Citalopram May Cease Alzheimer's Disease Progression

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Internal Medicine World ReportMay 2014

A frequently prescribed antidepressant can hinder the buildup of brain plaques linked to Alzheimer's disease development.

A frequently prescribed antidepressant can hinder the buildup of brain plaques linked to Alzheimer’s disease (AD) development, according to a study published May 14, 2014, in Science Translational Medicine.

Researchers at the Washington University School of Medicine in St. Louis and the University of Pennsylvania in Philadelphia recently conducted a pair of studies that focused on how the antidepressant citalopram influences amyloid-beta (Abeta) production in mice and humans. Although the peptide is also created in normal brains, AD patients have increased Abeta levels, which lead to the formation of brain plaques that have been associated with memory issues and cognitive impairment.

Over a 28-day period, the investigators used 2-photon imaging on mice that were treated with citalopram. Additionally, the researchers prescribed a single dose of either citalopram or placebo to 23 human patients aged 18-50 years without cognitive impairment or depression, and then extracted samples of the patients’ cerebrospinal fluid (CSF) within the next 24 hours.

At the conclusion of the trials, the investigators discovered citalopram decreased Abeta production in both mice and humans. In mice, the drug was responsible for stopping preexisting brain plaque growth and reducing the prevalence of new plaque by 78%, and in human subjects, Abeta production dropped by 37% in the CSF of those who received citalopram.

Although the investigators said their findings aid in understanding brain plaque development in AD patients, they cautioned against prescribing antidepressants based solely on the results.

“While antidepressants generally are well tolerated, they have risks and side effects,” senior author John Cirrito, PhD, said in a statement. “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.”

In the future, the investigators intend to study a possible association between serotonin and Abeta on a molecular level in mice. They also plan to observe older patients treated with antidepressants for 2 weeks.

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