The death of brain cells in Parkinson's disease may be caused by an energy crisis that causes neurons in the brain to exhaust themselves, dying prematurely, says a new study.
"Like a motor constantly running at high speed, these neurons need to produce an incredible amount of energy to function. They appear to exhaust themselves and die prematurely," said lead researcher Louis-Éric Trudeau, a professor at the University of Montreal's Departments of Pharmacology and Neurosciences.
Parkinson's disease is a progressive neurological disease, causing tremors, stiffness, and slowing of movements, that affects more than 1 million Americans, more than the combined number diagnosed with multiple sclerosis, muscular dystrophy, and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease). There is no cure.
Unlike Alzheimer's, which affects billions of brain neurons, the main symptoms of Parkinson's are caused by the death of tens or hundreds of thousands of neurons in a few more restricted areas of the brain, including the substantia nigra.
The key to unraveling the mystery of Parkinson's may be mitochondria, the powerhouses that allow cells to grow and neurons to emit electrical signals and release their chemical messengers such as dopamine, noradrenaline, and acetylcholine.
For the past three years, Trudeau's research team carried out numerous experiments in order to identify why mitochondria in neurons of the substantia nigra area of the brain work so hard and apparently lead neurons to "overheat."
Trudeau's findings could lead to the creation of better animal models of Parkinson's disease and the identification of new treatment strategies.
"For some unknown reason, it has been incredibly difficult to reproduce the symptoms of Parkinson's in mice, even when introducing in the genome of these animals the same mutations found in humans afflicted by familial forms of the disease," he said.
"Our discovery provides a new lead to potentially overcome such difficulties.
"It's possible that new medications could be developed to help the neurons in question reduce their energy consumption or produce energy more efficiently, which would reduce accumulated damage over the years," Trudeau said.
The study was published in Current Biology.
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