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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
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Mitochondrial DNA Manipulations Affect Tau Oligomerization.
Ian W Weidling1,2,3, Heather M Wilkins1,2, Scott J Koppel1,2,3
1University of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Journal of Alzheimer'S Disease : JAD
|August 18, 2020
Summary
Mitochondrial DNA (mtDNA) levels influence tau aggregation in brain cells. Reduced mtDNA and dysfunction increase tau oligomerization, suggesting a link to Alzheimer's disease pathogenesis.
Area of Science:
- Neuroscience
- Cell Biology
- Mitochondrial Biology
Background:
- Mitochondrial dysfunction and tau aggregation are hallmarks of Alzheimer's disease (AD).
- Mitochondrial toxins alter tau pathology in cellular and rodent models.
Purpose of the Study:
- To investigate the direct impact of mitochondrial DNA (mtDNA) on tau oligomerization.
- To determine if mtDNA alterations influence tau pathology in human neuronal cells relevant to AD.
Main Methods:
- Human neuronal SH-SY5Y cells were subjected to acute and chronic mtDNA depletion.
- Cell lines with chronic mtDNA depletion (ρ0 cells) were generated.
- Cytoplasmic hybrid (cybrid) cell lines were created using mtDNA from AD subjects.
Main Results:
- Acute mtDNA depletion impaired cytochrome oxidase activity.
- Metabolic reprogramming was observed in ρ0 cells.
- Reduced mtDNA content in AD cybrids correlated with increased tau oligomer levels and a monomer-to-oligomer shift.
Conclusions:
- Cellular mtDNA content directly affects tau oligomerization.
- Consistent tau changes across models confirm reproducibility.
- Findings in AD cybrids support the relevance of mtDNA to AD pathology.
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