It was a bit of a mystery to the scientists investigating the phenomenon: a brain disease driven by the death of specialized neurons was strongly linked to exposure to a particular pesticide. Why, then, didn’t exposing those same neurons directly to that same pesticide seem to affect them?
Parkinson’s disease (PD) is a neurodegenerative disease of aging, whose most obvious symptoms — tremors, gait disorders, and a “mask-like” facial appearance — involve the loss of fine motion control. These symptoms are the result of the loss of specialized cells in an area of the brain called the substantia nigra pars compacta (SNc) that specialize in producing the chemical signal-molecule dopamine and are responsible for turning off excess firing of neurons that control muscles. Once a critical number of these “dopaminergic” SNc neurons are lost, the unbalanced firing of those neurons begins to manifest itself in the main motion-related symptoms of the disease.
In all but a few people with rare mutations, degenerative aging processes (such as the accumulation of mitochondrial mutations in SNc neurons) are primarily responsible for the disease. But lifestyle and environmental factors also damage these neurons, and thus increase the risk of a person developing the disease clinically within a currently-normal
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