Reduced mitochondrial content in mouse dopaminergic neurons and astrocytes
Drug-induced Parkinson's disease is not well understood
Recently, researchers from the Guangzhou Institutes of Biomedicine and Health (GIBH) of the Chinese Academy of Sciences and the Second Affiliated Hospital of Zhejiang University School of Medicine revealed that FNZ induces Parkinson's disease by stimulating the integration of mitochondria and lysosomes (called mitosomes) mechanism of disease
The researchers noted that the FNZ-treated mice exhibited Parkinson's-like symptoms in the spin test, the open field test and the Morris water maze test, including decreased coordination and balance and decreased learning and memory
The research team detected increased glucose uptake in the brains of FNZ-treated mice by [18F]-fluoro-2-deoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) with significant mitochondrial proteins in the brains.
In studying the mechanism of mitochondrial elimination, the researchers found that FNZ induces direct entry of mitochondria into lysosomes to form mitosomes (a new organelle structure), which then mediates VAMP2/STX4-dependent extracellular effects leading to mitochondrial reduction in number
This study presents a FNZ-based approach to total mitochondrial depletion that can be used to explore new mitochondrial functions or replace mitochondrial DNA mutations in patients with mitochondrial function
Provided by the Chinese Academy of Sciences