Exposure to the banned pesticide DDT may play a role in the development of Alzheimer disease, results of a small case-control study suggest.
Levels of the main metabolite of DDT, dichlorodiphenyldichloroethylene (DDE), were 3.8-fold higher among individuals with an Alzheimer disease diagnosis than controls, Jason R. Richardson, PhD, of Rutgers Robert Wood Johnson Medical School in Piscataway, N.J., and colleagues reported in JAMA Neurology.
The researchers enrolled two cohorts from the University of Texas Southwestern Medical Center in Dallas and Emory University in Atlanta from 2002 to 2008. Participants had blood samples taken and researchers categorized them as having Alzheimer disease or being cognitively normal based on NINCDS-ADRDA Alzheimer’s Criteria.
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On average, DDE serum levels among the 86 individuals with an Alzheimer diagnosis were 2.64 ng/mg (SE 0.35) compared with 0.69 ng/mg in 79 controls (SE 0.1; P<0.001).
When the researchers compared Alzheimer cases to controls based on tertiles of serum DDE levels, participants in the highest tertile had nearly quadruple the risk of having an Alzheimer disease diagnosis than those in the lowest tertile (odd ratio 4.18; 95% CI: 2.54-5.82).
Furthermore, mean scores on the 30-point Mini-Mental State Examination (MMSE) were 1.605 points lower in the highest DDE serum tertiles versus the lower tertiles (95% CI: 0.114-3.095), the researchers found.
Although previous researchers have hypothesized that environmental factors may play a role in Alzheimer risk, there have been no leads on specific areas on which to focus.
“Richardson and colleagues have provided both a wake-up call to explore environmental influences and pointed us to a first area to assess — pesticides, which have already been implicated in other human illnesses,” Steven DeKosky, MD, of the University of Virginia in Charlottesville, and Sam Gandy, MD, PhD, of the Mount Sinai Alzheimer’s Disease Research Center in New York City, wrote in an accompanying editorial.
The researchers proposed a potential mechanism of action for DDT/DDE exposure and increased Alzheimer risk, noting that human neuroblastoma cells exposed to either DDT or DDE in in vitro strudies had higher secretions of amyloid precursor protein. Amyloid precursor protein is a considered the parent of beta-amyloid proteins, which cause the characteristic plaques in the brain associated with Alzheimer disease.
One study limitation was that the association between DDE and Alzheimer disease risk was not statistically significant when the two study cohorts were anlyzed separately, but only after the data were pooled.
Dekosky and Gandy called for more studies examining the role of environmental factors in Alzheimer disease.
“The time has arrived to direct resources toward the formation of collaborative teams of epidemiologists, toxicologists, geneticists and dementia researchers,” they wrote.
