Wallerian degeneration often occurs in the near the proximity of the injury site.

The provided axonal protection delays the onset of Wallerian degeneration.

Recovery takes place without wallerian degeneration.

Because axonal continuity is lost, Wallerian degeneration occurs.

The primary role of macrophages in peripheral regeneration is demylenation during Wallerian degeneration.

There is no wallerian degeneration.

Schwann cells are active in Wallerian degeneration.

He was the first to describe the degeneration of severed nerve fibers, now known as Wallerian degeneration.

Schwann cells are responsible for taking part in both Wallerian degeneration and bands of Bungner.

Wallerian degeneration does not occur, so recovery does not involve actual regeneration.

Following injury and wallerian degeneration, axons regrow and reinnervate their targets.

Wallerian degeneration in lesion-related tracts (lesion type 3).

Myelin clearance is the next step in Wallerian degeneration following axonal degeneration.

Experiments in Wallerian degeneration have shown that upon injury oligodendrocytes either undergo programmed cell death or enter a state of rest.

Digestion chambers are a histologic finding in nerves that are undergoing Wallerian degeneration.

Microglia play a vital role in CNS wallerian degeneration.

Macrophages also play a role in inducing the proliferation of Schwann cells that occurs during Wallerian degeneration.

When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its myelin sheath.

Wallerian degeneration is named after Augustus Volney Waller.

Degeneration appears distally in the paralysed facial nerve but this takes time, this process is called Wallerian degeneration.

In the mutant Ola mouse, Wallerian degeneration is significantly delayed following injury to peripheral nerves but nevertheless occurs.

The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains.

The basis of this hypothesis is as follows: after a lesion, axonal degeneration (via Wallerian degeneration) occurs.

Axonotmesis is a disruption of nerve cell axon, with Wallerian degeneration occurring below and slightly proximal to the site of injury.

Denervation studies at the neuromuscular junction of vertebrates have shown that the axon removal mechanism closely resembles Wallerian degeneration.