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Updated: Aug 16, 2026

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models
Published on: June 30, 2023
Differentiated Alzheimer's disease transmitochondrial cybrid cell lines exhibit reduced organelle movement
Patricia A Trimmer1, M Kathleen Borland
1Department of Neurology, University of Virginia, Charlottesville, VA 22908, USA. pat5q@virginia.edu
Abstract:
The axonal transport and function of organelles like mitochondria and lysosomes may be impaired and play an important role in the pathogenesis of Alzheimer's disease (AD). Unique cybrid cell lines that model AD pathology were created by fusing platelets containing mitochondria from age-matched AD and control volunteers with mitochondrial DNA-free SH-SY5Y human neuroblastoma cells. These cybrid lines were differentiated to form process-bearing neuronal cells. Mitochondria and lysosomes in the neurites of each cybrid line were fluorescently labeled to determine the kinetics of organelle movement. The mitochondria in AD cybrid neurites were elongate, whereas the mitochondria in control cybrid neurites were short and more punctate. The mean velocity of mitochondrial movement, as well as the percentage of moving mitochondria, was significantly reduced in AD cybrids. The velocity of lysosomal movement was also reduced in the processes of AD cybrid cells, suggesting that the axonal transport machinery may be compromised in cybrid cell lines that contain mitochondrial DNA derived from AD patients. Reduced mitochondrial and lysosomal movement in susceptible neurons may compromise function in metabolically demanding structures like synaptic terminals and participate in the terminal degeneration that is characteristic of AD.
Insights
Mitochondrial dysfunction in Alzheimer's disease (AD) impairs axonal transport of mitochondria and lysosomes. This cellular transport deficit in AD cybrid cells suggests a key role in neurodegeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Genetics
Background:
- Alzheimer's disease (AD) pathogenesis involves impaired axonal transport of organelles.
- Mitochondria and lysosomes are crucial for neuronal function and their transport is vital.
Purpose of the Study:
- To investigate the impact of Alzheimer's disease-associated mitochondrial DNA on axonal transport dynamics.
- To model AD pathology using unique cybrid cell lines.
Main Methods:
- Created cybrid cell lines by fusing AD patient platelets with neuroblastoma cells.
- Differentiated cybrids into neuronal cells and fluorescently labeled mitochondria and lysosomes.
- Quantified organelle movement kinetics in neurites.
Main Results:
- Mitochondria in AD cybrid neurites were elongated; control mitochondria were punctate.
- Significantly reduced velocity and percentage of moving mitochondria in AD cybrids.
- Reduced lysosomal movement velocity observed in AD cybrid cell processes.
Conclusions:
- Alzheimer's disease mitochondrial DNA compromises axonal transport machinery in neurons.
- Impaired mitochondrial and lysosomal transport may contribute to synaptic dysfunction and neurodegeneration in AD.
- Axonal transport deficits are a potential mechanism underlying Alzheimer's disease pathology.
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