ライフサイエンスコーパス: neuropathic pain

1 sm (eg, painful cramps, nociceptive pain, or neuropathic pain).

2 normalities in Schwann cells (SCs) may cause neuropathic pain.

3 cause of lower-limb amputation and disabling neuropathic pain.

4 a promising drug target for the treatment of neuropathic pain.

5 ting a potential role in the pathogenesis of neuropathic pain.

6 in chronic constriction injury (CCI)-induced neuropathic pain.

7 on of pain signalling and the maintenance of neuropathic pain.

8 ntial pharmacological target in migraine and neuropathic pain.

9 an potentially be exploited toward targeting neuropathic pain.

10 TRP-A1 facilitates MrgprD to development of neuropathic pain.

11 ntially damaging stimuli, are key drivers of neuropathic pain.

12 the analgesic action of these drugs against neuropathic pain.

13 TSP/alpha(2)delta-1 interaction to alleviate neuropathic pain.

14 nopioid therapy for the treatment of chronic neuropathic pain.

15 elieving effect against nerve injury-induced neuropathic pain.

16 owing promising efficacy in a mouse model of neuropathic pain.

17 for the control of inflammatory, chronic and neuropathic pain.

18 temporomandibular disorders, and trigeminal neuropathic pain.

19 patients with variable presence of radicular/neuropathic pain.

20 Facilitation of MrgprD by TRP-A1 promotes neuropathic pain.

21 acid receptor type 2 (HCAR2) in 2 models of neuropathic pain.

22 trials, eFT508, may be a new therapeutic for neuropathic pain.

23 le of Toll-like receptor 4 (TLR4) in driving neuropathic pain.

24 ht to drive aversion associated with chronic neuropathic pain.

25 id receptor type 2 in the pathophysiology of neuropathic pain.

26 ally-directed Y1R agonists to reduce chronic neuropathic pain.

27 h the cognitive and the sensory component of neuropathic pain.

28 which may contribute to nerve injury-induced neuropathic pain.

29 and treatment algorithms designed to target neuropathic pain.

30 hanical hypersensitivity, a major symptom of neuropathic pain.

31 ependent distribution resulting in disabling neuropathic pain.

32 del of peripheral nerve injury (PNI)-induced neuropathic pain.

33 e nociceptive system is a basic mechanism of neuropathic pain.

34 hanical hypersensitivity, a major symptom of neuropathic pain.

35 tic silencing as a new treatment modality in neuropathic pain.

36 ntion of chronic cancer chemotherapy-induced neuropathic pain.

37 the rat chronic constrictive injury model of neuropathic pain.

38 itivity in peripheral nerve injury models of neuropathic pain.

39 odone in pain-free states, and in a model of neuropathic pain.

40 nhibition of Panx1 may be useful in treating neuropathic pain.

41 n the rat spared nerve injury (SNI) model of neuropathic pain.

42 eurological disorders including epilepsy and neuropathic pain.

43 thus promotes post-traumatic axonal loss and neuropathic pain.

44 stically distinct models of inflammatory and neuropathic pain.

45 CXCL12/CXCR4 signaling pathway may alleviate neuropathic pain.

46 ined therapeutic target for inflammatory and neuropathic pain.

47 ovel strategy for preventing and controlling neuropathic pain.

48 nced amygdala activity in an animal model of neuropathic pain.

49 effective in the treatment of some types of neuropathic pain.

50 nctional role in SNI- and paclitaxel-induced neuropathic pain.

51 c pain, 100% had probable and 95.2% definite neuropathic pain.

52 apeutic target to alleviate inflammatory and neuropathic pain.

53 t and the development of novel therapies for neuropathic pain.

54 ent amnesia, dysautonomia, neuromyotonia and neuropathic pain.

55 a cellular target for treating this form of neuropathic pain.

56 expression in the injured DRG and attenuates neuropathic pain.

57 as modeling human neurological diseases like neuropathic pain.

58 a new role for the RGMa/Neogenin pathway on neuropathic pain.

59 cer pharmacotherapy, leading to debilitating neuropathic pain.

60 contribute to the pathogenesis of orofacial neuropathic pain.

61 y and retraction scars limiting movement) or neuropathic pain.

62 ovel therapeutic target for the treatment of neuropathic pain.

63 Mice deficient in PI16 are protected against neuropathic pain.

64 lue than common outbred strains for modeling neuropathic pain.

65 can cause acute peripheral pain and chronic neuropathic pain.

66 ymal transition (EMT), loss of sensation and neuropathic pain.

67 ied activity of PB neurons in a rat model of neuropathic pain.

68 ndritic spine dysgenesis and the presence of neuropathic pain.

69 ing of LPA(1) signaling in the PSNL model of neuropathic pain.

70 innings in the initiation and maintenance of neuropathic pain.

71 t an interesting therapeutic alternative for neuropathic pain.

72 that protects against spontaneous and evoked neuropathic pain.

73 sence epilepsy, cardiovascular diseases, and neuropathic pain.

74 microglia contribute to nerve injury-induced neuropathic pain.

75 regulation, oocyte development, epilepsy and neuropathic pain.

76 pharmacological target to treat SCI-induced neuropathic pain.

77 r synaptic plasticity in the pathogenesis of neuropathic pain.

78 erves (L3 and L4) would alleviate peripheral neuropathic pain.

79 ion mainly produced by fibroblasts, controls neuropathic pain.

80 ury and chemotherapy-induced mouse models of neuropathic pain.

81 eatment and control groups for patients with neuropathic pain (-0.1 points [95% CI, -0.8 to 0.5 point

82 ssociation for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite n

83 month) spinal cord injury (25 patients with neuropathic pain, 19 pain-free patients) and neuroimagin

84 for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain, a type of moderate to severe chronic p

85 s and a collection of TDPs in a rat model of neuropathic pain according to a longitudinal, double-bli

86 ions for therapeutics.SIGNIFICANCE STATEMENT Neuropathic pain affects up to 10% of the population, bu

87 Neuropathic pain afflicts millions of individuals and re

88 peutic target for SCI.SIGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in p

89 rom segments where patients had a history of neuropathic pain also showed electrophysiological and im

90 itical role in all modes of inflammatory and neuropathic pain, although the role of HCN3 in nocicepti

91 rgic receptor is a potential drug target for neuropathic pain, Alzheimer disease, and prostate cancer

92 and peripheral electrical NINMs could reduce neuropathic pain among DPN patients, without reported ad

93 ng contributes to various diseases including neuropathic pain and drug addiction.

94 As a result, attenuation of ocular neuropathic pain and dry eye will take place.

95 ular mechanisms engaged by the S1PR1 axis in neuropathic pain and establish S1PR1 as a target for the

96 this study we investigated the incidence of neuropathic pain and examined the presence of nerve dysf

97 changes that arise during the development of neuropathic pain and identify the activation of specific

98 rtant role in multiple preclinical models of neuropathic pain and in inherited human pain phenotypes,

99 ciated with the emergence and maintenance of neuropathic pain and increased pin-prick sensation.

100 ed nerve injury replicates symptoms of human neuropathic pain and induces upregulation of many genes

101 Its key role in neuropathic pain and its limited cellular and tissue dis

102 first-line treatment in chemotherapy-induced neuropathic pain and may be highly efficacious in neurop

103 es could serve as neuroimaging biomarkers of neuropathic pain and might be used for prediction and mo

104 which are associated with the persistence of neuropathic pain and motor dysfunction.

105 te that trkB.T1 in astrocytes contributes to neuropathic pain and neurological dysfunction following

106 se review of the role of dendritic spines in neuropathic pain and outline the potential for modulatio

107 ession, however, has been largely limited to neuropathic pain and perineural invasion.

108 ess behaviour), post-surgical pain, diabetic neuropathic pain and post-herpetic pain.

109 nize GPR160, identify it as a determinant of neuropathic pain and potential therapeutic target, and p

110 fibre damage in relation to the severity of neuropathic pain and quality of life (QoL) in patients w

111 anglion neurons is associated with radicular/neuropathic pain and radiographic nerve root compression

112 berrant afferent input in the maintenance of neuropathic pain and the potential for targeted chemogen

113 , and led to robust motosensory improvement, neuropathic pain and tissue damage mitigation, and myeli

114 play a critical role in mPFC deactivation in neuropathic pain and underlie the mPFC-specific cognitiv

115 ne contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorders; thus, i

116 in rats and dogs and was active in anxiety, neuropathic pain, and lower urinary tract models.

117 multiple sclerosis, asthma, atherosclerosis, neuropathic pain, and rheumatoid arthritis.

118 implicated in neurodevelopmental disorders, neuropathic pain, and schizophrenia.

119 Sensory problems such as neuropathic pain are common and debilitating symptoms in

120 Here, we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 (miR

121 ved in axon growth, whereas genes related to neuropathic pain are decreased.

122 The mechanisms underlying neuropathic pain are poorly understood.

123 Non-opioid therapeutics for the treatment of neuropathic pain are urgently needed to address the ongo

124 ng an important novel therapeutic avenue for neuropathic pain as a class.

125 al syndromes and diseases, including chronic neuropathic pain, autism, and epilepsy.

126 In the rodent nerve injury model of neuropathic pain, BDNF-mediated loss of inhibition (disi

127 P2, and DPP10 are potential drug targets for neuropathic pain because they form a channel complex wit

128 plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat spinal nerve ligat

129 al efficacy of nicotinic agents in relieving neuropathic pain best correlated with their activity on

130 predominant target in metastasis; MMP-9, in neuropathic pain), beta-secretase 1 (BACE-1, an aspartic

131 ciception in models of post-surgical and HIV neuropathic pain but only slightly blocked anti-nocicept

132 al dysrhythmia is a key pathology of chronic neuropathic pain, but few studies have investigated thal

133 ts long-lasting spinal inhibitory control of neuropathic pain, but its mechanism of action is complic

134 ormer is causally connected with the chronic neuropathic pain, but its mechanisms are poorly understo

135 st line analgesics used to treat SCI-induced neuropathic pain, but their efficacy is very limited.

136 showed that they reduce oxaliplatin-induced neuropathic pain by a mechanism involving the alpha7 sub

137 dings support a model in which PI16 promotes neuropathic pain by mediating a cross-talk between fibro

138 ndings suggest that DNMT3a may contribute to neuropathic pain by repressing Kcna2 expression in the D

139 inal cord in response to nerve injury drives neuropathic pain by selectively activating the S1P recep

140 Neuropathic pain can be a debilitating condition with bo

141 vel translational circuit for the genesis of neuropathic pain caused by chemotherapy with important i

142 Neuropathic pain caused by nerve injury presents with se

143 Neuropathic pain caused by peripheral nerve injuries sig

144 ry, emotional, and cognitive consequences of neuropathic pain (chronic constriction injury) in a rat

145 positive nociceptors in chemotherapy-induced neuropathic pain (CIPN) caused by paclitaxel treatment.

146 Chemotherapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitat

147 In the neuropathic pain condition, Homer1a, an activity-depende

148 he daily rhythmicity of pain sensation under neuropathic pain conditions.

149 nociceptor sensitization in inflammatory and neuropathic pain conditions.

150 dimorphism in the microglial contribution to neuropathic pain, depletion of DRG macrophages reduces n

151 not MMP-2/-12/-14 and significantly relieved neuropathic pain development in mice.

152 specific proteins during distinct phases of neuropathic pain development produces enhanced antinocic

153 golipid metabolism alterations contribute to neuropathic pain development.

154 onic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy.

155 istent post-surgical pain, fibromyalgia, and neuropathic pain disorders, is highly prevalent but rema

156 ntagonists retained their ability to inhibit neuropathic pain during sustained drug administration, a

157 esting paradigms for determining preclinical neuropathic pain efficacy and point to the MNK inhibitor

158 on mechanical allodynia, a standard test for neuropathic pain efficacy.

159 Neuropathic pain encompasses a diverse array of clinical

160 Neuropathic pain features were present in 50% (95% CI, 3

161 e-specific knockout of S1pr1 did not develop neuropathic pain following nerve injury, thereby identif

162 spinal nerves may be used to manage chronic neuropathic pain following peripheral nerve injury.

163 erlying cause for the development of chronic neuropathic pain following SCI.

164 type channels in SCI-nociceptors and chronic neuropathic pain following SCI.

165 erexcitable state and contributes to chronic neuropathic pain following SCI.SIGNIFICANCE STATEMENT Ch

166 critical role in the development of chronic neuropathic pain following spinal cord injury (SCI).

167 Our findings reveal a novel mechanism of neuropathic pain formation and highlight MrgprD as a pro

168 Neuropathic pain frequently leads to decisions about usi

169 l new mechanisms and therapeutic targets for neuropathic pain from different origins.

170 acts as the de novo DNMT and is required for neuropathic pain genesis likely through repressing at le

171 hypersensitivities, DRG DNMT1 contributes to neuropathic pain genesis partially through repression of

172 mary sensory neurons of DRG are critical for neuropathic pain genesis.

173 om molecular discoveries in animal models of neuropathic pain have failed to translate following unsu

174 artial sciatic nerve ligation (PSNL)-induced neuropathic pain, however, the cell types that are funct

175 citatory dorsal horn interneurons facilitate neuropathic pain hypersensitivity.

176 ch as paclitaxel are known to elicit chronic neuropathic pain in cancer patients and seriously compro

177 knowledge of the mechanisms contributing to neuropathic pain in diabetes.

178 venues and that has the potential to predict neuropathic pain in future cohorts.

179 lular determinants of nerve regeneration and neuropathic pain in humans.

180 on in the spinal cord prevented and reversed neuropathic pain in male and female rodents without alte

181 nic pain, and notably in oxaliplatin-induced neuropathic pain in mice.

182 receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice.

183 s of colorectal carcinoma, causes peripheral neuropathic pain in patients.

184 dose of RgIA4 prevented chemotherapy-induced neuropathic pain in rats.

185 t not agonists, attenuated and even reversed neuropathic pain in rodents of both sexes and in two mod

186 B2) agonist, suppresses chemotherapy-induced neuropathic pain in rodents without producing tolerance

187 ding to altered sensory phenotypes including neuropathic pain in SFN.SIGNIFICANCE STATEMENT This work

188 Symptomatic treatment of neuropathic pain in small fibre neuropathy is often disa

189 vidence suggests that cannabis may alleviate neuropathic pain in some patients, but insufficient evid

190 n a well-established mouse model of diabetic neuropathic pain in vivo film implantation showed effect

191 Although NIBS can alleviate neuropathic pain (including PLP), both disease and treat

192 a potential new target for the treatment of neuropathic pain, including chemotherapy (paclitaxel)-in

193 unctional perceptual changes associated with neuropathic pain, including pain aversion to light touch

194 on of various ion channels can be altered in neuropathic pain, including T-type Ca(2+) channels that

195 Pin-prick score of the 25 patients with neuropathic pain increased from 1 to 12 months (Deltamea

196 We show that chronic neuropathic pain increases PACAP expression at multiple

197 The spared nerve injury (SNI) model of neuropathic pain increases PI16 protein levels in fibrob

198 expression of Cdk5 in a preclinical model of neuropathic pain increases the functional expression of

199 nociceptors in naive mice and at the peak of neuropathic pain induced by paclitaxel treatment.

200 phrine, TNFalpha, and interleukin-6, and the neuropathic pain induced by the cancer chemotherapy pacl

201 Identifying the molecular players underlying neuropathic pain induced structural and functional malad

202 iors across sensory modalities and abolished neuropathic pain-induced mechanical (hyper-)sensitivity.

203 nth is the strongest predictor for 12 months neuropathic pain intensity (1.90+/-2.26 and 3.83+/-1.19,

204 tions, drug discovery, prosthetic design and neuropathic pain investigations.

205 We conclude that development of neuropathic pain involves abnormal homeostatic activity

206 Neuropathic pain involves long-lasting modifications of

207 Chronic, intractable neuropathic pain is a common and debilitating consequenc

208 Neuropathic pain is a complex, chronic pain state that o

209 ced tactile allodynia.SIGNIFICANCE STATEMENT Neuropathic pain is a current public health challenge.

210 Neuropathic pain is a debilitating condition caused by t

211 following SCI.SIGNIFICANCE STATEMENT Chronic neuropathic pain is a major comorbidity of spinal cord i

212 Neuropathic pain is a significant public health challeng

213 Neuropathic pain is an intractable medical condition wit

214 Neuropathic pain is believed to arise from damage to noc

215 Treating neuropathic pain is challenging and novel non-opioid-bas

216 Neuropathic pain is common in peripheral neuropathy.

217 echanisms responsible for the maintenance of neuropathic pain is imperative for the development of mo

218 a primary dermatological disorder can cause neuropathic pain is still unclear.

219 Pain creams compounded for neuropathic pain (ketamine, gabapentin, clonidine, and l

220 re severe dry eye symptoms, ocular pain, and neuropathic pain-like ocular symptoms.

221 e blockage of the mGluR5 resulted in chronic neuropathic pain-like symptoms even in the absence of ne

222 vealing potential peripheral DRG targets for neuropathic pain management.

223 that DRG DNMT1 may be a potential target for neuropathic pain management.SIGNIFICANCE STATEMENT In th

224 ifth lumbar (L5) nerve injury in rats causes neuropathic pain manifested with thermal and mechanical

225 ent of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in r

226 between altered dendritic spine dynamics and neuropathic pain may serve as a structure-based opportun

227 Here, we used a neuropathic pain model of perineural HIV envelope glycop

228 In a neuropathic pain model of perineural HIV gp120 applicati

229 In a neuropathic pain model, LC(:SC) activation reduced hind-

230 r cingulate cortex in a chemotherapy-induced neuropathic pain model.

231 howed significant effects on the CCI-induced neuropathic pain model.

232 tenance of neuropathic nociception in either neuropathic pain model.

233 ute inflammatory pain and paclitaxel-induced neuropathic pain models during cancer chemotherapy.

234 fects in myriad preclinical inflammatory and neuropathic pain models.

235 ne tolerance, in both acute pain and chronic neuropathic pain models.

236 in the spinal cord in a nerve injury-induced neuropathic pain mouse model.

237 Neuropathic pain (NeuP) arises due to injury of the soma

238 Neuropathic pain (NP) is a complex chronic pain state wi

239 icated in neuronal excitation, seizures, and neuropathic pain (NP).

240 In the spared nerve injury (SNI) model of neuropathic pain, NPY-saporin decreased mechanical and c

241 isingly, these striking positive outcomes on neuropathic pain occurred in the absence of any effect o

242 Skin biopsies from patients with neuropathic pain often show changes in epidermal innerva

243 x-specific transcriptome changes, leading to neuropathic pain only in female mice.

244 steroidal anti-inflammatory drugs, drugs for neuropathic pain, opioids, and cannabinoids, to physical

245 nged in a sciatic nerve transection model of neuropathic pain or in the Complete Freund's adjuvant mo

246 Patients suffering from neuropathic pain, or nerve damage, experience an inversi

247 Given that Kcna2 is a key player in neuropathic pain, our findings suggest that DRG DNMT1 ma

248 ical hypersensitivity that characterizes the neuropathic pain phenotype.

249 ting the mechanisms by which HCAR2 regulates neuropathic pain plasticity.

250 arget of rapamycin complex 1 is activated in neuropathic pain pointing to a key role of MNK1-eIF4E-me

251 though it has no major influence on acute or neuropathic pain processing.

252 . x 12 days) suppressed chemotherapy-induced neuropathic pain produced by paclitaxel without producin

253 gonist EHD2-sc-mTNF(R2) in mice with chronic neuropathic pain promoted long-lasting pain recovery.

254 ty in vivo in an experimental mouse model of neuropathic pain, raising the possibility that it might

255 yer 5 mPFC pyramidal neurons is abolished in neuropathic pain rats due to a severe reduction of a mus

256 udy therefore reveals a function of TNFR2 in neuropathic pain recovery and demonstrates that both TNF

257 e in silencing sensory neurons and reversing neuropathic pain-related hypersensitivity.

258 increased 5-HT2CR in the BLA contributes to neuropathic-pain-related amygdala plasticity by driving

259 e, decreases neuronal activity, and inhibits neuropathic-pain-related behaviors.

260 Neuropathic pain remains a therapeutic challenge because

261 e underlying mechanism of MrgprD involved in neuropathic pain remains elusive.

262 the involvement of CB(2) from these cells in neuropathic pain remains unresolved.

263 old allodynia and models of inflammatory and neuropathic pain, respectively, following intraperitonea

264 RGMa antibody also attenuated neuropathic pain responses, which was associated with fe

265 olecular level, the beneficial reductions in neuropathic pain resulting from S1PR1 inhibition were dr

266 neuropathy symptom inventory questionnaire, neuropathic pain scale) and QoL (SF-36, pre-R-ODS and ho

267 These findings also support the use of neuropathic pain screening tools in these patients and t

268 questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of

269 y, we report that individuals with orofacial neuropathic pain show altered functional connectivity be

270 adigms in a rat model of oxaliplatin-induced neuropathic pain, showed the better antihypersensitive p

271 phage TLR9 signaling in chemotherapy-induced neuropathic pain.SIGNIFICANCE STATEMENT Chemotherapy-ind

272 subunits could be potential drug targets for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain

273 ic cognitive deficits that are comorbid with neuropathic pain.SIGNIFICANCE STATEMENT The medial prefr

274 including chemotherapy (paclitaxel)-induced neuropathic pain.SIGNIFICANCE STATEMENT This work demons

275 therapeutic target against inflammatory and neuropathic pain.SIGNIFICANCE STATEMENT We demonstrate t

276 Using the Neuropathic Pain Special Interest Group of the Internati

277 triggers pC/EBPbeta in the HIV gp120-induced neuropathic pain state.

278 pathic pain and may be highly efficacious in neuropathic pain states that are refractive to opioid an

279 Cold allodynia occurs as a major symptom of neuropathic pain states.

280 ains present in sensory neurons may modulate neuropathic pain states.

281 l horn and contributes to characteristics of neuropathic pain such as mechanical and thermal hypersen

282 ion by MRI and patient-based questionnaires (Neuropathic Pain Symptom Inventory and 36-Short Form Hea

283 Neuropathic pain symptoms respond poorly to available th

284 ads to spinal cord central sensitization and neuropathic pain symptoms.

285 and neuronal plasticity related to radicular/neuropathic pain that may suggest therapeutic avenues an

286 We explored spontaneous neuropathic pain through on-demand self-administration o

287 s essential in cold allodynia in CCI-induced neuropathic pain through the PKA-TRP-A1 pathway.

288 In this study we used a mouse model of neuropathic pain to dissociate these factors.

289 atform for treating pathologies ranging from neuropathic pain to epilepsy.

290 tivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch

291 (eFT508) as an important drug candidate for neuropathic pain treatment.

292 aviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and

293 Neuropathic pain was induced by partial sciatic nerve li

294 enerated by the spared nerve injury model of neuropathic pain was reversed by ivermectin treatment.

295 development and/or maintenance of acute and neuropathic pain, we selectively ablated Y1R-expressing

296 In these well-established models of neuropathic pain, we show that the onset of chronic pain

297 T2 represents a valuable strategy to relieve neuropathic pain, we synthesized novel activators (4a-f)

298 us CARTp signaling in spinal cord attenuated neuropathic pain, whereas exogenous intrathecal CARTp ev

299 B1 signaling would suppress inflammatory and neuropathic pain without producing cannabimimetic effect

300 agonist drugs for treating inflammatory and neuropathic pain without the psychoactivity of CB1.