Antidepressant May Reduce Amyloid Levels

Results from a new study published in Science Translational Medicine suggest that the antidepressant citalopram (Celexa™) may benefit people with Alzheimer’s disease. Scientists observed a drop in levels of beta-amyloid, one of the proteins suspected to cause the disease, in the spinal fluid of healthy volunteers after they took citalopram. The scientists also reported that citalopram stopped the growth of beta-amyloid plaques in preclinical animal studies, a promising finding that suggests the drug might slow disease progression. Prior research in mice and isolated human neurons found that citalopram stimulates the formation of new neurons in the hippocampus, the part of the brain responsible for memories that is greatly affected in Alzheimer’s disease.

Citalopram belongs to a class of antidepressant drugs called selective serotonin reuptake inhibitors (SSRIs), which function by increasing serotonin levels in the brain. A separate study published in February 2014 in the New England Journal of Medicine reported that citalopram improved symptoms of agitation in patients with Alzheimer’s disease. However, it remains unknown if citalopram has any impact on cognitive function or disease progression in people with Alzheimer’s. Past clinical trials with another SSRI, sertraline (Zoloft™), did not significantly improve cognition in Alzheimer's patients.

While these research findings are encouraging, much more work is needed to determine if citalopram or any other antidepressants will be viable treatments for Alzheimer’s disease. 

This website does not provide, and should not be used for, medical advice, diagnosis, or treatment. You should consult with your healthcare providers when making decisions regarding your health. Your use of this site constitutes your agreement to the Terms & Conditions.

Sign up for more information!

To stay connected with us, please provide your contact details below. We will share the latest Alzheimer's and related research news, along with information on our signature events.

Fill out my online form.
Go to top