Potential Treatment for Parkinson’s Targets Mitochondrial Dysfunction
Kim Tieu, Ph.D.
University of Rochester
NIEHS Grants P30ES001247, R01ES014899, R01ES022274, R21ES017470
Research supported in part by NIEHS showed that inhibiting a protein required for mitochondrial fission brought positive effects in experimental mouse models of Parkinson’s disease. The findings could lead to a treatment that would target the neuronal mitochondrial dysfunction that is associated with Parkinson’s disease.
Mitochondria frequently change shape, size, number, and location through the processes of fission and fusion. To determine whether targeting fission and fusion might have a therapeutic effect on Parkinson’s disease, the researchers used mice that model the mitochondrial impairments seen in the disease.
The researchers found that targeting fission, which produces smaller and more motile mitochondria, was beneficial in the animal models studied. Fission requires the recruitment of the GTPase dynamin-related protein 1 (Drp1) from the cytosol to the outer mitochondrial membrane. By blocking Drp1 using gene-therapy or a chemical approach, the researchers reduced both cell death and the deficits in dopamine release, effectively reversing the Parkinson’s disease process.
Citation: Rappold PM, Cui M, Grima JC, Fan RZ, de Mesy-Bentley KL, Chen L, Zhuang X, Bowers WJ, Tieu K. 2014. Drp1 inhibition attenuates neurotoxicity and dopamine release deficits in vivo. Nat Commun 5:5244.
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