Early detection remains to be a major challenge for experts and researchers studying dementia. But new research by Harvard University suggests the protein thought to cause Alzheimer’s, accumulates in the brain a decade or more before symptoms occur.
The findings give hope to researchers struggling to move beyond a rash of high-profile Alzheimer’s failures in clinical drug trials. Researchers are reconsidering their approach and wondering whether the problem is in trying to reverse, rather than prevent, dementia.
"I think we’ve failed in 11 phase 3 trials, which is not a good track record," said Reisa Sperling, a neurology professor at Harvard Medical School, a physician at Brigham and Women’s Hospital, and co-director of the Harvard Aging Brain Study at Massachusetts General Hospital (MGH). "From a clinical point of view, it’s a dismal failure."
Catch it Early
Now, the "catch it early" idea is being put to the test in a new study called A4, or Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease, led by Sperling and the University of Southern California’s Paul Aisen. Researchers will try an anti-amyloid drug on people who show no signs of cognitive decline, but who do have abnormally high levels of amyloid beta in their brains.
"It’s the first trial in a population we refer to as ’preclinical Alzheimer’s disease.’ We believe this is identifying an early stage of the disease, not just ’at risk’ [patients].... If we wait for people to have symptoms, there’s already substantial neuro-degeneration." said Paul Aisen, lead author of the study from the University of Southern California.
The A4 study rests on a foundation laid by the Harvard Aging Brain Study, which began in 2009 and is headed by Sperling and Keith Johnson, a professor of radiology at HMS and MGH. The study, which has funding to run through 2019, images the brains of 60- to 90-year-olds to follow changes over time.
The inflammation associated with the disease—part of the process of clearing amyloid and tau proteins from the brain, but itself destructive to tissue—amounts to another unanswered question, Sperling said. It’s possible that inflammation has to be reduced or avoided entirely to avoid cognitive damage. Another possibility is that Alzheimer’s is part of an underlying problem, an inability to handle waste proteins and, as Sperling put it, "empty the body’s protein garbage can." Potentially pointing to a broader problem is the fact that other neurodegenerative diseases, such as amyotrophic lateral sclerosis and Parkinson’s, are also related to abnormal protein accumulation.
Despite these questions, Sperling, Aisen, and Rentz agree that there’s a sense of hope in the Alzheimer’s community, a feeling that progress in several areas has put science on the verge of a breakthrough.
"I am very hopeful about the field in general," Aisen said. "There’s a number of promising therapies. I believe we’re going to be successful and I believe dramatically successful. This is an enormous world health problem and a major problem in this country’s health."
Should A4 fail, Sperling has a plan for trying to catch the disease earlier still. While A4 is targeting cognitively normal patients with high amyloid levels, she’s designing A3, which would test interventions on people age 60—or even 50—who are cognitively normal and whose amyloid levels have yet to rise.
Source of this article:
Plotting the demise of Alzheimer’s
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