Blood Levels of Beta Amyloid May Predict Cognitive Decline
Accumulation of beta-amyloid protein fragments in the brain is one of the characteristic features of Alzheimer’s disease. Currently, definitive evidence of these plaques can only be detected upon autopsy. A focus area of Alzheimer’s research today is finding other biomarkers that can detect the disease earlier in its process, before symptoms such as memory loss begin to occur.
Kristine Yaffe MD, of the University of California San Francisco, and colleagues studied the relationship between plasma (blood) beta-amyloid accumulation and cognitive decline in 997 older adults (average age 74 years) registered in the Health ABC study, a prospective observational study that initially began in 1997-1998, and who were dementia-free at enrollment.
Beta-amyloid is a short peptide consisting of about 40 amino acids. While A-beta40 is the most prominent peptide, A-beta42 is the neurotoxic form and the main component of senile plaques. Together, the A-beta42/A-beta40 ratio – also called beta amyloid 42/40 - is thought to be a predictive biomarker for cognitive impairment and eventual Alzheimer’s disease.
Dr. Yaffe and her team found that low beta-amyloid 42/40 levels was strongly associated with a cognitive decline over a period of nine years. Plasma beta-amyloid 40 was also strongly associated.
The researchers also studied the effects of “cognitive reserve”, or levels of education and literacy that may contribute to prevention of cognitive decline. Those with less education (below high school graduate) or who were less literate (equal to sixth grade or below) had a lower beta-amyloid 42/40 levels and a higher risk of developing dementia.
"To identify those at risk of dementia, biomarkers like plasma beta-amyloid levels that are relatively easy to obtain and minimally invasive could be useful. In addition, our finding of an interaction of cognitive reserve with the association of plasma beta-amyloid level and cognitive decline could have public health importance because it may suggest pathways for modifying beta-amyloid effects on cognition," the authors of the study conclude.
Source: JAMA. 2011;305:261-266.