Up to 47 Million Americans May Have Brain Amyloidosis the Finding That Defines Preclinical AD, Study Estimates

By Sullivan, Michele G. | Clinical Psychiatry News, January 2018 | Go to article overview

Up to 47 Million Americans May Have Brain Amyloidosis the Finding That Defines Preclinical AD, Study Estimates


Sullivan, Michele G., Clinical Psychiatry News


A treatment that would cut the risk of developing amyloid plaques in the brain by 50% could save more than 4 million U.S. residents from mild cognitive impairment and 2.5 million from Alzheimer's disease by 2060.

The conclusion that even modestly effective preventive therapy could vastly improve the Alzheimer's outlook is especially important given another startling finding in a new mathematical modeling study by Ron Brookmeyer, PhD, and his colleagues: Right now, they assert, almost 47 million cognitively normal people in the United States may have brain amyloidosis, the physical finding used to define preclinical Alzheimer's disease.

The study, published online in Alzheimer's & Dementia, is the first to quantify the number of cognitively healthy U.S. residents who could eventually experience cognitive changes that put them on the path to Alzheimer's dementia, according to a statement released by the Alzheimer's Association.

This is the first major attempt to forecast how many people will have either preclinical Alzheimer's disease or mild cognitive impairment due to Alzheimer's, according to Dr. Brookmeyer. "If confirmed, these data provide essential information for public health planning, and for informing and guiding the public and private investment in Alzheimer's and dementia research. We need more research to confirm the findings from this model, and more Alzheimer's and dementia research that includes diverse populations."

In an interview, Dr. Brookmeyer, a biostatistician at the University of California, Los Angeles, attempted to put those numbers into perspective.

"I want to emphasize that of the 47 million with these Alzheimer's brain changes but without clinical symptoms, most will not progress to clinical disease during their lifetimes. In fact, perhaps only 1 in 7 will progress to full-blown dementia."

Nevertheless, the numbers are disturbing and represent a reality that must be confronted and managed proactively if at all possible, Dr. Brookmeyer said. "The numbers are what they are," he said. "They may sound alarmist, but I have every confidence in them. And they're important because they allow us to understand how many people could potentially benefit from treatment, at what point on the disease continuum it would be useful to implement treatment, and how those treatments could impact public health."

To carry out the modeling, Dr. Brookmeyer extrapolated from data in two prospective longitudinal cohort studies: the Mayo Clinic Study of Aging and one by Stephanie J. Vos, PhD, of Maastricht (the Netherlands) University

The Mayo study followed 1,541 cognitively normal older adults and provided data on the rate of transition from normal cognition to mild cognitive impairment (MCI). The study by Dr. Vos and her associates followed 353 subjects with MCI and brain amyloid and 222 with late MCI as they progressed. It's the largest prospective study of progression from MCI to AD that also contained data on baseline neurodegeneration and amyloid burden (Brain. 2015;138[5]:1327-38).

"These studies gave us the rates of transition from one state to another," Dr. Brookmeyer said. "For example; the Mayo study gave us rates of transition from normal to amyloidosis: 3% of normal 60-year-olds will convert to this state every year."

The Vos study, Dr. Brookmeyer said, determined rates of progression from MCI to Alzheimer's dementia, given two preclinical states: asymptomatic amyloid brain plaques alone, or plaques with evidence of neurodegeneration and cognitive signs. Both of these transitional states were first defined in 2011 in a joint paper by the Alzheimer's Association and the National Institute on Aging (Alzheimers Dement. 2011;7[3]:280-92). While acknowledging that the root causes of Alzheimer's are unknown, and probably multifactorial, the paper hypothesized a pathophysiologic time line beginning with a three-stage preclinical phase:

* Stage 1: Asymptomatic cerebral amyloidosis: amyloid-positive PET brain imaging with an amyloid-binding ligand and/or a cerebrospinal fluid assay with low amyloid-beta 42 in the presence of normal cognition. …

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