Study explores effects of DDT exposure on Alzheimer’s risk

Researchers from Florida International University recently discovered a mechanism in the brain which linked the pesticide, dichlorodiphenyltrichloroethane, or DDT, to Alzheimer’s disease, which could lead to a more targeted approach to early detection and treatment for the condition.

The study, published in the journal, Environmental Health Perspectives, was led by Jason Richardson, PhD, a professor at Florida International University’s (FSI) College of Public Health & Social Work. Previous studies have shown an association between the DDT, a pesticide used in the 1940s and 1970s to combat insect borne diseases, and Alzheimer’s, but the exact details of the connection remained unclear, according to the study. For this investigation, Richardson and his team of researchers sought to better understand the mechanisms associated with DDT and Alzheimer’s.

"The vast majority of research on the disease has been on genetics—and genetics are very important—but the genes that actually cause the disease are very rare," Richardson said in a statement. “Environmental risk factors like exposure to DDT are modifiable. So, if we understand how DDT affects the brain, then perhaps we could target those mechanisms and help the people who have been highly exposed.”

The study’s researchers focused on sodium channels, a feature of the nervous system that allows brain cells to communicate. Previous research had shown that DDT causes these channels to remain open, increasing the firing of neurons and the release of amyloid-beta peptides. Using cultured cells, transgenic flies, and mice models, the study found that when neurons were treated with a compound that blocks sodium channels in the brain, tetrodotoxin, overproduction of the amyloid precursor protein and toxic amyloid-beta species, was prevented.

"We found that if we block sodium channels with the compound tetrodotoxin and then dose neurons with DDT, then they don't increase the amyloid precursor protein and don't secrete excess amyloid-beta," Richardson said.

For their future studies, Richardson and his team plan to test the efficacy of therapeutic drugs that target sodium channels.