Washington, May 15 (IANS) A commonly prescribed antidepressant may reduce production of a brain protein related to the development of Alzheimer's disease, showed a new US study conducted in mice and healthy people.
Although the findings are encouraging, the researchers cautioned that it would be premature for people to take antidepressants solely to slow the development of the disorder, according to Xinhua.
Alzheimer's is characterised by the buildup of amyloid beta, a protein that accumulates in the brains of those with the disease. The accumulated clumps of amyloid beta are known as plaques, which are tied closely to memory problems and other cognitive impairments. Plaques also are sometimes present in cognitively normal brains.
In the new study, researchers at the Washington University and the University of Pennsylvania found antidepressant citalopram can reduce amyloid beta production by an average of 25 percent within two days in a mouse model of Alzheimer's disease.
In addition, giving the mice the antidepressant stopped the growth of existing plaques and reduced the formation of new plaques by 78 percent.
In a second experiment, 23 healthy people aged 18-50 who were not cognitively impaired or depressed, were administered 60 mg citalopram, roughly equivalent to the dose used in mice.
Samples of spinal fluid taken from the participants over the next 24 hours showed a 37 percent drop in amyloid beta production.
"Antidepressants appear to be significantly reducing amyloid beta production, and that's exciting," said senior author John Cirrito, assistant professor of neurology at the Washington University.
"But while antidepressants generally are well tolerated, they have risks and side effects. 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," Cirrito said.
The researchers next planned to test the effects of citalopram on amyloid beta production in individuals 65 and over.
The findings were published Wednesday in the US journal Science Translational Medicine.