Exposure to synthetic pesticide DDT may increase the risk of developing Alzheimer's disease, according to a new study.
Patients with Alzheimer's disease have significantly higher levels of DDE, the long-lasting metabolite of Dichlorodiphenyltrichloroethane (DDT), in their blood than healthy people, researchers have found.
In a case-control study involving 86 Alzheimer's patients and 79 healthy elderly controls, researchers found that DDE levels were almost four times higher in serum samples from Alzheimer's patients than in controls.
Having DDE levels in the highest third of the range in the study increased someone's risk of Alzheimer's by a factor of four.
"This is one of the first studies identifying a strong environmental risk factor for Alzheimer's disease," said co-author Allan Levey, director of Emory's Alzheimer's Disease Research Center.
"The magnitude of the effect is strikingly large - it is comparable in size to the most common genetic risk factor for late-onset Alzheimer's," said Levey.
Researchers led by Jason Richardson from Rutgers-Robert Wood Johnson Medical School, have also identified a plausible mechanism by which DDE and DDT have Alzheimer's-related effects on the brain.
Exposure of cultured neural cells to high concentrations of DDT or DDE - comparable to those seen in highly exposed humans - increases levels of the protein that is a precursor to beta-amyloid, the main component of plaques found in the brains of Alzheimer's patients.
DDT's half-life in the body is very long, between 8 and 10 years. Because of continuing exposure and long half-life, the DDE metabolite accumulates in tissues as people age.
This observation could help explain why age is by far the largest risk factor for Alzheimer's disease, Levey said.
DDE levels weren't the sole determinant of whether someone gets Alzheimer's; some Alzheimer's patients had non-detectable levels of DDE and some healthy control samples had DDE levels that were relatively high.
The researchers said that genetic risk factors may combine with environmental exposures to drive disease development.
The results appear in the journal JAMA Neurology.
