The complement receptor-1 (CR1) gene has recently been linked with the risk of late-onset Alzheimer's disease. Researchers from the National Institute on Aging (NIA) at the National Institutes of Health have found that a variant in the gene, a single change in a single letter in the genetic code, affects the levels of beta amyloid, the protein that accumulates in the brain in Alzheimer's disease, in the brains of cognitively healthy older people.
The researchers looked at the brains of older people in the Baltimore Longitudinal Study of Aging (BLSA) and the Alzheimer's Disease Neuroimaging Initiative (ADNI), and found that having the variant form of the gene was actually linked with lower levels of beta amyloid, and this was statistically significant in some areas of the brain. The researchers also found that the gene variant interacted with APOE, a well-known genetic risk factor for Alzheimer's disease, and this had an effect on the levels of brain amyloid. The results were published in Biological Psychiatry.
"The prevailing hypothesis has implicated factors increasing beta amyloid in the brain as an integral element of Alzheimer's disease pathology," said NIA Director Richard J. Hodes. " This study indicates the importance of exploring and understanding other distinct mechanisms that may be at work in this disease."
According to lead author Madhav Thambisetty, chief of the Clinical and Translational Neuroscience Unit at the NIA, it could be "that the CR1 risk factor gene, if it contributes to Alzheimer's disease, does it in a way unrelated to increasing amyloid burden." Thambisetty suggests that the disease may be a result of multiple genetic risk factors in combination.
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