ライフサイエンスコーパス: Wallerian degeneration

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 the dorsal funiculus, i.e., axons undergoing Wallerian degeneration.

5 and unmyelinated axons, or the byproducts of Wallerian degeneration.

6 d with the macrophage-dependent processes of Wallerian degeneration.

7 n (Ca2+) concentrations can slow the rate of Wallerian degeneration.

8 ut site rapidly degenerate, a process termed Wallerian degeneration.

9 ry and are likely critical to the process of Wallerian degeneration.

10 g the Wld(S) mutation which leads to delayed Wallerian degeneration.

11 ld not be suppressed by mutations that block Wallerian degeneration.

12 ruction pathways, including axons undergoing Wallerian degeneration.

13 ffects they might produce by facilitation of Wallerian degeneration.

14 or receptor super family (TNFRSF) members in Wallerian degeneration.

15 2s lacking ISTID regions substantially delay Wallerian degeneration.

16 ty, attenuated roGFP2 oxidation, and delayed Wallerian degeneration.

17 un in Schwann cells is a global regulator of Wallerian degeneration.

18 um, likely related to both demyelination and wallerian degeneration.

19 evation in axons, and thereby suppression of Wallerian degeneration.

20 effects on normal development, maturation or Wallerian degeneration.

21 n axonal swelling, fragmentation, and distal Wallerian degeneration.

22 ed axons and dendrites, and axons undergoing Wallerian degeneration.

23 ic pathways that have become established for Wallerian degeneration.

24 n damage may occur by a mechanism similar to Wallerian degeneration.

25 rase (NMNAT) act as a powerful suppressor of Wallerian degeneration and ataxin- and tau-induced neuro

26 ess the question in a novel way by assessing Wallerian degeneration and axon numbers in the medullary

27 Injection of ATP at 150 mum caused little Wallerian degeneration and behavioral tests showed no si

28 l to further probe the mechanisms underlying Wallerian degeneration and its prevention.

29 al to the lesion site, which correlates with Wallerian degeneration and nerve oedema.

30 pe, emphasizing the mechanistic link between Wallerian degeneration and peripheral neuropathy.

31 inflammation-induced axonal loss followed by Wallerian degeneration and post-inflammatory neurodegene

32 lphaBC plays an important role in regulating Wallerian degeneration and remyelination after PNS injur

33 Demyelination, Wallerian degeneration and Renaut bodies were induced in

34 is required for clearance of tissue debris (Wallerian degeneration) and effective regeneration.

35 mportant role for inductive autophagy during Wallerian degeneration, and point to potential mechanist

36 ty is both necessary and sufficient to delay Wallerian degeneration, and that promoting axonal and sy

37 ic factor withdrawal, but not injury-induced Wallerian degeneration, and we define a biochemical casc

38 eneration, arguing TDP-43(Q331K)-induced and Wallerian degeneration are genetically distinct processe

39 GSK3, hat-trick, or xmas-2 does not suppress Wallerian degeneration, arguing TDP-43(Q331K)-induced an

40 he degeneration of transected axons, termed "Wallerian degeneration," as a model to examine the possi

41 at1) fusion protein that potently suppresses Wallerian degeneration, but the mechanistic action of Wl

42 s after demyelination, followed by prominent Wallerian degeneration by 21 days in the Ptprz-deficient

43 ons in Wld(S) mutant mice are protected from Wallerian degeneration by overexpression of a chimeric U

44 a therapeutic window in which the course of Wallerian degeneration can be delayed even after injures

45 logy domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved tr

46 ven within white matter undergoing fulminant Wallerian degeneration despite intimate contact with mye

47 med NMNAT1 from a molecule unable to inhibit Wallerian degeneration, even at high expression levels,

48 ond established CST locations do not undergo Wallerian degeneration following a large lesion of the s

49 domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy.

50 In later stages of Wallerian degeneration, however, Schwann cell mitogenesi

51 of this degeneration cascade, also known as Wallerian degeneration; however, the mechanism of SARM1-

52 show that axons exhibit the early stages of wallerian degeneration if they are conducting impulses a

53 a mutation (WldS) which delays the onset of Wallerian degeneration in damaged axons.

54 show that Wlds protein substantially delays Wallerian degeneration in flies.

55 eneration that is morphologically similar to Wallerian degeneration in mammals and can be suppressed

56 Enzyme-dead Wld(S) is unable to delay Wallerian degeneration in mice.

57 Mutations in hiw strongly inhibit Wallerian degeneration in multiple neuron types and deve

58 ts provide additional evidence for a role of Wallerian degeneration in neuropathic pain.

59 In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is d

60 Wld(s) mutant mouse, which undergoes delayed Wallerian degeneration in response to axonal injury, sug

61 and paranodal changes consistent with acute wallerian degeneration in roots stimulated at 50 or 100

62 Here, we describe an approach to study Wallerian degeneration in the Drosophila L1 wing vein th

63 16 nerve roots (31.2%) demonstrated moderate wallerian degeneration in the survival group.

64 rescently tagged Nmnat2 significantly delays Wallerian degeneration in these mice.

65 and preserving mitochondria, and peripheral Wallerian degeneration in vivo.

66 and central fiber pathways undergo very slow Wallerian degeneration in Wlds mutant mice.

67 d C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37 degrees C.

68 ignal that initiates myelin breakdown during Wallerian degeneration induces multiple MTOCs and MT bun

69 nal swelling, axonal fragmentation and loss, Wallerian degeneration, inflammatory infiltrates, Schwan

70 mulation in the distal nerve was reduced and Wallerian degeneration inhibited, regeneration was delay

71 he spontaneous mutant Wld(s) mouse, in which Wallerian degeneration is characteristically slow, provi

72 elinated axons and myelinated sensory axons; Wallerian degeneration is restricted to myelinated effer

73 /6 strain and mutant mice (Wld(S)), in which Wallerian degeneration is substantially delayed.

74 Wld(S) (slow Wallerian degeneration) is a remarkable protein that can

75 cal response of peripheral nerves to injury (Wallerian degeneration) is the cornerstone of nerve repa

76 we hypothesize that products associated with Wallerian degeneration lead to an alteration in the prop

77 mage recruits inflammatory cells to sites of Wallerian degeneration, leading to demyelination.

78 We postulated that Wallerian degeneration leads to an alteration in the pro

79 es and the molecular mechanisms underpinning Wallerian degeneration may further delineate its pathoge

80 However, in the Wallerian degeneration model of nerve injury, the mitoti

81 The slow Wallerian degeneration mouse (C57BL/Wld(s)) is a mutant

82 ges were compared in C57BL and WldS (delayed Wallerian degeneration mutation) mice.

83 In addition to Wallerian degeneration, nerve injury was significantly a

84 n) is a remarkable protein that can suppress Wallerian degeneration of axons and synapses, but how it

85 This suggests that Wallerian degeneration of axons transected in the demyel

86 Wallerian degeneration of injured neuronal axons and syn

87 We have used a Drosophila model to study the Wallerian degeneration of motoneuron axons and their neu

88 th macrophage invasion and activation during Wallerian degeneration of peripheral nerve.

89 Axonal injury due to prostatectomy leads to Wallerian degeneration of the cavernous nerve (CN) and e

90 The cortical lesion also caused Wallerian degeneration of the cortical descending effere

91 is similar in mechanism to the more delayed Wallerian degeneration of the disconnected distal axon,

92 nsects the subepidermal plexus, resulting in Wallerian degeneration of the nerve fibers that enter th

93 rocyte stress, is followed by demyelination, wallerian degeneration of the ON, and oligodendrocyte an

94 rve MTR is consistent with demyelination and Wallerian degeneration of transected axons.

95 basis of these data, we hypothesize that the Wallerian degeneration of white matter axons that follow

96 ography), assuming that marked hypoplasia or Wallerian degeneration on the lesioned side in patients

97 t Schwann cell proliferation associated with Wallerian degeneration or axon regeneration or the clear

98 emyelination (P < 0.005), without increasing Wallerian degeneration or nerve fiber loss, a pattern qu

99 The dominant slow Wallerian degeneration phenotype is conferred by a hybri

100 time that the WldS mouse is more than a slow Wallerian degeneration phenotype, emphasizing the mechan

101 nerves, unlike the others, had all undergone Wallerian degeneration previously and the loss of hIK1-l

102 nsible for Schwann cell proliferation during Wallerian degeneration, probably acting via autocrine or

103 acity to levels that exceed that of the slow Wallerian degeneration protein, Wld(S).

104 Wallerian degeneration provides a model to study axon-to

105 s of synaptic degeneration in the absence of Wallerian degeneration resemble synapse elimination in n

106 Thus, Wld(S)-mediated suppression of Wallerian degeneration results from VCP-N16 interactions

107 lture showed that CM101 protected axons from Wallerian degeneration; reversed gamma-aminobutyrate-med

108 ne externalization was slowed and delayed in Wallerian degeneration slow (Wld(S)) axons and this phen

109 When we expressed the neuroprotective gene Wallerian degeneration slow (Wld(S)) in receptor neurons

110 +) may explain the potent axon protection in Wallerian degeneration slow (Wld(s)) mutant mice.

111 l degeneration is delayed in the striatum of Wallerian degeneration slow (Wld(s)) mutant mice.

112 Overexpression of the Wallerian degeneration slow (Wld(s)) protein can delay a

113 The Wallerian degeneration slow (Wld(S)) protein protects ax

114 generation of transected axons is delayed in Wallerian degeneration slow (Wlds) mice with the overexp

115 In Wallerian degeneration slow (wlds) mice, Wallerian degen

116 The expression of the mutant Wallerian degeneration slow (WldS) protein significantly

117 ose in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerv

118 xpressing the axon-protective fusion protein Wallerian degeneration slow (WldS).

119 of ubiquitylation and overexpression of the Wallerian degeneration slow protein (Wld(S)) lengthened

120 The chimeric Wallerian degeneration slow protein (Wld(S)) protects ax

121 In addition, we show that the Wallerian degeneration slow protein (Wld(S)), a more sta

122 The expression of a fusion protein, named "Wallerian degeneration slow" (Wld(S)), can protect axons

123 ndria in both degeneration and NMNAT/WLD(S) (Wallerian degeneration slow)-mediated protection.

124 ion morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying me

125 ime, supposedly through their involvement in Wallerian degeneration, the process by which the distal

126 onse in the distal nerves in an event termed Wallerian degeneration: the Schwann cells degrade their

127 In the setting of Wallerian degeneration, this stagger will expose growth

128 Wallerian degeneration, thus, appears to progress throug

129 e hypothesis that neuronal damage, including Wallerian degeneration, triggers inflammatory responses

130 nerve and characterised the early events in Wallerian degeneration using an unbiased proteomics scre

131 nation were diminished in double-Tg mice and Wallerian degeneration was markedly decreased.

132 Wallerian degeneration (WD) and inherited demyelinating

133 veral hours post axotomy, early hallmarks of Wallerian degeneration (WD) are delayed in aged flies.

134 Using laser axotomy to induce Wallerian degeneration (WD) in zebrafish peripheral sens

135 Wallerian degeneration (WD) is considered an essential p

136 Wallerian degeneration (WD) is the set of molecular and

137 odels to address the role of mitochondria in Wallerian degeneration (WD).

138 down by the molecularly regulated process of Wallerian degeneration (WD).

139 In C5-d mice, inflammatory demyelination and Wallerian degeneration were followed by axonal depletion

140 ation, and mucoid degeneration, appearing as Wallerian degeneration, were observed.

141 rliest detectable change in axons undergoing Wallerian degeneration, which among other degenerative e

142 Slow Wallerian degeneration (Wld(S)) encodes a chimeric Ube4b

143 In two mutant strains of mice, the slow Wallerian degeneration (Wld(s)) mouse and the chemokine

144 The slow Wallerian degeneration (Wld(S)) mutation, which results

145 The slow Wallerian degeneration (Wld(S)) protein protects injured

146 transferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons