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1 rolonged survival of transected axons ("slow Wallerian degeneration").
2 ayed degeneration of transected nerves (slow Wallerian degeneration).
3 scending and descending fiber tracts undergo Wallerian degeneration).
4 n damage may occur by a mechanism similar to Wallerian degeneration.
5 ly distinct from macrophages associated with Wallerian degeneration.
6 the dorsal funiculus, i.e., axons undergoing Wallerian degeneration.
7 and unmyelinated axons, or the byproducts of Wallerian degeneration.
8 d with the macrophage-dependent processes of Wallerian degeneration.
9 n (Ca2+) concentrations can slow the rate of Wallerian degeneration.
10 ut site rapidly degenerate, a process termed Wallerian degeneration.
11 ry and are likely critical to the process of Wallerian degeneration.
12 g the Wld(S) mutation which leads to delayed Wallerian degeneration.
13 out mice, evidence of some independence from Wallerian degeneration.
14 ation) by accelerating axon regeneration and Wallerian degeneration.
15 nitude of cytokine production is crucial for Wallerian degeneration.
16  that conductive scaffolds with ES minimized Wallerian degeneration.
17 or receptor super family (TNFRSF) members in Wallerian degeneration.
18 ic pathways that have become established for Wallerian degeneration.
19 ld not be suppressed by mutations that block Wallerian degeneration.
20 ruction pathways, including axons undergoing Wallerian degeneration.
21 ffects they might produce by facilitation of Wallerian degeneration.
22 2s lacking ISTID regions substantially delay Wallerian degeneration.
23 ty, attenuated roGFP2 oxidation, and delayed Wallerian degeneration.
24 un in Schwann cells is a global regulator of Wallerian degeneration.
25 um, likely related to both demyelination and wallerian degeneration.
26 evation in axons, and thereby suppression of Wallerian degeneration.
27 effects on normal development, maturation or Wallerian degeneration.
28 n axonal swelling, fragmentation, and distal Wallerian degeneration.
29 ed axons and dendrites, and axons undergoing Wallerian degeneration.
30 ctivated in response to injury that mediates Wallerian degeneration(4), was sufficient to break this
31  injury promotes gliomagenesis by triggering Wallerian degeneration, a targetable active programme of
32 ate of axon regeneration and debris removal (Wallerian degeneration) after nerve injury.
33 ese phenotypes are not prevented by blocking Wallerian degeneration and are independent of Perlecan's
34 rase (NMNAT) act as a powerful suppressor of Wallerian degeneration and ataxin- and tau-induced neuro
35 ess the question in a novel way by assessing Wallerian degeneration and axon numbers in the medullary
36 on regenerative capacity but display delayed Wallerian degeneration and axonal fusion, observed so fa
37    Injection of ATP at 150 mum caused little Wallerian degeneration and behavioral tests showed no si
38 l to further probe the mechanisms underlying Wallerian degeneration and its prevention.
39 al to the lesion site, which correlates with Wallerian degeneration and nerve oedema.
40 rve response to injury, contributing to both Wallerian degeneration and nerve regeneration, and their
41 pe, emphasizing the mechanistic link between Wallerian degeneration and peripheral neuropathy.
42 inflammation-induced axonal loss followed by Wallerian degeneration and post-inflammatory neurodegene
43 lphaBC plays an important role in regulating Wallerian degeneration and remyelination after PNS injur
44                               Demyelination, Wallerian degeneration and Renaut bodies were induced in
45 damaged but intact sensory axons complements Wallerian degeneration and suggests the therapeutic pote
46 odegeneration, with axonal damage leading to Wallerian degeneration and toxic proteinopathies of amyl
47  is required for clearance of tissue debris (Wallerian degeneration) and effective regeneration.
48 mportant role for inductive autophagy during Wallerian degeneration, and point to potential mechanist
49 ty is both necessary and sufficient to delay Wallerian degeneration, and that promoting axonal and sy
50 ic factor withdrawal, but not injury-induced Wallerian degeneration, and we define a biochemical casc
51 eneration, arguing TDP-43(Q331K)-induced and Wallerian degeneration are genetically distinct processe
52 GSK3, hat-trick, or xmas-2 does not suppress Wallerian degeneration, arguing TDP-43(Q331K)-induced an
53 ires activation of Sarm1, a key regulator of Wallerian degeneration, as mice lacking the Sarm1 gene d
54 he degeneration of transected axons, termed "Wallerian degeneration," as a model to examine the possi
55 xic insult from neurodegenerative disorder), Wallerian degeneration associated with injury is precede
56 leotide in its oxidized form (NAD(+)) during Wallerian degeneration associated with neuropathies.
57  cell death pathways, including necroptosis, Wallerian degeneration, autophagic cell death, and pyrop
58 rapid SARM1-dependent programmed axon death (Wallerian degeneration), but a potential role for Sarm1
59 at1) fusion protein that potently suppresses Wallerian degeneration, but the mechanistic action of Wl
60 s after demyelination, followed by prominent Wallerian degeneration by 21 days in the Ptprz-deficient
61 ons in Wld(S) mutant mice are protected from Wallerian degeneration by overexpression of a chimeric U
62  a therapeutic window in which the course of Wallerian degeneration can be delayed even after injures
63 logy domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved tr
64 ledge of the molecular mechanisms underlying Wallerian degeneration, demonstrated its involvement in
65 ven within white matter undergoing fulminant Wallerian degeneration despite intimate contact with mye
66 med NMNAT1 from a molecule unable to inhibit Wallerian degeneration, even at high expression levels,
67 ond established CST locations do not undergo Wallerian degeneration following a large lesion of the s
68 domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy.
69                           In later stages of Wallerian degeneration, however, Schwann cell mitogenesi
70  of this degeneration cascade, also known as Wallerian degeneration; however, the mechanism of SARM1-
71  show that axons exhibit the early stages of wallerian degeneration if they are conducting impulses a
72  a mutation (WldS) which delays the onset of Wallerian degeneration in damaged axons.
73  show that Wlds protein substantially delays Wallerian degeneration in flies.
74  previously implicated in the progression of Wallerian degeneration in injury-induced spheroid format
75 eneration that is morphologically similar to Wallerian degeneration in mammals and can be suppressed
76        Enzyme-dead Wld(S) is unable to delay Wallerian degeneration in mice.
77 long rescue of a lethal condition related to Wallerian degeneration in mice; the discovery of 'drugga
78            Mutations in hiw strongly inhibit Wallerian degeneration in multiple neuron types and deve
79 ts provide additional evidence for a role of Wallerian degeneration in neuropathic pain.
80 detection of NMNAT2 mutations that implicate Wallerian degeneration in rare human diseases; the capac
81  In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is d
82 Wld(s) mutant mouse, which undergoes delayed Wallerian degeneration in response to axonal injury, sug
83  and paranodal changes consistent with acute wallerian degeneration in roots stimulated at 50 or 100
84       Here, we describe an approach to study Wallerian degeneration in the Drosophila L1 wing vein th
85 16 nerve roots (31.2%) demonstrated moderate wallerian degeneration in the survival group.
86 rescently tagged Nmnat2 significantly delays Wallerian degeneration in these mice.
87  and preserving mitochondria, and peripheral Wallerian degeneration in vivo.
88 and central fiber pathways undergo very slow Wallerian degeneration in Wlds mutant mice.
89 d C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37 degrees C.
90 ignal that initiates myelin breakdown during Wallerian degeneration induces multiple MTOCs and MT bun
91 nal swelling, axonal fragmentation and loss, Wallerian degeneration, inflammatory infiltrates, Schwan
92 mulation in the distal nerve was reduced and Wallerian degeneration inhibited, regeneration was delay
93                                              Wallerian degeneration is a widespread mechanism of prog
94 he spontaneous mutant Wld(s) mouse, in which Wallerian degeneration is characteristically slow, provi
95 tly confirmed with Sarm1(-/-) mice, in which Wallerian degeneration is greatly delayed.
96 elinated axons and myelinated sensory axons; Wallerian degeneration is restricted to myelinated effer
97 /6 strain and mutant mice (Wld(S)), in which Wallerian degeneration is substantially delayed.
98                                 Wld(S) (slow Wallerian degeneration) is a remarkable protein that can
99 cal response of peripheral nerves to injury (Wallerian degeneration) is the cornerstone of nerve repa
100 we hypothesize that products associated with Wallerian degeneration lead to an alteration in the prop
101 mage recruits inflammatory cells to sites of Wallerian degeneration, leading to demyelination.
102                           We postulated that Wallerian degeneration leads to an alteration in the pro
103 ation ameliorates the axonopathy, implying a Wallerian degeneration-like pathomechanism.
104 es and the molecular mechanisms underpinning Wallerian degeneration may further delineate its pathoge
105                              However, in the Wallerian degeneration model of nerve injury, the mitoti
106                                     The slow Wallerian degeneration mouse (C57BL/Wld(s)) is a mutant
107 ges were compared in C57BL and WldS (delayed Wallerian degeneration mutation) mice.
108                               In addition to Wallerian degeneration, nerve injury was significantly a
109 mistry demonstrated that CES does not induce Wallerian degeneration, nor does it cause macrophage inf
110 n) is a remarkable protein that can suppress Wallerian degeneration of axons and synapses, but how it
111                           This suggests that Wallerian degeneration of axons transected in the demyel
112 hat underwent dorsal root axotomy triggering Wallerian degeneration of axons-a pathological process w
113                                              Wallerian degeneration of injured neuronal axons and syn
114 We have used a Drosophila model to study the Wallerian degeneration of motoneuron axons and their neu
115 th macrophage invasion and activation during Wallerian degeneration of peripheral nerve.
116  Axonal injury due to prostatectomy leads to Wallerian degeneration of the cavernous nerve (CN) and e
117              The cortical lesion also caused Wallerian degeneration of the cortical descending effere
118  is similar in mechanism to the more delayed Wallerian degeneration of the disconnected distal axon,
119 nsects the subepidermal plexus, resulting in Wallerian degeneration of the nerve fibers that enter th
120 rocyte stress, is followed by demyelination, wallerian degeneration of the ON, and oligodendrocyte an
121 rve MTR is consistent with demyelination and Wallerian degeneration of transected axons.
122 basis of these data, we hypothesize that the Wallerian degeneration of white matter axons that follow
123 ography), assuming that marked hypoplasia or Wallerian degeneration on the lesioned side in patients
124 t Schwann cell proliferation associated with Wallerian degeneration or axon regeneration or the clear
125 can be rescued either by genetic blockade of Wallerian degeneration or caspase-dependent death.
126 emyelination (P < 0.005), without increasing Wallerian degeneration or nerve fiber loss, a pattern qu
127 ral injury, severed axons undergo programmed Wallerian degeneration over several following days.
128                            The dominant slow Wallerian degeneration phenotype is conferred by a hybri
129 time that the WldS mouse is more than a slow Wallerian degeneration phenotype, emphasizing the mechan
130 nerves, unlike the others, had all undergone Wallerian degeneration previously and the loss of hIK1-l
131 nsible for Schwann cell proliferation during Wallerian degeneration, probably acting via autocrine or
132 acity to levels that exceed that of the slow Wallerian degeneration protein, Wld(S).
133                                              Wallerian degeneration provides a model to study axon-to
134 s of synaptic degeneration in the absence of Wallerian degeneration resemble synapse elimination in n
135 , triggered by mechanical nerve wounding and Wallerian degeneration, respectively.
136         Thus, Wld(S)-mediated suppression of Wallerian degeneration results from VCP-N16 interactions
137 lture showed that CM101 protected axons from Wallerian degeneration; reversed gamma-aminobutyrate-med
138 ne externalization was slowed and delayed in Wallerian degeneration slow (Wld(S)) axons and this phen
139   When we expressed the neuroprotective gene Wallerian degeneration slow (Wld(S)) in receptor neurons
140 the three decades since the discovery of the Wallerian degeneration slow (Wld(S)) mouse, research has
141 +) may explain the potent axon protection in Wallerian degeneration slow (Wld(s)) mutant mice.
142 l degeneration is delayed in the striatum of Wallerian degeneration slow (Wld(s)) mutant mice.
143                        Overexpression of the Wallerian degeneration slow (Wld(s)) protein can delay a
144    Using this assay, we found that the mouse Wallerian degeneration slow (Wld(S)) protein can protect
145                                          The Wallerian degeneration slow (Wld(S)) protein protects ax
146 generation of transected axons is delayed in Wallerian degeneration slow (Wlds) mice with the overexp
147                                           In Wallerian degeneration slow (wlds) mice, Wallerian degen
148                 The expression of the mutant Wallerian degeneration slow (WldS) protein significantly
149 ose in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerv
150 xpressing the axon-protective fusion protein Wallerian degeneration slow (WldS).
151  of ubiquitylation and overexpression of the Wallerian degeneration slow protein (Wld(S)) lengthened
152                                 The chimeric Wallerian degeneration slow protein (Wld(S)) protects ax
153                In addition, we show that the Wallerian degeneration slow protein (Wld(S)), a more sta
154   The expression of a fusion protein, named "Wallerian degeneration slow" (Wld(S)), can protect axons
155 ndria in both degeneration and NMNAT/WLD(S) (Wallerian degeneration slow)-mediated protection.
156 ion morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying me
157 ime, supposedly through their involvement in Wallerian degeneration, the process by which the distal
158 onse in the distal nerves in an event termed Wallerian degeneration: the Schwann cells degrade their
159                            In the setting of Wallerian degeneration, this stagger will expose growth
160                                              Wallerian degeneration, thus, appears to progress throug
161 e hypothesis that neuronal damage, including Wallerian degeneration, triggers inflammatory responses
162  nerve and characterised the early events in Wallerian degeneration using an unbiased proteomics scre
163 nation were diminished in double-Tg mice and Wallerian degeneration was markedly decreased.
164                                              Wallerian degeneration (WD) and inherited demyelinating
165 veral hours post axotomy, early hallmarks of Wallerian degeneration (WD) are delayed in aged flies.
166                Using laser axotomy to induce Wallerian degeneration (WD) in zebrafish peripheral sens
167                                              Wallerian degeneration (WD) is a process of autonomous d
168                                              Wallerian degeneration (WD) is considered an essential p
169                                              Wallerian degeneration (WD) is the set of molecular and
170 f injured axons is controlled by a conserved Wallerian degeneration (WD) pathway, which is thought to
171 We now describe a role for ADAM17 during the Wallerian degeneration (WD) process.
172  myelination, has never been investigated in Wallerian degeneration (WD).
173 odels to address the role of mitochondria in Wallerian degeneration (WD).
174 down by the molecularly regulated process of Wallerian degeneration (WD).
175  been associated with programmed axon death (Wallerian degeneration, WD), a widespread and potentiall
176 In C5-d mice, inflammatory demyelination and Wallerian degeneration were followed by axonal depletion
177 the early phase of innate-immune response of Wallerian degeneration, were found to be upregulated in
178 ation, and mucoid degeneration, appearing as Wallerian degeneration, were observed.
179 rliest detectable change in axons undergoing Wallerian degeneration, which among other degenerative e
180                                         Slow Wallerian degeneration (Wld(S)) encodes a chimeric Ube4b
181      In two mutant strains of mice, the slow Wallerian degeneration (Wld(s)) mouse and the chemokine
182                                     The slow Wallerian degeneration (Wld(S)) mutation, which results
183                                     The slow Wallerian degeneration (Wld(S)) protein protects injured
184 transferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons

 
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