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An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons
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Synaptic Contacts Enhance Cell-to-Cell Tau Pathology Propagation
Sara Calafate1, Arjan Buist2, Katarzyna Miskiewicz3
1Neuroscience Department, Janssen Research and Development, a Division of Janssen Pharmaceutica NV, 2340 Beerse, Belgium; VIB Center for the Biology of Disease, 3000 Leuven, Belgium; KU Leuven Department for Human Genetics, 3000 Leuven, Belgium.
Cell Reports
|May 19, 2015
Summary
Synapses enhance the spread of Tau pathology between neurons, not just proximity. This finding suggests synaptic repair therapies might inadvertently worsen Tau protein aggregation in diseases like Alzheimer's.
Area of Science:
- Neuroscience
- Neurodegenerative Diseases
- Cell Biology
Background:
- Tau protein aggregation and spread are hallmarks of tauopathies, including Alzheimer's disease (AD).
- Propagation of Tau pathology is thought to occur along connected neurons, but the role of synaptic contacts is unclear.
Purpose of the Study:
- To investigate whether synaptic contacts, independent of mere proximity, facilitate the propagation of Tau pathology between neurons.
- To determine the role of synaptic activity in promoting Tau pathology spread within neuronal networks.
Main Methods:
- Utilized quantitative in vitro models with acceptor hippocampal neurons and Tau donor cells.
- Employed artificial neuronal networks in microfluidic devices to study synaptic transmission and Tau pathology propagation.
Main Results:
- Synapses, not just cell proximity, significantly enhance Tau pathology propagation between neurons.
- Synaptic activity in artificial neuronal networks promotes the spread of Tau pathology, alongside non-synaptic mechanisms.
Conclusions:
- Physical synaptic contacts between neurons facilitate the propagation of Tau pathology.
- Synaptic repair therapies could potentially have adverse effects by promoting Tau pathology spread.
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