Researchers at FIU’s Robert Stempel College of Public Health & Social Work are one-step closer to understanding how inhibiting dynamin related protein-1 (Drp1) in the brain might be a protective mechanism that can be used as a therapeutic strategy for Parkinson’s disease (PD) patients.
A team led by Kim Tieu, professor and chair of the department of Environmental Health Sciences, targeted an important protein linked to PD, α-synuclein. In cell models the researchers observed how α-synuclein impaired mitochondria (the powerhouse of the cell), increased oxidative stress, accumulation and spread of toxic protein.
The team found that blocking Drp1 significantly improved the function of mitochondria and autophagy, a cellular process highly critical to removing misfolded and toxic proteins such as α-synuclein. In combination, through genetic and pharmacological approaches, the team found that blocking Drp1 was protective against toxicity caused by α-synuclein.
“Increased Drp1 function is suggested to have negative effects on conditions such as Parkinson’s disease. Before this publication, the pathogenic mechanism of Drp1 had been attributed to impaired mitochondrial function. Our work identified an additional exciting and novel role of Drp1 in autophagy; therefore, further strengthening the therapeutic potential of blocking Drp1,” said Rebecca Fan, who remains in Tieu’s lab as a post-doctoral research associate after her recent successful PhD defense.
“Most of the data in this paper were generated from Rebecca’s dissertation project. I am proud of her novel and significant work because it helped us secure a highly competitive R35 RIVER grant award and these data now serve as the basis for multiple studies that my lab is pursuing,” said Tieu.
Other investigators from the Plymouth University and Fudan University also contributed to this publication.
To read the full study, click here .