BI European Studentship: Variations in axon survival within the human population

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

In this project we will study an enzyme whose activity appears to be harmful for axons, at least in the absence of the next enzyme in the pathway. When an axon in a nerve is injured it undergoes a characteristic degeneration process known as ‘Wallerian degeneration’ and there is evidence that similar mechanisms account for axon loss in some neurodegenerative conditions such as multiple sclerosis, Parkinson’s disease and glaucoma. Starting from a mutant strain of mice in which the process of Wallerian degeneration is delayed by tenfold, we first identified the protein that confers this neuroprotective property on these mice, and now we have identified a second enzyme in the same pathway, Nampt, whose inhibition seems to protect axons. This indicates a potential for intervening in axonal disorders pharmacologically but to do this we need to understand much more about the biology of Nampt in axons. This project will investigate how Nampt is delivered to axons and what regulates its stability and removal from axons. There is significant pharmaceutical industry interest in Nampt and this project will be carried out in collaboration with Takeda (Cambridge) Ltd.

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