The outcome of a new study on a common antidepressant is pointing to the possibility of it preventing Alzheimer’s disease also known as dementia, which is not medically known to have a cure, but worsens as it progresses until it leads to death.
The study, published in Science Translational Medicine, included people and mice, found that the selective serotonin re-uptake inhibitor (SSRI) citalopram (Celexa) stopped growth of amyloid beta, a brain peptide that clumps into the plaques believed to trigger Alzheimer’s.
According to the lead author of the study, Yvette Sheline, Professor of Psychiatry, Radiology and Neurology and Director of the Centre for Neuromodulation in Depression and Stress, at University of Pennsylvania’s Perelman School of Medicine, “The study isn’t evidence that this drug can slow Alzheimer’s disease, but it’s an exciting first step towards greater understanding of the capabilities of SSRIs, which offer promise as preventive measures”.
Currently, Alzheimer’s ranks as the sixth-leading cause of death in the US and the rates of the disorder are expected to more than triple over coming decades, unless a way to prevent it is discovered.
Since Alzheimer’s symptoms begin about 15 years after plaques start to form, says Dr. Sheline, “the hope is that early treatment could slow or even prevent the disease.”
However, it’s too soon to tell if antidepressants can ward off the much-feared disorder, the doctor adds. Here’s a closer look at the research.
The study is the first to identify a previously unknown effect of citalopram, which was approved by the FDA in 1998 for treatment of depression.
While the drug typically takes a few weeks to help relieve depression, the researchers discovered that it has an immediate – and significant – effect on amyloid beta, says Dr. Sheline.
In the double-blinded controlled study, 23 healthy adults, ages 18 to 50, who had no previous history of antidepressant use, received the drug. Compared to people who took a placebo, those treated with citalopram had a 38 percent lower level of amyloid beta in their cerebrospinal fluid, which was tested hourly over a 37-hour period.
In a parallel study with mice that are genetically predisposed to develop brain plaques, treatment with the drug reduced levels of the peptide by 25 per cent, compared to baseline levels.
In addition, over a two-month period, the treated mice had no new growth of plaques, compared to a control group of mice given sugar water.
The research builds on a 2011 study by Dr. Sheline and colleagues linking antidepressant use to reduced amyloid levels in the brains of elderly volunteers.
“That was an astonishing discovery, since depression is a risk factor for developing Alzheimer’s,” says Dr. Sheline. In that retrospective study, the team analysed PET scans of the brains of 186 cognitively normal adults with late-life depression.
During the analysis, the researchers didn’t know which volunteers had taken antidepressants. After the results were un-blinded, the team found that volunteers who had taken citalopram during the previous five years had significantly less plaque development, compared to people who hadn’t taken the drug.
What’s more, the longer the volunteers had been treated with the antidepressant, the fewer plaques they had. The researchers also found that mice genetically predisposed to develop Alzheimer’s had a 50 per cent reduction in brain plaques if they were treated with the drug, compared to mice given sugar water.
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