Study reveals mechanism linking DDT exposure to Alzheimer’s disease

A new study by researchers at Florida International University (FIU) reveals a mechanism linking the pesticide DDT to Alzheimer’s disease.

Posted in Environmental Health Perspectives, the study shows how the persistent environmental pollutant DDT causes increased amounts of toxic beta-amyloid, which forms the characteristic amyloid plaques found in the brains of people with Alzheimer’s disease.

According to Jason Richardson, a professor at CRF’s Robert Stempel College of Public Health & Social Work and corresponding author, the study further demonstrates that DDT is an environmental risk factor for Alzheimer’s disease. In 2014, he led a team of scientists from Rutgers University, Emory University and UT Southwestern Medical School who presented evidence linking DDT to disease. Now they have data demonstrating a mechanism that may explain the association.

The vast majority of disease research has focused on genetics – and genetics is very important – but the genes that actually cause the disease are very rare. Environmental risk factors such as DDT exposure are modifiable. So if we understand how DDT affects the brain, we might be able to target those mechanisms and help people who have been heavily exposed.”

Jason Richardson, professor at CRF’s Robert Stempel College of Public Health & Social Work

DDT was widely used between the 1940s and 1970s to control insect-borne diseases like malaria and to treat crop and animal production. People who were heavily exposed to DDT at the time are now starting or are already in the age group with a higher risk of developing Alzheimer’s disease. Although prohibited in the United States, exposure to DDT is likely possible today through inherited contamination or imported foods.

The study focused on sodium channels, which the nervous system uses to communicate between brain cells (neurons), as a potential mechanism. DDT causes these channels to stay open, resulting in increased firing of neurons and increased release of beta-amyloid peptides. In the study, the researchers demonstrate that if neurons are treated with tetrodotoxin, a compound that blocks sodium channels in the brain, increased production of amyloid precursor protein and toxic beta-amyloid species is prevented.

“This finding could potentially provide a roadmap for future therapies for people with high DDT exposure,” Richardson said.

The study was carried out in collaboration with Rutgers University.

The researchers used cultured cells, transgenic flies and mouse models to demonstrate the effect of DDT on the amyloid pathway, a hallmark of Alzheimer’s disease.

By exposing all models to DDT; in the range of what people were exposed to decades ago; the researchers observed increased production of the amyloid precursor protein, as well as elevated levels of toxic amyloid species, such as amyloid beta peptides and plaques.

“We found that if we block the sodium channels with the compound tetrodotoxin and then dose the neurons with DDT, they do not increase amyloid precursor protein and do not secrete excess beta-amyloid,” explains Richardson.

The next step for researchers will be to test therapeutic drugs using the information they know now. Richardson shares that there are already several drugs that target sodium channels.
“We’re doing these studies to see if we can take a drug that’s already FDA-approved and see if it reduces toxic amyloid buildup,” he adds.


Florida International University

Journal reference:

Aid, A. et al. (2022) Effects of DDT on amyloid precursor protein levels and beta-amyloid pathology: mechanistic links to Alzheimer’s disease risk. Environmental Health Perspectives.

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