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Discovering how toxic proteins traffic from cell to cell in Alzheimer’s disease

Alzheimer’s disease (AD) is a progressive and unremitting neurodegenerative disorder characterized by impairments in cognition and memory.

Aims

This project aims to examine the effect of tau hyperphosphorylation and Aβ on the release of exosomes in cell culture systems, and to determine the potential impact of this mechanism in the propagation of pathology in Alzheimer’s disease.

On a macroscopic level, widespread neuronal degeneration is interspersed with the presence of the key pathological hallmarks of AD: neurofibrillary tangles composed of hyperphosphorylated tau and amyloid plaques comprised of amyloid-β (Aβ).

Recent studies have strongly implicated cell-to-cell transmission of tau and Aβ in progression of AD, however the mechanism of transfer between cells is unclear.

Small extracellular vesicles, called exosomes, play an important role in cell to cell trafficking. Once released from the donor cell, exosomes act as discrete vesicles travelling to distant and proximal recipient cells to alter cell function and phenotype. The idea that exosomes may be involved in the spreading of pathology from cell to cell in AD has recently gained considerable attention with our recent findings suggesting tau and Aβ are associated with human brain derived exosomes.

Techniques employed will include cell culture, the use of pharmacological tools to manipulate tau phosphorylation, western-blotting, and exosome isolation and characterisation using transmission electron microscopy and density gradients.

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