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Issue 47
, 2014
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DDT, other Environmental Toxins Linked to Late-Onset Alzheimer’s Disease

Source: Scientific American, Date: , 2014

Scientists suspect that, along with genetic factors, toxins and pollutants may increase the risk of developing this debilitating disorder

Alzheimer’s disease is now the sixth leading cause of death in the U.S., but researchers still do not know what causes the degenerative neurological disorder. In recent years they have pinpointed several genes that seem largely responsible for those cases in which the disorder develops early on, prior to age 60. They have also identified about 20 genes that can increase or decrease risk for the more common late-onset variety that starts appearing in people older than 60.But genetics simply cannot explain the whole picture for the over five million Americans with late-onset Alzheimer’s. Whereas genetics contribute some risk of developing this version of the disorder, no combination of genes inevitably leads to the disease.
Scientists are now urgently searching for the other missing pieces to explain what causes late-onset Alzheimer’s. Some researchers have shifted their attention from genes to the environment—especially to certain toxins. Their studies of pesticides, food additives, air pollution and other problematic compounds are opening a new front in the battle against this devastating malady. Here’s a roundup of some of the possibilities being studied:
DDT (dichlorodiphenyltrichloroethane)

Scientists have already found a strong potential link between pesticides and Parkinson’s disease. Now, a preliminary study released in January suggests that the pesticide DDT, which degrades so slowly that it continues to linger in the environment more than 40 years after the U.S. Environmental Protection Agency banned its use in the U.S., may also contribute to Alzheimer’s.
Jason Richardson and his team at Rutgers University tested blood samples of people with and without late-onset Alzheimer’s. They
found that most participants with the disease had levels of DDT and DDE (a metabolite of DDT) four times greater than the control group. Researchers also observed that participants with the most severe cases of Alzheimer’s had both a genetic predisposition and high pesticide blood levels, indicating that DDT/DDE may interact with genes to trigger the disease.
Richardson doesn’t have a definitive mechanism for how DDT exposure might lead to Alzheimer’s, however. But he speculates that DDT/DDE somehow encourage growth of the amyloid proteins that make up the plaques associated with the disease. He emphasized that his study is preliminary and his results will have to be replicated by future research on a larger scale.
In addition, some of the findings seem to contradict the study’s main conclusion. “The people I find most interesting are the ones who have really high levels of DDT and DDE, but don’t have Alzheimer’s,” Richardson says, “Maybe we’re a little early on those guys and they’ll ultimately end up with the disease. Or what would be more interesting is if their genetic makeup or lifestyle protects them from the disease.”

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