Overview of Nerve Degeneration and Regeneration Nerve damage produces a well characterized cascade of cellular and molecular events, described as Wallerian degeneration, throughout the distal stump. This process involves several phases, some concurrent, others consecutive, in which the distal stump degenerates; the myelin associated with degenerating axons are degraded and removed by Schwann cells (SC), and blood-recruited macrophages. SC can dedifferentiate, proliferate and align within the basal lamina tubes, called Bügner bands, which may subsequently be penetrated by regrowing axons. Once the SC-axon attachment is re-established, the remyelination process begins [1]. Growth cones emerge from the proximal stump of severed axons, induced by local factors released in response to the injury [2-4] and elongate if they find a favorable environment. It is known that regeneration of injured axons following trauma depends on a delicate balance between growth-promoting and growth-inhibiting factors. Several neurotrophic factors, cytokines, extracellular matrix molecules and hormones are secreted by neurons, SC, macrophages, the target tissue and cells present in the injury site, promoting neuronal survival, thus creating a permissive microenvironment for axon regeneration [5]. In this sense, SC in the vicinity of the transected axon synthesize a variety of growth factors including glial-derived neurotrophic factor (GDNF), insulin-like growth factor (IGF-1), and nerve growth factor (NGF), which have effects on axon growth [6]. The neurotrophins (NTs) family, which includes the brain-derived neurotrophic factor (BDNF), NGF and NTs 3 and 4/5, also play a crucial role in the regeneration process, serving as molecular cues and activators of the key signaling pathways that will support neuronal survival and growth [7].