Hardeep S Puri

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Hardeep S Puri

Further proof of link between pesticides and Parkinson’s uncovered

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Researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research by neurologists at UCLA suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain.

When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms — including tremor, rigidity, and slowed movements and speech — increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra.

This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.

While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.

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