Modeling Alzheimer's disease on-chip using microfluidic and tissue engineering approaches

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Alzheimer's Disease (AD) is a progressive neurodegenerative disease associated with cognitive dysfunction in the brain. An estimated 500,000 Canadian have AD, including 70,000 age <65 years. The main cause of AD has not been clearly discovered, and therefore the effective treatment to stop the disease or reverse its progression has not yet been established. It is mainly believed that a group of soluble folded proteins like Amyloid beta (Aβ) aggregates to insoluble forms in the brain where they play an essential role in neuronal degeneration functions. Aβ in AD patients can impair synaptic function extracellularly via the direct deposition on synapses or intracellularly through interrupting the axonal transmission. The existing models are not able to determine the contribution of any of these two ways in synaptic dysfunction due to inability in local delivery of molecules into specific cellular compartments. Microfluidics, in particular, has the capability for spatiotemporal delivery of molecules to the synaptic site. The overall objective of the proposed work is to understand how extracellular Aβ peptides spatiotemporally delivered to synapses contribute