An ongoing drug trial has linked higher levels of amyloid protein in the brain to early Alzheimer’s disease and functional decline.

Study participants were chosen based on the results of amyloid positron emission tomography imaging. About 1,300 fit the eligibility profile: high levels of amyloid beta, but no clinical signs of Alzheimer’s disease. These study subjects underwent cognitive testing, clinical assessments and genotyping.

Data analysis revealed that more amyloid deposits are linked not only to early Alzheimer’s, but also to family history of the disease, lower cognitive test scores, and self-reported declines in daily cognitive function, wrote lead author Reisa A. Sperling, M.D., from Brigham and Women’s Hospital and Harvard Medical School. 

The screenings were part of the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease study, launched in 2014 to test the effects of the drug solanezumab. The study is expected to be completed in late 2022. Solanezumab has failed in past trials in people with mild dementia and Alzheimer’s. It is currently being studied in people with a certain genetic risk factor, and in the current study of people with no memory loss, but evidence of amyloid beta buildup.

“[P]revious trials may have been intervening too late in the disease process to be effective,” said Richard J. Hodes, M.D., director of the National Institute on Aging, which funded the study. “A4 is pioneering in the field because it targets amyloid accumulation in older adults at risk for developing dementia before the onset of symptoms.”

“Alzheimer’s disease is never going to have a one-size-fits-all treatment,” concluded Sperling. “We’re likely to need different treatments, even combinations of therapies, for different individuals based on their risk factors.”

Amyloid proteins are seen as a hallmark of Alzheimer’s disease.

The study was published online Monday in JAMA Neurology.