By the time someone begins to experience the clinical symptoms of Alzheimer’s disease, the damage has already been done. An accumulation of toxic proteins is causing brain cells to whither and die, taking with them a lifetime of precious memories.

But what if we had a definitive test that could predict one’s risk of developing Alzheimer’s, even before the onset of symptoms? Could we use it to develop an early-detection method and—even more importantly—a way to slow or halt the disease before it is too late?

While this may seem closer to fiction than reality, scientists from the Western University of Health Sciences are reporting that they’ve done just that: a simple blood test that can accurately predict one’s Alzheimer’s risk—up to ten years before symptoms begin to develop.

Reporting in the latest issue of Translational Psychiatry, senior author Dr. Doug Ethell and his research team describe their ingenious method of tracking the earliest stages of Alzheimer’s via a simple blood test.

Their test, called the CD4see assay, tracks the body’s early immune response to toxic proteins—called amyloid beta proteins—that accumulate and form harmful plaques in the brains of Alzheimer’s patients.

Ethell has long been studying how a class of immune cells, called T cells, responds to the buildup of amyloid beta. Previously, he showed that these so-called amyloid beta-specific T cells could actually counter the cognitive decline seen in Alzheimer’s. So, lower amyloid T cell levels should correlate with symptoms. As he explained in an interview:

“If our mouse studies were correct, then there should be fewer of those cells in Alzheimer’s patients. Translating those studies from mouse to man was going to take a big effort—characterizing the small proportion of T cells that respond to amyloid-beta from the millions of other kinds of T cell would require technology that didn’t exist yet.”

So Ethell turned to stem cells. With support from CIRM, Ethell and his team took human embryonic stem cells (hESCs) and developed a type of immune system cell called dendritic cells. These cells stimulated the growth of amyloid-beta T cells—effectively bringing them out of hiding and allowing the researchers to locate and count them.

“Everyone showed a decrease in these T cells as they aged, but the decline occurred earliest in women with the apoE4 gene (the single greatest genetic risk factor for Alzheimer’s), often right around the same time as menopause,” explained Ethell. “When our raw data was pasted on foam boards all over my office it seemed to us that older women had lower responses than men, and when the data was finally plotted the dramatic decline around menopause was clear.”

Interestingly, this observation seems to correlate with the fact that Alzheimer’s is more prevalent in women than in men.

Ethell and his team propose that the CD4see assay could soon be used to measure amyloid-beta-specific T cells against one’s age, sex and whether they carry apoE4. This could then be used to calculate the individual’s risk for developing Alzheimer’s symptoms in the future.

This assay could also prove helpful when looking to test new therapeutic strategies that treat early-stage Alzheimer’s—something that has proven difficult without a reliable early detection method.

“Alzheimer’s disease is a puzzle and every bit of knowledge adds a new piece,” added Ethell. “We now view Alzheimer’s disease very differently than we did even just a few years ago.”