Alzheimer’s Detection May Occur Earlier Than Ever

Discovering Alzheimer’s disease early is critical to slowing down the progression of memory loss and cognitive decline. For years, scientists have been searching for new methods or clues to identify those brain changes in people. The hope is not only that they might be able to stop the destructive protein that causes Alzheimer’s, but possibly even reverse the damage.

Which is why researchers at Washington University School of Medicine in St. Louis hope they’re onto something.

The compound could be used in brain scans to identify the signs of early-stage Alzheimer’s disease or to monitor response to treatment.

They’ve developed a chemical compound, named fluselenamyl, that detects amyloid clumps better than current Food and Drug Administration-approved compounds, according to a new report. If a radioactive atom is incorporated into the compound, its location in a living brain can be monitored using positron emission tomography (PET) scans.

The compound, they believe, could potentially be used in brain scans to identify the signs of early-stage Alzheimer’s disease or to monitor response to treatment. Their findings are outlined in the latest issue of Scientific Reports.

“Fluselenamyl is both more sensitive and likely more specific than current agents,” said Vijay Sharma, Ph.D., a professor of radiology, neurology, and biomedical engineering, and the study’s senior author, in a statement. “Using this compound, I think we can reduce false negatives, potentially do a better job of identifying people in the earliest stages of Alzheimer’s disease, and assess the effects of treatments.”

Amyloid plaques are one of the telltale findings in the brains of people with Alzheimer’s disease. The neurons near such plaques are often dead or damaged, and this loss of brain cells is thought to account for difficulty with thinking, memory loss, and confusion experienced by Alzheimer’s patients.

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“A huge obstacle with existing state-of-the-art PET agents approved for plaque detection is that they tend to bind indiscriminately to the brain’s white matter, which creates false positives on the scans,” Sharma said. Nonspecific binding to other parts of the brain creates “noise,” which makes it difficult to distinguish samples with plaques from those without.

Amyloid plaques can be either diffuse or compact. The compact kind has long been associated with the disease, but conventional wisdom has held that diffuse plaques are benign, since they can be found in the brains of elderly people without any symptoms of Alzheimer’s disease, as well as the brains of those with Alzheimer’s. Sharma believes diffuse plaques may mark the earliest stages of the disease — and fluselenamyl bound to such proteins two to 10 times better than each of the three FDA-approved imaging agents for detecting amyloid beta.

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In other words, fluselenamyl detected much smaller clumps of the protein, indicating it may be able to detect the brain changes associated with Alzheimer’s disease earlier.

Sharma already has submitted an application to the National Institutes of Health (NIH) for a phase 0 trial, to establish whether fluselenamyl is safe for use in humans and behaves in the human body the same way it behaves in mice.