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MONDAY, Jan. 27, 2014 (HealthDay News) -- Exposure to the banned pesticide DDT appears to increase a person's risk of Alzheimer's disease, a new study reveals.
Blood drawn from a small sample of Alzheimer's patients contained nearly four times greater levels of a DDT byproduct than blood taken from a group of healthy people, researchers found.
Exposure to DDT appears to promote the development of amyloid beta plaques, which clog the neurons of Alzheimer's patients and are suspected to be a cause of the disease, said study author Jason Richardson, an assistant professor of environmental and occupational medicine at Rutgers-Robert Wood Johnson Medical School in New Jersey.
The pesticide also might further increase Alzheimer's risk for people who already have a genetic predisposition toward developing the degenerative disease, Richardson said.
People scored significantly lower on logic and reasoning tests if they had high levels of the DDT byproduct and an Alzheimer's-prone version of the apolipoprotein E (ApoE) gene, compared with people who had similarly high levels of DDT but no genetic risk.
However, Richardson added that it's too soon to tell if the pesticide and the faulty gene have some sort of interaction or simply pose their own individual risk for Alzheimer's.
"They may just act separately, or they may converge. We don't know yet," he said of the two risk factors. "If both were on board, you did worse than if you had only one of them."
U.S. officials banned DDT in 1972 due to concerns over the pesticide's effect on wildlife, especially birds. Since the 1940s, it had been used extensively in agriculture and for mosquito control.
A worldwide ban on DDT use in agriculture has been in effect since 2004, but it has lingered in the environment and it is still in limited use in foreign countries where mosquitos carry malaria and other infectious diseases.
This research, published online Jan. 27 in JAMA Neurology, grew out of earlier research in which Richardson and colleagues linked the banned pesticide beta-hexachlorocyclohexane (beta-HCH) to Parkinson's disease.
That earlier study also contained a small sample of Alzheimer's patients, Richardson said. Those patients did not have elevated levels of beta-HCH but they did have higher levels of a byproduct of DDT called DDE. The researchers decided to go back and look into a possible link between DDT and Alzheimer's.
This new research is based on blood samples drawn from 86 Alzheimer's patients between 2002 and 2008.
Even though DDT has been banned for decades, it still turns up in human blood samples due to its long half-life, the authors noted. DDE can remain in a person's body for up to a decade, and despite the ban people still are exposed to DDT through imported food or contamination that remains in United States soil and waterways.
Researchers found that people with Alzheimer's disease had 3.8 times the level of DDE in their blood when compared to healthy people.
The investigators further found that people with DDE levels in the top third of the sample had four times the risk of developing Alzheimer's.
The team did some follow-up lab research involving human brain cell cultures to investigate possible explanations for the link. They found that when they exposed the cells to DDE for 48 hours, levels of a protein linked to beta amyloid plaques increased by nearly 50 percent.
"Levels of DDE that correspond to that of people who are highly exposed increases the levels of a protein associated with the plaques that build up in the brains of people with Alzheimer's," Richardson said.
People who want to limit their exposure to DDT should avoid eating fish caught in contaminated waterways and be careful eating food grown or raised in countries where the pesticide is still used to control mosquitos.
While the results are interesting, the study's small sample makes it difficult to draw any firm conclusions about the link between DDT exposure and Alzheimer's disease risk, said Heather Snyder, director of medical and scientific operations for the Alzheimer's Association.
"This requires further study, but it does give us valuable information that will help better ask future research questions," Snyder said. "It gives us some good reasons that we as a field should explore elements in the environment that could influence Alzheimer's risk."
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SOURCES: Jason Richardson, assistant professor, environmental and occupational medicine, Rutgers-Robert Wood Johnson Medical School, Piscataway, N.J.; Heather Snyder, director, medical and scientific operations, Alzheimer's Association, Chicago; Jan. 27, 2014, JAMA Neurology, online
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