Inflammation may contribute to Alzheimer’s disease
By Will Boggs
Wed Jun 6, 2007
NEW YORK (Reuters Health) – People with high levels of inflammatory markers are more likely to develop Alzheimer’s disease than those who do not, according to a report in the Neurology.
“Physicians should take our research findings as further evidence of the involvement of inflammation in the pathogenesis of Alzheimer’s disease,” Dr. Zaldy S. Tan from Harvard Medical School, Boston, told Reuters Health. The findings can be used to develop strategies to “advance research in Alzheimer’s disease diagnosis and treatment.”
Tan and associates compared the relationship between proteins produced by the immune system to generate an inflammation response and the risk of developing Alzheimer’s disease in 691 men and women without dementia who were living in the community.
The participants were 79 years old on average. During an average follow-up of 7 years, 44 subjects developed Alzheimer’s disease and 262 died.
Higher levels of interleukin-1 were associated with more than a twice the risk of developing Alzheimer’s disease, the authors report, and individuals with the highest production of tumor necrosis factor-alpha were 30 percent more likely to develop Alzheimer’s disease than those with the lowest production of tumor necrosis factor-alpha.
Subjects with highest levels of both interleukin-1 and tumor necrosis factor-alpha had a 61 percent greater risk of developing Alzheimer’s disease than did individuals with the lowest levels, the investigators found.
However, neither C-reactive protein nor interleukin-6 levels were related to the risk of Alzheimer’s disease.
Higher production of a blocker of interleukin-1, call interleukin-1 receptor antagonist, was not associated with a significantly lower risk of developing Alzheimer’s disease, the results indicate.
“These data strengthen the evidence for a pathophysiologic role of inflammation in the development of clinical Alzheimer’s disease,” the researchers conclude.
“There are still many unanswered questions in Alzheimer’s disease research, and information such as this can help get us closer to finding the answers,” Tan said.
SOURCE: Neurology May 29, 2007.

