Organochlorine pesticides, which persist in the environment and accumulate in fatty tissues, have been evaluated for their potential role in endocrine disorders, cancers, and neurodegenerative diseases—including Alzheimer’s disease (AD). Perhaps the best known organochlorine pesticide is DDT (dichlorodiphenyltrichloroethane); however, its lesser known cousin, DDE (dichlorodiphenyldichloroethylene), also gives rise to health concerns. Besides being present in commercial DDT formulations, DDE is a long-lived breakdown product and metabolite of DDT.

DDE, when present in elevated amounts in blood, appears to be associated with an increased risk of AD. This sobering finding appeared in an article published January 27 in JAMA Neurology (“Elevated Serum Pesticide Levels and Risk for Alzheimer Disease”). The article also considered another dimension of DDE exposure—whether it has an effect on a previously established risk factor for late-onset AD. As it turns out, this risk factor—a particular variant of the apolipoprotein E4 (APOE4) gene—does appear to be relevant. According to the article, “carriers of an APOE4 ε4 may be more susceptible to the effects of DDE.”

The JAMA Neurology article was prepared by a team of researchers led by Jason R. Richardson, Ph.D., of the Rutgers Robert Wood Johnson Medical School and Environmental and Occupational Health Sciences Institute in Piscataway, NJ. After Dr. Richardson and his colleagues examined existing blood samples from 86 AD patients and 79 controls, they detected DDE in the blood of 70% of control and 80% of AD patients.

DDE levels were associated with increased risk for AD, with average levels 3.8 times higher in the blood of AD patients. Scores on a test of cognitive function (the Mini-Mental State Examination) were lower in the group with the highest levels of DDE who carried the ε4 version of the APOE gene compared with those carrying another version.

The DDE found in the blood samples could have had any of several origins, the researchers noted. For example, DDE could have come from food imported from countries where DDT is still used. Also, given DDE’s long half-life, the blood-borne DDE could have come from legacy contamination of soil and waterways in the United States.

Whatever its source, DDE is of abiding concern to Dr. Richardson and other scientists who explore the interactions between environmental exposures and genetic susceptibilities in the etiology of neurological disease. In the current study led by Dr. Richardson, a key goal was to identify a novel and specific biomarker of DDE exposure and disease for early detection of disease or dysfunction of the nervous system. According to this study, “Identifying people who have elevated levels of DDE and carry an APOE ε4 allele may lead to early identification of some cases of AD.”

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