Journal
PLOS ONE
Volume 17, Issue 8, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0272511
Keywords
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Categories
Funding
- Florida health department grant
- Ed and Ethel Moore 747 Alzheimer Research
- University of Central Florida [7AZ11]
- Antibody targeting of IL1RAP and 749 studying their therapeutic effects in mouse models of Alzheimer's disease
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Mitochondrial dysfunction is a characteristic of neurodegenerative diseases, and the expression level of Tom40 protein is significantly reduced in patients with these diseases. The delivery of Tom40 protein to the brain using engineered exosomes has been found to protect neurons from oxidative stress, suggesting its potential as a novel therapy for neurodegenerative diseases.
Mitochondrial dysfunction is a hallmark of neurodegeneration. The expression level of Tom40, a crucial mitochondrial membrane protein, is significantly reduced in neurodegenerative disease subjects. Tom40 overexpression studies have shown to protect the neurons against oxidative stress by improving mitochondrial function. Thus, successful delivery of Tom40 protein to the brain could lead to a novel therapy for neurodegenerative diseases. However, delivering protein to the cell may be difficult. Especially the blood-brain barrier (BBB) is a big hurdle to clear in order to deliver the protein to the brain. In the current study, we engineered exosomes, which are the extracellular vesicles of endosomal origin, and able to cross BBB as delivery vehicles packing human Tom40. We found Tom40 protein delivery by the exosome successfully protected the cells against hydrogen peroxide-induced oxidative stress. This result suggests that exosome-mediated delivery of Tom40 may potentially be useful in restoring mitochondrial functions and alleviating oxidative stress in neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases.
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