New research shows that a common antidepressant may cut production of one of the chief suspects in the investigation of Alzheimer’s disease. These findings open 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 citalopram, which is sold as Celexa. “This is not the great new hope. This is a small step,” cautioned Yvette Sheline of the University of Pennsylvania, who is leading the research with John Cirrito of Washington University in St. Louis.

Alzheimer’s is characterized by sticky plaques that form in the brain 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.

The latest study involves a somewhat different approach, exploring whether it’s possible to slow the plaque buildup by altering the body’s production of amyloid.

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

Next, the researchers gave a single dose of citalopram or a placebo to 23 healthy young adults, people who were neither 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 percent, the researchers reported.

It will take years of additional research to tell whether that translates into any protective effect. Citalopram and similar drugs called selective serotonin reuptake inhibitors, or 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 to study the effect of using citalopram for two weeks.

More than 5 million Americans have Alzheimer’s or related dementia; that number is expected to jump to 16 million by 2050. There is no cure; today’s medications only temporarily ease symptoms.

Scientists 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 important to investigate ways to intervene in the years before symptoms arise, said Heather Snyder of the Alzheimer’s Association, who was not 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 this year suggested that citalopram also might calm the agitation that people with advanced Alzheimer’s can suffer.