Disease relevance of Wallerian Degeneration

• However, dividing the lesion volumes by the mean F in T2w lesions resulted in a quantity that correlated well with NAWM NAA/Cr (r = -0.78, P = 0.038), possibly reflecting the association of Wallerian degeneration in the NAWM with axonal transection associated with demyelination within lesions [1].
• Twenty percent L-fucose diet resulted in significant axonal atrophy, paranodal swelling (P < 0.001), and paranodal demyelination (P < 0.005), without increasing Wallerian degeneration or nerve fiber loss, a pattern qualitatively similar to that seen in early murine diabetic neuropathy [2].
• METHODS: Twenty-six patients with supratentorial hemorrhage were examined on the coronal T2-weighted image of the pons 3 months or later after stroke, and the percentage of Wallerian degeneration in the pons was calculated [3].
• We speculate that perineural clonidine reduces signals, likely proinflammatory cytokines and prostaglandins produced during Wallerian degeneration after nerve injury, which drive changes in ion channel expression in DRG somata leading to hyperexcitability and hypersensitivity [4].
• Differences in the location of leuko-araiosis between the four groups might be due to differences in the location of the grey matter disorder and Wallerian degeneration rather than amyloid in Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy and normal ageing [5].

High impact information on Wallerian Degeneration

• Important insight into the mechanisms of axon degeneration arose from findings that the degeneration of transected axons is delayed in Wallerian degeneration slow (Wlds) mice with the overexpression of a fusion protein with the nicotinamide adenine dinucleotide (NAD) synthetic enzyme, nicotinamide mononucleotide adenylyltransferase (Nmnat1) [6].
• The mechanisms responsible for the induction of Schwann cell proliferation in peripheral nerves undergoing wallerian degeneration and segmental demyelination are not understood [7].
• Wallerian degeneration involves Rho/Rho-kinase signaling [8].
• In 7 rats with acrylamide-induced axonopathy or wallerian degeneration, the rate-dependent block was not observed [9].
• These results suggest that local apolipoprotein synthesis may be involved in the mobilization of myelin cholesterol which occurs during Wallerian degeneration [10].

Chemical compound and disease context of Wallerian Degeneration

• Intraneural injection of pure glycerol induces Wallerian degeneration with subsequent regeneration [11].
• The pattern of change of histamine in the distal and proximal nerve sheaths was different: it dropped at 2 h and then rose in the later stages of Wallerian degeneration [12].
• The effect of diabetes, insulin and Wallerian degeneration on leucine metabolism of isolated rat sciatic nerves [13].
• Early stimulation of phosphatidylcholine biosynthesis during Wallerian degeneration of rat sciatic nerve [14].
• Tumor necrosis factor-alpha in immune-mediated demyelination and Wallerian degeneration of the rat peripheral nervous system [15].

Biological context of Wallerian Degeneration

• Specifically, the down-regulation of the MEK/Erk pathway by the proteasome plays roles in Wallerian degeneration of severed axons and axonal pruning in response to local NGF deprivation [16].
• Analysis of the CRII-7/rMDC15 transcript levels following peripheral nerve lesions demonstrated regulated mRNA expression during Wallerian degeneration and nerve regeneration [17].
• Thus, it is concluded that an increase in cholesterol esterifying activity in degenerating nerve is primarily responsible for cholesterol esterification during Wallerian degeneration [18].
• Here we show that upregulation of Mts1 is a consistent feature of astrocytes in white matter undergoing Wallerian degeneration [19].
• Rats evaluated at 14 weeks had histological evidence of graft rejection with inflammatory cell infiltration, extensive demyelination and remyelination, and some Wallerian degeneration [20].

Anatomical context of Wallerian Degeneration

• The transient induction of NF-M mRNA is also apparent in dedifferentiating Schwann cells during Wallerian degeneration [21].
• This study to demonstrates long-term induction of HO-1 and HSP70 in microglia and macrophages after traumatic injury and an association between induction of HO-1 and Wallerian degeneration [22].
• The number of cells expressing the myelin-supporting oligodendrocyte marker PLP-exon 3b remains unchanged in Wallerian degeneration [23].
• Demyelination, Wallerian degeneration and Renaut bodies were induced in the medial plantar nerve in rats housed in cages with wire-grate flooring [24].
• Even more striking is the appearance of CGRP immunoreactivity in normally non-reactive motor endplates during axon regeneration after an experimentally induced Wallerian degeneration of the motor axons [25].

Gene context of Wallerian Degeneration

• These data indicate that endoneurial TNFR1 and TNFR2 proteins are differentially regulated during Wallerian degeneration [26].
• Desert hedgehog-patched 2 expression in peripheral nerves during Wallerian degeneration and regeneration [27].
• Tumor necrosis factor-alpha (TNF-alpha) injected into nerve induces Wallerian degeneration, whereas, interleukin-1 (IL-1) production promotes detersion by scavenger macrophages, and synthesis of neurotrophic factors (nerve growth factor-NGF- and leukemia inhibitory factor-LIF) [28].
• In SCGx rats, significantly lower serum GH and PRL and higher MBH GRH and TRH content as compared to controls was observed 16-24 h after surgery, during the wallerian degeneration phase after SCGx [29].
• Regulation of Wallerian degeneration and nerve growth factor withdrawal-induced pruning of axons of sympathetic neurons by the proteasome and the MEK/Erk pathway [16].

Analytical, diagnostic and therapeutic context of Wallerian Degeneration

• To delineate a role in the regenerative response to axotomy we examined the expression of OPN in Wallerian degeneration of the sciatic nerve in rats [30].
• Northern blots were used to examine the expression of genes encoding receptors for IgG (FcRIII) and for C3b/C4b (Crry) in rat sciatic nerve during development and Wallerian degeneration [31].
• The increase of FcRIII mRNA that occurred in Wallerian degeneration was most likely due to infiltration of macrophages, as FcRIII mRNA-positive macrophages were demonstrated in the degenerating nerves by in situ hybridization [31].
• Electron microscopy revealed fibers with Wallerian degeneration establishing asymmetric synapses exclusively on the distal dendrites and spines of TRH neurons [32].
• Hypothalamic luteinizing hormone-releasing hormone content and serum luteinizing hormone levels in male rats during wallerian degeneration of sympathetic nerve terminals after superior cervical ganglionectomy [33].

References