ライフサイエンスコーパス: axonal degeneration

1 utive activation of SARM1 and thereby led to axonal degeneration.

2 for white matter injury, axonal growth, and axonal degeneration.

3 coln1(-/-) mice, which indicates progressive axonal degeneration.

4 lay a critical role in mediating progressive axonal degeneration.

5 ant mitochondrial energy metabolism precedes axonal degeneration.

6 f Fig4 in motor neurons display neuronal and axonal degeneration.

7 tion, and full reversal of spongy myelin and axonal degeneration.

8 nt is both necessary and sufficient to delay axonal degeneration.

9 n this interaction causes dysmyelination and axonal degeneration.

10 ompanied by cessation of TBI-induced chronic axonal degeneration.

11 f demyelination with no evident white matter axonal degeneration.

12 tion, mitochondrial function, apoptosis, and axonal degeneration.

13 ble neuroprotective effect of lamotrigine on axonal degeneration.

14 ent of drugs to prevent chemotherapy-induced axonal degeneration.

15 o we propose this phenotype is important for axonal degeneration.

16 the caspase6 apoptotic cascade that fosters axonal degeneration.

17 ligodendrocyte apoptosis, demyelination, and axonal degeneration.

18 sis in the injurious cascade associated with axonal degeneration.

19 ow that ACs are released from SCs and induce axonal degeneration.

20 rs, in which prolonged inflammation leads to axonal degeneration.

21 while sparing transport, and did not induce axonal degeneration.

22 in vivo does not affect guidance but causes axonal degeneration.

23 s and provide a target for new therapies for axonal degeneration.

24 rovides trophic support for axons to prevent axonal degeneration.

25 a conserved mechanism, in the initiation of axonal degeneration.

26 sis pathway implicated in protection against axonal degeneration.

27 Peripheral nerves showed axonal degeneration.

28 y promotes mitochondrial movement and delays axonal degeneration.

29 tion mechanism connecting hyperlipidemia and axonal degeneration.

30 e of Bcl-w and of mitochondria in preventing axonal degeneration.

31 orticospinal tract, consistent with a distal axonal degeneration.

32 es are consistent with structural changes of axonal degeneration.

33 an adaptive mechanism that protects against axonal degeneration.

34 ecreased nuclear CREB activation and induced axonal degeneration.

35 assess the aberrant activity responsible for axonal degeneration.

36 tant in specific types of disease-associated axonal degeneration.

37 been proposed as a major contributor to this axonal degeneration.

38 r optic nerve cross-sections were graded for axonal degeneration.

39 red axons via virus-like particles prevented axonal degeneration.

40 efects in long-range axonal connectivity and axonal degeneration.

41 vo as well as in vitro hyperglycemia-induced axonal degeneration.

42 oreactivity within axon tracts suggestive of axonal degeneration.

43 n automated quantitative assay for assessing axonal degeneration.

44 and define a model for the steps leading to axonal degeneration.

45 equires JNK, Fos, and Jun, JNK also promotes axonal degeneration.

46 l neurodegenerative diseases, is involved in axonal degeneration.

47 tore the mitochondria morphology and prevent axonal degeneration.

48 n pathological mechanism of length-dependent axonal degeneration.

49 ropagation of membrane polarity asymmetry in axonal degeneration.

50 involving dysmyelination, demyelination and axonal degeneration.

51 tic receptors may alleviate synapse loss and axonal degeneration.

52 paraplegia (HSP), a disease characterized by axonal degeneration.

53 B3, protects against excitotoxicity-induced axonal degeneration.

54 onally distinct, into a unifying pathway for axonal degeneration.

55 echanism by which MAPK signaling facilitates axonal degeneration.

56 tion as causes of axonal ovoid formation and axonal degeneration.

57 human degenerative diseases characterized by axonal degeneration.

58 abolic changes preceded any demyelination or axonal degeneration.

59 acterized by hypomyelination and progressive axonal degeneration.

60 NEDD4L, and of TNFRSF21, a key regulator of axonal degeneration.

61 enerative clusters (50%), increased rates of axonal degeneration (91%) and increased numbers of empty

62 However, late onset of progressive axonal degeneration, accompanied by astrogliosis, microg

63 axons to promote axonal NAD(+) depletion and axonal degeneration after injury.

64 thways that contribute to early and subacute axonal degeneration after stroke.

65 primary cultured mouse motor neurons showed axonal degeneration after transient expression of the TT

66 Axonal degeneration after traumatic brain injury and ner

67 We found that although Nmnat blocks axonal degeneration after trophic factor withdrawal, it

68 ascular insult to the sixth nerve trunk with axonal degeneration, allowing for substitutive innervati

69 The loss of MOCA in mice leads to axonal degeneration and causes sensorimotor impairments

70 t is not known how mitofusin mutations cause axonal degeneration and CMT2A disease.

71 axons followed by examination of progressive axonal degeneration and debris clearance alongside uninj

72 crostructural changes suggest trauma-related axonal degeneration and demyelination, which are related

73 009) was observed, suggesting co-presence of axonal degeneration and demyelination.

74 l analysis of either sex revealed widespread axonal degeneration and disruption to the axo-glial junc

75 indings have important implications for both axonal degeneration and dysfunction during the progressi

76 autophagy-lysosomal function and exacerbates axonal degeneration and gain of toxicity in C9ALS/FTD mo

77 on of nodes and paranodes is associated with axonal degeneration and may lead to impaired conduction

78 PCs, markers of proteotoxic stress preceded axonal degeneration and motor dysfunction, indicating a

79 mice that develop forebrain tau inclusions, axonal degeneration and MT deficits.

80 ie-Tooth type 4B (CMT4B) is characterized by axonal degeneration and myelin outfoldings.

81 ochemical studies support the involvement of axonal degeneration and neuroinflammation--ubiquitous co

82 Intestinal inflammation causes initial axonal degeneration and neuronal death but subsequent ax

83 vidence for spinal motor neuron loss, distal axonal degeneration and p75 neurotrophin receptor (p75(N

84 symptoms likely reflect combined effects of axonal degeneration and plasticity, inappropriate firing

85 available data suggest that it results from axonal degeneration and reduced regenerative capacity.

86 ansmission, postsynaptic receptor abundance, axonal degeneration and regeneration.

87 The pathological findings suggest axonal degeneration and repair.

88 o be multifactorial including causes such as axonal degeneration and retrograde degeneration.

89 uggest an ON-limited infarct with subsequent axonal degeneration and selective neuronal loss similar

90 to be recognized as regulators of selective axonal degeneration and synaptic function, thus playing

91 of C9ORF72 patients, resulting in rescue of axonal degeneration and TDP-43 pathology.

92 d at remyelination failure, which results in axonal degeneration and ultimately disease progression,

93 impaired rotarod performance and widespread axonal degeneration and was more pronounced in shiverer

94 system, and the cerebellum, which result in axonal degeneration and WM loss.

95 uron death and neurotoxin-induced retrograde axonal degeneration, and axon regeneration.

96 wed the PAI-1 treatment reduced brain edema, axonal degeneration, and cortical cell death at 24-48 h

97 reased lesion size, PhMN loss, phrenic nerve axonal degeneration, and diaphragm neuromuscular junctio

98 e of tissue responses leading to cell death, axonal degeneration, and glial scar formation, exacerbat

99 osis (MS) is characterized by demyelination, axonal degeneration, and inflammation.

100 myelitis (gray matter inflammation), chronic axonal degeneration, and inflammatory demyelination due

101 an result in tissue disruption, neuronal and axonal degeneration, and neurological dysfunction.

102 erve biopsies identified mild demyelination, axonal degeneration, and perivascular inflammation.

103 evolutionarily conserved genes that promote axonal degeneration, and so could identify candidate the

104 es cannot distinguish neuroinflammation from axonal degeneration, and therefore provide little specif

105 Selective synaptic and axonal degeneration are critical aspects of both brain d

106 the underlying molecular pathways leading to axonal degeneration are incompletely understood, accumul

107 s, downstream mechanisms that lead to distal axonal degeneration are unknown.

108 of myelin gene expression and development of axonal degeneration as the mice aged.

109 ency in the brain, produce both neuronal and axonal degeneration as well as more moderate and potenti

110 vo, p75(NTR-/-) mice exhibited resistance to axonal degeneration associated with oxidative injury fol

111 ent with an intra-axonal redox mechanism for axonal degeneration associated with the initiation and p

112 significant motoneurons loss, accompanied by axonal degeneration, astrogliosis and microglial activat

113 Axonal degeneration (AxD) following nerve injury, chemot

114 sion of extracellular NR delays NMDA-induced axonal degeneration (AxD) much more strongly than extrac

115 = 0.75, P = 0.0015) and to a lesser extent, axonal degeneration (beta = -0.48, P = 0.043).

116 tes resistance to axonal injury and prevents axonal degeneration both in cell culture and in vivo.

117 neuron (MN)-selective protein inclusions and axonal degeneration but the underlying mechanisms of suc

118 on of JNK activity during this period delays axonal degeneration, but critical JNK substrates that fa

119 d subcellular events have been implicated in axonal degeneration, but researchers have so far been un

120 tinjury during which the course of Wallerian axonal degeneration can be halted.

121 er time, and that once a threshold is passed axonal degeneration can become functionally apparent in

122 Progressive axonal degeneration can lead to both Charcot-Marie-Tooth

123 at augmenting expression of MFN1 rescued the axonal degeneration caused by MFN2 mutants, suggesting a

124 of these proteins resulted in prevention of axonal degeneration caused by paclitaxel.

125 e tested whether this pathway is involved in axonal degeneration caused by withdrawal of other trophi

126 red for transmission of sensory information; axonal degeneration causes impaired tactile sensation an

127 hanism of its involvement in the progressive axonal degeneration characteristic of these diseases is

128 sure [IOP], retinal ganglion cell death, and axonal degeneration) closely resembling those seen in pa

129 ose that even after completed remyelination, axonal degeneration continues to progress at a low level

130 The extent to which large-caliber axonal degeneration contributes to Alzheimer disease (AD

131 Axonal degeneration contributes to permanent neurologica

132 Molecules that promote axonal degeneration could represent potential targets fo

133 SARM1, an executor of axonal degeneration, displays NADase activity that deple

134 mic insult but go on to experience a delayed axonal degeneration driven in part by changes in axoglia

135 t that three distinct patterns of retrograde axonal degeneration exist: (i) direct retrograde axonal

136 of mitochondrial volume and distribution in axonal degeneration following acute CNS demyelination.

137 ilure of prompt remyelination contributes to axonal degeneration following demyelination.

138 e of intra-axonal Ca(2+) stores in secondary axonal degeneration following spinal cord injury.

139 Progressive axonal degeneration follows demyelination in many neurol

140 ion slow (WldS) protein significantly delays axonal degeneration from various nerve injuries and in m

141 Axonal degeneration has been proposed to be mediated by

142 Axonal degeneration has been recognized as a predominant

143 is APP/DR6/caspase 6 pathway and resulted in axonal degeneration, however, APP cleavage and caspase 6

144 is known to regulate neuronal apoptosis and axonal degeneration; however, the contribution of microg

145 al degeneration exist: (i) direct retrograde axonal degeneration; (ii) rapid and self-terminating RTD

146 Intraepidermal nerve fiber loss, axonal degeneration, immune cell infiltration, alteratio

147 luate if genetic deletion of SARM1 decreases axonal degeneration in a mouse model of neuropathy induc

148 ta indicate N-APP is not the sole culprit in axonal degeneration in adult nerves.

149 lies mutant SOD1-mediated NF aggregation and axonal degeneration in ALS MNs.

150 esults in amelioration of acrylamide-induced axonal degeneration in an EPO-dependent manner.

151 Thus, a decrease in axonal degeneration in Bim deficient DBA/2J mice may not

152 s a defined degenerative pathway involved in axonal degeneration in both the peripheral nervous syste

153 ovides new insights into the pathogenesis of axonal degeneration in Charcot-Marie-Tooth disease type

154 ted model thus mimics some of the aspects of axonal degeneration in chronic progressive MS.

155 The axonal degeneration in CMT causes distal muscle weakness

156 genic precursors preceding demyelination and axonal degeneration in CMT1C patients.

157 type specificity and molecular mechanisms of axonal degeneration in CMT2A and dominant optic atrophy.

158 b delayed chemotherapy-induced and Wallerian axonal degeneration in culture by preventing axotomy-ind

159 e Nmnat alone is clearly sufficient to delay axonal degeneration in cultured neurons, we sought to de

160 Taxol-induced axonal degeneration in Drosophila shares molecular execu

161 protection against neurological deficit and axonal degeneration in experimental autoimmune encephalo

162 ed microglia converge on the initial site of axonal degeneration in human glaucoma, yet their part in

163 However, there are no signs of axonal degeneration in les rats up to 9 months.

164 e, we investigated oxidative stress-mediated axonal degeneration in mice lacking the antioxidant enzy

165 t the mouse ortholog of rtp, MORN4, promotes axonal degeneration in mouse sensory axons following axo

166 In this review, we discuss the role of axonal degeneration in neurodegenerative disorders, with

167 s and may thus represent long-segment severe axonal degeneration in optic nerves in patients with GON

168 f bclw mRNA to the axon, and thereby prevent axonal degeneration in rat and mouse sensory neurons.

169 ysis revealed that CMT2B Rab7 mutants caused axonal degeneration in rat E15.5 DRG neurons.

170 Na(+) and Ca(2+) currents that contribute to axonal degeneration in response to inflammatory conditio

171 SARM1 induces axonal degeneration in response to various insults and i

172 Here we show that Mtmr13 loss leads to axonal degeneration in sciatic nerves of older mice.

173 onfocal microscopy has been used to identify axonal degeneration in several peripheral neuropathies.

174 Knockdown of rtp also delays axonal degeneration in severed olfactory axons.

175 that expression of MFN2(R94Q) induces distal axonal degeneration in the absence of overt neuronal dea

176 (Wld(S)) mutation, which results in reduced axonal degeneration in the central and peripheral nervou

177 f Fbxo7 in myelinating glia, however, led to axonal degeneration in the CNS and peripheral neuropathy

178 It however triggered axonal degeneration in the CNS and resulted in the sever

179 elevated susceptibility of CD4(-/-) mice to axonal degeneration in the CNS, with augmented progressi

180 ing acute demyelination and protects against axonal degeneration in the CNS.

181 nt significantly attenuated the PBBI-induced axonal degeneration in the corpus callosum and ipsilater

182 oteins, especially mutant M1, contributes to axonal degeneration in the corticospinal tracts.

183 hat neuroinflammation is more prominent than axonal degeneration in the early stage of schizophrenia,

184 This mutation leads to axonal degeneration in the in vitro neuronal cell line.

185 retina was determined by fundus imaging, and axonal degeneration in the optic nerves was determined b

186 e RIPK1 using necrostatin-1 strongly delayed axonal degeneration in the peripheral nervous system and

187 ycans and exhibited abnormal myelination and axonal degeneration in the PNS.

188 dies target the nodal axolemma, induce acute axonal degeneration in the presence of complement, and i

189 RGCs in the peripheral retina, and exhibited axonal degeneration in the retina and optic nerve as com

190 The pattern of axonal degeneration in the simulations mirrored both vis

191 Axonal degeneration in the spinal cord and muscle atroph

192 sequences, is all that is required to delay axonal degeneration in vivo.

193 om other neurodegenerative diseases suggests axonal degeneration, in the absence of neuronal loss, ca

194 imary dorsal root ganglion cultures prevents axonal degeneration induced by acrylamide in a dose-depe

195 nd caspase 6 activation were observed during axonal degeneration induced by dynactin 1(Dctn1) dysfunc

196 nd caspase 6 activation were not involved in axonal degeneration induced by mechanical or toxic insul

197 degeneration slow (Wld(s)) protein can delay axonal degeneration initiated via axotomy, chemotherapeu

198 pheral neuropathies or CNS diseases in which axonal degeneration is a common factor.

199 Axonal degeneration is a critical, early event in many a

200 Axonal degeneration is a hallmark of many debilitating n

201 Axonal degeneration is a hallmark of many neurological d

202 Axonal degeneration is a hallmark of many neuropathies,

203 Axonal degeneration is a key component of a variety of n

204 Axonal degeneration is a key pathology of neurodegenerat

205 Axonal degeneration is a major cause of permanent disabi

206 to stress and injury.SIGNIFICANCE STATEMENT Axonal degeneration is a major feature of neuropathies a

207 Axonal degeneration is a molecular self-destruction casc

208 ization after axotomy.SIGNIFICANCE STATEMENT Axonal degeneration is a neuronal process independent of

209 Axonal degeneration is a pathophysiological mechanism co

210 Axonal degeneration is a primary cause of permanent neur

211 Axonal degeneration is an early and important component

212 Axonal degeneration is an early and prominent feature of

213 of neurodegenerative diseases indicate that axonal degeneration is an early event in the disease pro

214 cation of necroptosis as a key mechanism for axonal degeneration is an important step toward the deve

215 Axonal degeneration is central to clinical disability an

216 Therefore, understanding the mechanisms of axonal degeneration is critical for developing new thera

217 , it has been recognized that the process of axonal degeneration is distinct from somal degeneration

218 portance in other conditions in which distal axonal degeneration is found.

219 (ER), but the relevance of this function to axonal degeneration is not understood.

220 lic, and toxic insults, but the mechanism of axonal degeneration is poorly understood.

221 Injury-induced (Wallerian) axonal degeneration is regulated via the opposing action

222 Axonal degeneration is the major cause of permanent neur

223 Although axonal degeneration is thought to be a predominant featu

224 the GTPase Rab7 cause a dominantly inherited axonal degeneration known as Charcot-Marie-Tooth type 2B

225 zed by retinal ganglion cell (RGC) death and axonal degeneration leading to irreversible blindness.

226 s with MS eventually experience results from axonal degeneration, little is known about the mechanism

227 , deletion of PrP(C) expression rescues 5-HT axonal degeneration, loss of synaptic markers, and early

228 erative disease characterized by progressive axonal degeneration mainly affecting motor neurons.

229 o control levels, and both soluble Abeta and axonal degeneration markers decreased in parallel.

230 sruption might, over time, contribute to the axonal degeneration observed in peripheral demyelinating

231 otein complexes, which may contribute to the axonal degeneration observed in SMA.

232 However, a late onset of demyelination and axonal degeneration occurred at hyperelevated, but not m

233 Axonal degeneration occurred when intra-axonal concentra

234 explored the relationship between markers of axonal degeneration occurring after the stroke and visua

235 Axonal degeneration occurs in multiple neurodegenerative

236 Neuro-axonal degeneration occurs progressively from the onset

237 The mechanisms by which axonal degeneration occurs, even in the presence of appa

238 ized by spasticity of the leg muscles due to axonal degeneration of corticospinal neurons.

239 ly ameliorated the motor deficits as well as axonal degeneration of dnc-1 KD animals.

240 However, the selective vulnerability and axonal degeneration of motor neurons in ALS pose the que

241 2 expression in zebrafish is associated with axonal degeneration of motor neurons that can be rescued

242 Axonal degeneration of the CST in the atrophic cervical

243 Here, we asked whether axonal degeneration or axonal regeneration in adult nerv

244 tically induced depletion of NMNAT2 triggers axonal degeneration or defective axon growth.

245 glial, or inflammatory cells in models where axonal degeneration or inflammation occur as potential c

246 whether this defect plays a critical role in axonal degeneration or simply reflects sequelae of gener

247 RM1, which has been previously implicated in axonal degeneration (p = 1.76 x 10(-08) with amyotrophic

248 SARM1 is the central executioner of the axonal degeneration pathway that culminates in depletion

249 as the central determinant of a fundamental axonal degeneration pathway that is activated by diverse

250 Our results demonstrate that axonal degeneration proceeds by necroptosis, thus defini

251 but whether such changes play a role in the axonal degeneration process is not clear.

252 rmissive for execution of the injury-induced axonal degeneration program.

253 tent with a linear molecular pathway for the axonal degeneration program.

254 critical and early ER-dependent step during axonal degeneration, providing novel targets for axonal

255 he molecular mechanisms responsible for this axonal degeneration remain to be elucidated, dysfunction

256 excitability, peripheral polyneuropathy, and axonal degeneration reminiscent of CMT and HSP.

257 Axonal degeneration represents an early pathological eve

258 osis, which requires caspase 3, we show that axonal degeneration requires caspase 6, which is activat

259 ructural loss of retinal ganglion cells, and axonal degeneration, resembling glucocorticoid-induced g

260 The JNK pathway promotes axonal degeneration shortly after axonal injury, hours b

261 mutant mice have demonstrated that delaying axonal degeneration slows disease course and prolongs su

262 rgo selective motor and sensory neuronal and axonal degeneration specific to the spinal cord and peri

263 Seventeen biopsies had increased axonal degeneration suggesting active neuropathy.

264 ssed to generate a fragment that can trigger axonal degeneration, suggesting a vital role for BACE1 i

265 not only halted neuronal loss, but prevented axonal degeneration, symptom onset, weight loss, and par

266 that lead to ischemia, amyloid accumulation, axonal degeneration, synaptic loss, and eventually irrev

267 EphB3 null mutant mice exhibited more severe axonal degeneration than wild type littermates after tre

268 eparated out to reveal abnormalities such as axonal degeneration that affect diffusion characteristic

269 s one of the key mechanisms of delayed neuro-axonal degeneration that contributes to disability accru

270 vidence for existence of acquired retrograde axonal degeneration that is truly trans-synaptic (RTD) h

271 ollowing demyelination may contribute to the axonal degeneration that occurs in peripheral demyelinat

272 Our findings reveal focal axonal degeneration that occurs in the ventral side of t

273 rts the identification of a new regulator of axonal degeneration: the transmembrane protein Raw.

274 f OPTN led to progressive dysmyelination and axonal degeneration through engagement of necroptotic ma

275 meability transition pore and contributes to axonal degeneration triggered by both mechanical and tox

276 pairment.SIGNIFICANCE STATEMENT We show that axonal degeneration triggered by diverse stimuli is medi

277 igated the reaction of fibrous astrocytes to axonal degeneration using a transgenic mouse strain expr

278 in-3, kif1b, or its adaptor kbp, exacerbates axonal degeneration via a nonmitochondrial cargo common

279 results indicate that diverse insults induce axonal degeneration via multiple pathways and that these

280 Axonal degeneration was evident in brain stem, spinal co

281 roptotic pathway early during injury-induced axonal degeneration was made evident by increased phosph

282 Distal Wallerian axonal degeneration was observed 14 days after ablation.

283 ify where WldS activity is required to delay axonal degeneration, we adopted a method to alter the te

284 over agents that suppress neuronal death and axonal degeneration, we performed drug screens on primar

285 Utilizing an in vitro model of axonal degeneration, we studied a subset of mouse periph

286 ctivation of SARM1 prevents various forms of axonal degeneration, we tested whether it might protect

287 In contrast, significant signs of axonal degeneration were limited to focal areas in the f

288 uses dose-dependent neuronal dysfunction and axonal degeneration, which are rescued by genetic or pha

289 Axonal degeneration, which contributes to functional imp

290 ested to cause axonal swellings that lead to axonal degeneration, which is known as "diffuse axonal i

291 igate the effect of a conditioning lesion on axonal degeneration, which occurs in the distal stump af

292 ins abolishes the ability of SARM to promote axonal degeneration, while a SARM mutant containing only

293 Optic nerves displayed axonal degeneration with a modest axon loss of 6% and in

294 disease is characterized by length-dependent axonal degeneration with distal sensory loss and weaknes

295 We studied early molecular events in axonal degeneration with single-axon laser axotomy and t

296 , whereas the adult-onset phenotype reflects axonal degeneration without antecedent demyelination.

297 , and produced classic features of segmental axonal degeneration without cell body death, including n

298 onset vision loss and neurological deficits, axonal degeneration without cell body loss, and cytoplas

299 es endogenous remyelination and/or minimizes axonal degeneration would reduce the rate and degree of

300 such neuropathies are characterized by early axonal degeneration, yet therapies that inhibit this axo