DDT, one of the once most popular pesticides, was banned some time ago due to its harmful effects on human health. This measure contributed, inter alia, to the development of Alzheimer’s disease. Now scientists have managed to figure out how this happens. The research results were published in the journal Environmental Health Perspectives.
- DDT was first used to control insects in 1939
- In the 70s, many countries banned its use, in Poland it began to be withdrawn in 1976.
- This agent is possibly carcinogenic and may cause Alzheimer’s disease
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DDT – what does it do?
DDT (Dichlorodiphenyltrichlorethane) is an insecticide that has historically been widely used around the world to combat malaria and lice, and to protect plants.
The insecticidal effect of DDT was discovered by the Swiss professor Paul Hermann Mueller, for which he was awarded the Nobel Prize in Medicine and Physiology in 1948. This pesticide was discontinued after it was found to have serious side effects.
Although the use of DDT was banned in most countries decades ago, it is still circulating in the environment and its amount is slowly declining. It accumulates in living organisms, and its effects are observed in the next generations. It is still found, for example, in breast milk. The data published in 2001 show that DDT adversely affects, for example, the development of children. DDT metabolites affect, inter alia, on the endocrine system and increase the risk of breast cancer.
People who were particularly vulnerable to DDT between the 40s and 70s are already at or near an increased risk of developing Alzheimer’s disease. This substance is also constantly circulating in food chains.
DDT a Alzheimer
Researchers from Florida International University (FIU) conducted new research on the effects of DDT. As already demonstrated in 2014, the team of prof. Jason Richardson, DDT pollution increases the amount of toxic beta-amyloid that forms the characteristic amyloid plaques found in the brains of people with Alzheimer’s disease.
Now, FIU researchers have data that may explain the link between DDT and amyloid plaques. They used cell cultures, transgenic flies, and mouse models to demonstrate the effects of DDT on the amyloid pathway that characterizes Alzheimer’s disease. By subjecting all models to DDT – to the extent to which humans were exposed decades ago – scientists observed an increase in amyloid precursor protein production as well as elevated levels of toxic amyloid variants.
A study in collaboration with Rutgers University focused on sodium channels that the nervous system uses to communicate between brain cells (neurons). DDT keeps these channels open, leading to increased neuronal excitation and enhanced release of beta-amyloid peptides. As has been shown, when neurons are exposed to tetrodotoxin, a sodium channel blocker in the brain, this prevents increased production of amyloid precursor and toxic beta-amyloid variants.
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DDT affects the brain
The new discovery could help develop early detection methods and potential therapies for people at high risk of the pesticide.
– The vast majority of research on Alzheimer’s disease is concerned with genetics. Genetics are very important, but the genes that actually cause the disease are very rare, says Prof. Richardson. – Environmental risk factors such as exposure to DDT can be modified. So if we understand how DDT affects the brain, perhaps we could target these mechanisms and help people who were particularly vulnerable, she adds.
“We found that if we block sodium channels with tetrodotoxin and then act on DDT neurons, amyloid precursor protein levels do not rise, and no excess beta-amyloid is released,” Richardson says.
The next step will be to test potential drugs – several substances that act on sodium channels are already known. Tetrodotoxin is widely known as a deadly poison – it is its inaccurate removal that makes fugu fish served in Japanese restaurants deadly poisonous. On the other hand, trace amounts of this poison, acting on the nerve endings, give the dish a special taste.
– We are currently conducting research whether we can take a drug already approved by the FDA and check whether it reduces the accumulation of toxic amyloid – noted Prof. Richardson.
Author: Paweł Wernicki.