Studies with the WldS mutant mouse have shown that axon and synapse pathology in several models of neurodegenerative diseases are mechanistically related to injury-induced axon degeneration (Wallerian degeneration). Crucially, an absence of SARM1 delays Wallerian degeneration as robustly as WldS, but their relative capacities to confer long-term protection against related, non-injury axonopathy...

This review focuses on recent developments in our understanding of neurodegeneration at the mammalian neuromuscular junction. We provide evidence to support a hypothesis of compartmental neurodegeneration, whereby synaptic degeneration occurs by a separate, distinct mechanism from cell body and axonal degeneration. Studies of the spontaneous mutant Wld(s) mouse, in which Wallerian degeneration ...

1. The Wallerian degeneration occurring in peripheral nerves by incubation in Ringer solution and serum does not occur in plasma. 2. Peripheral nerves incubated in plasma give rise to no growth. The same is true of peripheral nerves in a Wallerian degeneration up to the 4th day. 3. Peripheral nerves in Wallerian degeneration from the 5th day give rise to a growth of the syncytium of Schwann. In...

Axon pruning by degeneration remodels exuberant axonal connections and is widely required for the development of proper circuitry in the nervous system from insects to mammals. Developmental axon degeneration morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying mechanisms. As previously reported for mice, we show that Wlds protein substantially delays W...

Wallerian axon degeneration is a form of programmed subcellular death that promotes axon breakdown in disease and injury. Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enzyme NMNAT2 prevents degeneration. New studies reveal that these pathways cooperate in a locally mediated axon destruction program, with NAD+ metabolism playing a central role. Here...

Wallerian degeneration is the degeneration of the distal stump of an injured axon. It normally occurs over a time course of around 24 hr but it is delayed in the slow Wallerian degeneration mutant mouse (C57BL/Wlds) for up to 3 weeks. The gene, which protects from rapid Wallerian degeneration, Wld, previously has been mapped to distal chromosome 4. This paper reports the fine genetic mapping of...

Macrophages are important effector cells in immune-mediated demyelination. Current concepts regarding their entry and activation focus on the effects of T-cell-derived cytokines. This presentation describes the responses of macrophages and microglia to a non-inflammatory, non-immune injury, Wallerian degeneration. During Wallerian degeneration in the peripheral nervous system (PNS), macrophages...

A model of endoneurial oedema is presented which produces localised nerve fibre injury including Wallerian degeneration, endoneurial oedema and increased endoneurial fluid pressure. A carbon dioxide laser was used to irradiate rat sciatic nerve and quantitative results were collected 2 days and 6 days after irradiation. The increase in endoneurial fluid pressure is compared with other models of...