Previous work had shown that a spontaneous dominant mutation in the mouse, Wlds (slow Wallerian degeneration), is associated with the protection of axons from a process known as peripheral nerve Wallerian degeneration -- that is, degeneration of axons following a physical insult that disconnects the axons from neuronal cell bodies. The Wlds mutation results in the formation of an abnormal fusion protein whose molecular effects aren't well understood, but the axonal protection conferred by the mutation suggests therapeutic potential for manipulating the biological pathways involved.
In the present work, these scientists sought to assess the effects of the Wlds protein in mouse model of Parkinson's disease. The researchers found that following injection of a dopamine toxin in the brain (a technique that mimics Parkinson's Disease), Wlds mutant mice exhibited strong protection of dopaminergic axons. Moreover, the ability of the preserved axons to synthesize and release dopamine was confirmed by behavioural data. Interestingly, while axons were protected, there was no accompanying protection of the dopaminergic cell bodies in Wlds mice, highlighting subtle differences in the degeneration proces
Contact: Heidi Hardman