Abstract: Augustus Volney Waller was a renowned British neurophysiologist who birthed the axon degeneration field in 1850 by describing curdling and fragmentation of the glossopharyngeal and hypoglossal cranial nerves of a frog following a transection injury. The degeneration of axons after a transection injury is now known as Wallerian degeneration (WD). Waller’s work was expanded by Santiago Ramón y Cajal who described in detail the morphological stages of WD from monitory fragmentation of the axon and the granular disintegration of the neurofibrils to the final resorption of the axon. Interest in this field burgeoned in the early 1990’s with the fortuitous discovery of a mutant mouse, known as the Wallerian degeneration Slow (WldS) mouse. Although overtly normal, its remarkable phenotype was discovered when the animals were subjected to a physical nerve injury and a profoundly slowed rate of axonal degeneration was revealed. This slow axon breakdown is intrinsic to neurons, present in central and peripheral nervous system axons, and associated with structural preservation and retention of the ability to conduct axon potentials for up to 2 weeks (a 10-fold delay).