MONDAY, July 10, 2006 (HealthDay News) -- Measuring levels of a protein in the cerebrospinal fluid of middle-aged adults at high genetic risk for Alzheimer's disease may reveal early signs of disease development, U.S. researchers report.
A team from the University of Washington, Seattle, noted that aging, plus the presence of a copy of a gene called apolipoprotein E*4 (APOE*4) are the two strongest known risk factors for Alzheimer's. People with APOE*4 develop clinical dementia about 10 to 15 years earlier than people without this particular allele (copy).
Previous research had found that Alzheimer's-related plaques in the brain begin forming years before a person shows any symptoms of the disease. These plaques are made of proteins called beta-amyloids, predominately a type known as "A beta 42." As these proteins clump together into plaques, there are fewer circulating through the nervous system.
According to the researchers, this means that lower levels of A beta 42 in the cerebrospinal fluid surrounding the brain and spinal cord are an indicator of the development of Alzheimer's disease.
The study, published in the July Archives of Neurology, included 184 adults, average age 50 years, who had no symptoms of Alzheimer's disease. Researchers checked each participant for the APOE*4 allele and took samples of cerebrospinal fluid to check their levels of A beta 42.
People who were older and had the APOE*4 allele were more likely to have lower levels of A beta 42 than people without the APOE*4 allele. The researchers concluded that people with the APOE*4 allele experienced a slight decline in A beta 42 in their younger years and then a dramatic decline between 50 and 60 years old.
Those without the APOE*4 allele have a slight increase in A beta 42 levels until age 50, and then experience a gradual decline in those levels.
"In persons with the APOE*4 allele, decline in cerebrospinal fluid A beta 42 concentration possibly begins in young adulthood, followed by marked acceleration of this decline beginning in midlife-decades before clinical manifestation of Alzheimer's disease," the study authors wrote.
"These findings have implications for the preclinical diagnosis of Alzheimer's disease, as well as for treatment," they added. "Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid deposition. Primary prevention trials for Alzheimer's disease targeting elderly persons may [already] be too late to affect the early stages of disease pathology."
The U.S. National Institute on Aging has more about Alzheimer's disease.