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Research finds clue that antidepressant may cut protein involved in Alzheimer's development

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WASHINGTON - Research shows a common antidepressant may cut production of one of the chief suspects behind Alzheimer's, a new avenue in the hunt for drugs to prevent the devastating brain disease.

It's far too early for anyone worried about dementia to try the drug citalopram, which sells as the brand Celexa — and comes with side effects.

"This is not the great new hope. This is a small step," cautioned Dr. Yvette Sheline of the University of Pennsylvania, who is leading the research with Dr. John Cirrito of Washington University in St. Louis.

Alzheimer's is characterized by sticky plaques that form in patients' brains 10 to 15 years before the first memory symptoms are noticed. Scientists have tried treatments to clear away those plaques, made of a protein named beta-amyloid that somehow goes awry and starts clumping together, but with no success yet.

Wednesday's study is a somewhat different approach, beginning to explore if it's possible to slow the plaque from building up by altering the body's production of amyloid.

First, researchers gave citalopram to older mice with Alzheimer's-like brain damage. The animals' existing plaques didn't go away but they quit growing — and dramatically fewer new plaques formed compared to mice given sugar water, the research team reported in the journal Science Translational Medicine.

Next, researchers gave a single dose of citalopram or a placebo to 23 healthy young adults, people who neither were depressed nor old enough to have brain plaques. Tests of the volunteers' spinal fluid over the next day and a half showed their normal amyloid production dropped by 37 per cent, the researchers reported.

It will take years of additional research to tell if that translates into any protective effect. Citalopram and similar drugs called SSRIs alleviate depression by affecting levels of the brain chemical serotonin; Sheline said citalopram probably alters amyloid production in a completely different way.

In fact, the next question is whether it's even possible to tamp amyloid production down for long periods or if the body would just get used to the drug and adjust. Sheline has begun enrolling healthy older adults into a study to see if using citalopram for two weeks has the same effect.

More than 5 million Americans already have Alzheimer's or related dementia, numbers expected to jump to 16 million by 2050 as the population ages. There is no cure, and today's medications only temporarily ease symptoms.

Scientists still don't know exactly what causes Alzheimer's. The leading theory is that those amyloid plaques somehow start the disease process but that it takes another abnormal protein, named tau, to push someone over the edge.

It's crucial to investigate ways to intervene in the years before symptoms arise, said Heather Snyder of the Alzheimer's Association, who wasn't involved in the new research.

Whether antidepressants pan out or not, the researchers are using an intriguing method of analyzing spinal fluid "that gives us new information that will open the door to further discoveries around Alzheimer's disease," she said.

Citalopram has been used to treat depression for nearly two decades, but it does have side effects and the Food and Drug Administration has warned that higher doses may trigger dangerous irregular heartbeats. Still, separate research published earlier this year suggested citalopram also might calm the agitation that people with advanced Alzheimer's can suffer.

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