A potent LRRK2 inhibitor rebuilt primary cilia, revived dopamine signaling, and doubled nerve-ending density
in mice with Parkinson’s mutations, suggesting enzyme-blocking therapy could slow or reverse disease.
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Putting the brakes on an enzyme might rescue neurons that are dying due to a type of Parkinson's disease that's caused by a single genetic mutation, according to a new Stanford Medicine-led study conducted in mice.
The genetic mutation causes an enzyme called leucine-rich repeat kinase 2, or LRRK2, to be overactive. Too much LRRK2 enzyme activity changes the structure of brain cells in a way that disrupts crucial communication between neurons that make the neurotransmitter dopamine and cells in the striatum, a region deep in the brain that is part of the dopamine system and is involved in movement, motivation and decision making.
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