often prescribed might slow production of amyloid beta, which is part of what causes Alzheimer's disease, according to new research from Washington University School of Medicine in St. Louis and the University of Pennsylvania. Science Translational Medicine published the research, which described mouse studies examining a variety of antidepressants.

Brain plaques are related to memory issues involved with Alzheimer's, and scientists showed that the antidepressant citalopram halted plaque growth in a mouse model of the disease. Also, one dose of the antidepressant reduced the production of amyloid beta by 37 percent in health young adults.

The research is promising, but researches warned people should not take antidepressants just to help reduce the risk of Alzheimer's disease. ". . . While antidepressants generally are well tolerated, they have risks and side effects," said senior author John Cirrito, PhD, assistant professor of neurology at Washington University. "Until we can more definitively prove that these drugs help slow or stop Alzheimer's in humans, the risks aren't worth it. There is still much more work to do."

Normal brain activity produces amyloid beta, but when too much is present, it can clump into plaques. Some of Cirrito's previous research revealed that serotonin, one of the brain's chemical messengers, decreases amyloid beta production. Because many antidepressants help serotonin circulate in the brain, Cirroto and first author Yvetter Sheline, MD, speculated about whether antidepressants might help slow the development of Alzheimer's.

"We also plan to study older adults who will be treated for two weeks with antidepressants," said Sheline. "If we see a drop in levels of amyloid beta in their spinal fluid after two weeks, then we will know that this beneficial reduction in amyloid beta is sustainable." (Read more)




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