ライフサイエンスコーパス: narcolepsy

1 taplexy in orexin knock-out mice, a model of narcolepsy.

2 of HDC cells in any of the animal models of narcolepsy.

3 radoxical sleep, and cataplexy, hallmarks of narcolepsy.

4 attention-deficit hyperactivity disorder and narcolepsy.

5 understand the function of HCRT neurons and narcolepsy.

6 e recruited to block the muscle paralysis in narcolepsy.

7 st of CNS autoimmune complications including narcolepsy.

8 tom of the neurodegenerative sleep disorder, narcolepsy.

9 xin-ataxin-3 transgenic mouse model of human narcolepsy.

10 sm may contribute to sleep disorders such as narcolepsy.

11 associated with the sleep/arousal disorder, narcolepsy.

12 tes wakefulness and their destruction causes narcolepsy.

13 p-wake regulators and HCRT deficiency causes narcolepsy.

14 aking, is an important diagnostic symptom of narcolepsy.

15 excessive sleepiness in adult patients with narcolepsy.

16 d allow improved management of children with narcolepsy.

17 and loss of Hcrt function has been linked to narcolepsy.

18 uces a condition similar to canine and human narcolepsy.

19 gulation of sleep and the pathophysiology of narcolepsy.

20 oss of these cells causes the sleep disorder narcolepsy.

21 sudden, unwanted transitions-for example, in narcolepsy.

22 ing of behavioural states, such as occurs in narcolepsy.

23 sed in most patients with the sleep disorder narcolepsy.

24 a role in the loss of hypocretin neurons in narcolepsy.

25 ic rat could provide a useful model of human narcolepsy.

26 s or mutation of hypocretin receptors causes narcolepsy.

27 uld be of potential value for treating human narcolepsy.

28 or of its receptors causes human and animal narcolepsy.

29 of orexin appears to be the primary cause of narcolepsy.

30 nd muscle tone and in the pathophysiology of narcolepsy.

31 transmitter system as a key target for human narcolepsy.

32 stasis; the absence of hypocretin results in narcolepsy.

33 r mechanisms underlying REM disregulation in narcolepsy.

34 Hcrt function results in the sleep disorder narcolepsy.

35 wakefulness, and disorders of sleep, such as narcolepsy.

36 he multiple sleep disturbances that occur in narcolepsy.

37 peptides linked to the human sleep disorder narcolepsy.

38 xin(+) neurons or clinical manifestations of narcolepsy.

39 ce have symptoms similar to human and canine narcolepsy.

40 eceptor 2 gene has been implicated in canine narcolepsy.

41 ating axons are present here in canines with narcolepsy.

42 ate wakefulness, and loss of orexin produces narcolepsy.

43 ate sleep-wake stability and are affected in narcolepsy.

44 ently implicated in the human sleep disorder narcolepsy.

45 indicates increased body mass index (BMI) in narcolepsy.

46 ement (REM) sleep and the pathophysiology of narcolepsy.

47 was found in a single case with early onset narcolepsy.

48 ess being the cause of the Hcrt cell loss in narcolepsy.

49 spected or confirmed to have OSA rather than narcolepsy.

50 lved in the pathophysiological mechanisms of narcolepsy.

51 tant dogs, the only known monogenic model of narcolepsy.

52 er an autoimmune process could be at play in narcolepsy.

53 ers such as REM sleep behaviour disorder and narcolepsy.

54 fectors of the immunopathological process in narcolepsy.

55 to the treatment of sleep disorders such as narcolepsy.

56 , Huntington's disease (HD), depression, and narcolepsy.

57 tudying the neurobiological underpinnings of narcolepsy.

58 mal dominant cerebellar ataxia, deafness and narcolepsy.

59 ad beneficial effects in two mouse models of narcolepsy.

60 macogenetic approach for the amelioration of narcolepsy.

61 ave been implicated in Parkinson disease and narcolepsy.

62 2), rather than stage 1 sleep (NREM1), as in narcolepsy.

63 nts with narcolepsy and in 2 mouse models of narcolepsy.

64 l, and loss of the orexin neurons results in narcolepsy, a condition characterized by chronic sleepin

65 ide hypocretin (Hcrt) has been implicated in narcolepsy, a debilitating disorder characterized by exc

66 Narcolepsy, a disorder associated with HLA-DQB1*06:02 an

67 Type 1 narcolepsy, a disorder caused by a lack of hypocretin (o

68 unction or deletion of the orexin system and narcolepsy, a disorder characterized by hypersomnolence

69 at orexin knockout mice are a model of human narcolepsy, a disorder characterized primarily by rapid

70 Narcolepsy, a disorder of rapid eye movement (REM) sleep

71 drome remarkably similar to human and canine narcolepsy, a sleep disorder characterized by excessive

72 mal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN).

73 mitter and its unique therapeutic effects in narcolepsy and alcoholism.

74 et group whose function is altered in canine narcolepsy and appears pivotal for normal REM and wakefu

75 ng are responsible for the human diseases of narcolepsy and cataplexy; inhibition of orexin receptors

76 ns, and mice lacking the orexin neurons have narcolepsy and fail to rouse in response to hunger.

77 , and supportive therapy are recommended for narcolepsy and hypersomnia; continuous positive airway p

78 Narcolepsy and idiopathic hypersomnia are chronic brain

79 es have strengthened the association between narcolepsy and immune system gene polymorphisms, includi

80 mined histaminergic neurons in patients with narcolepsy and in 2 mouse models of narcolepsy.

81 Genetic studies in a canine model of narcolepsy and in knock-out mice have led to the identif

82 relevant to human diseases such as obesity, narcolepsy and infertility.

83 ng the hypocretin neurotransmitter system in narcolepsy and normal sleep.

84 nce, and disruption of their function causes narcolepsy and obesity.

85 contributing to the complex pathogenesis of narcolepsy and OSRDs.

86 cell survival, with possible implications in narcolepsy and other autoimmune diseases.

87 ry), and treatment options for children with narcolepsy and other hypersomnias of central origin in o

88 ethnic groups, we found association between narcolepsy and polymorphisms in the TRA@ (T-cell recepto

89 n shown to be involved in the sleep disorder narcolepsy and possibly in the normal regulation of slee

90 dogs exhibit all the major symptoms of human narcolepsy and respond to drugs that increase or decreas

91 g susceptibility to sleep disorders, such as narcolepsy and restless leg syndrome.

92 orders of known cellular etiology, including narcolepsy and retinopathies.

93 t), whose loss results in the sleep disorder narcolepsy and that has also been implicated in feeding

94 1 have high sensitivity for the diagnosis of narcolepsy and that SOREM periods from NREM1 are a marke

95 In this study, 11 sporadic cases of canine narcolepsy and two additional multiplex families were in

96 wakefulness, and reward; their loss produces narcolepsy and weight gain.

97 uraged efforts to discover agonists to treat narcolepsy and, alternatively, antagonists to treat inso

98 eurotransmitter system in the sleep disorder narcolepsy and, potentially, in the regulation of normal

99 which promote wakefulness (their loss causes narcolepsy) and also regulate metabolism and reward.

100 a single gene underlying the sleep disorder narcolepsy, and identification of loci that make quantit

101 s study establishes zebrafish as a model for narcolepsy, and indicating a role of HCRT neurons in reg

102 animals, may be effective in treating human narcolepsy, and may affect a broad range of motivated be

103 n, attention deficit/hyperactivity disorder, narcolepsy, and obesity.

104 genetic predisposition, most cases of human narcolepsy are associated with a deficient hypocretin sy

105 mal dominant cerebellar ataxia, deafness and narcolepsy are located in the C-terminus end of the TS d

106 Currently available treatments for narcolepsy are only palliative, symptom-oriented pharmac

107 so indicates genetic heterogeneity in canine narcolepsy, as reported previously in humans.

108 ied an apparent increase in the incidence of narcolepsy associated with a specific adjuvanted pandemi

109 This diagnosis was defined as narcolepsy associated with cataplexy plus HLA-DQB1*06:02

110 In this Review, we discuss how the narcolepsy association was detected, and we present the

111 in B cells, may mediate type 1 diabetes and narcolepsy associations in the chromosome 15q25.1 region

112 ke and energy metabolism in a mouse model of narcolepsy (ataxin-ablation of hypocretin-expressing neu

113 The current animal models of narcolepsy, based on either disruption of the orexinergi

114 s are not required for the major symptoms of narcolepsy, because all animal models have these symptom

115 man narcolepsy through histopathology of six narcolepsy brains and mutation screening of Hcrt, Hcrtr1

116 ibute to the genetic predisposition to human narcolepsy but that additional susceptibility loci are a

117 None of the patterns were exclusive for narcolepsy but were also detected in the OSRD group at s

118 and sex-matched patients with a diagnosis of narcolepsy but with normal hypocretin levels.

119 pocretin (Hcrt) cell loss is responsible for narcolepsy, but Hcrt's role in normal behavior is unclea

120 ake-promoting drug used for the treatment of narcolepsy, but its precise mechanism of action is unkno

121 NT Cataplexy is one of the major symptoms of narcolepsy, but little is known about how strong, positi

122 Murine and canine narcolepsy can be caused by mutations of the hypocretin

123 some sleep disorders such as parasomnias and narcolepsy can be confused with those of other neurologi

124 Canine narcolepsy can readily be quantified.

125 In humans and canines with narcolepsy, cataplexy is considered to be a separate and

126 The encephalitic process, responsible for narcolepsy-cataplexy and hypocretin deficiency, reflects

127 affected 32% of the patients, sometimes with narcolepsy-cataplexy and low CSF hypocretin.

128 e compared with those obtained in idiopathic narcolepsy-cataplexy and with normal control brains.

129 CSF hypocretin was examined in 38 successive narcolepsy-cataplexy cases [36 human leukocyte antigen (

130 Narcolepsy-cataplexy is a neurological disorder associat

131 Here, we demonstrate rescue of the narcolepsy-cataplexy phenotype of orexin neuron-ablated

132 egulation of REM sleep control unique to the narcolepsy-cataplexy syndrome emerges from loss of signa

133 Narcolepsy-cataplexy, a neurological disorder associated

134 Human narcolepsy-cataplexy, a sleep disorder associated with a

135 tion of hypocretin-containing cells in human narcolepsy-cataplexy.

136 ORX, or their receptors, is associated with narcolepsy/cataplexy, a disorder characterized by an inc

137 A) receptor-expressing PF neurones may cause narcolepsy/cataplexy.

138 In narcolepsy caused by hypocretin/orexin deficiency, catap

139 ep and wake signals, a process that fails in narcolepsy caused by OH loss.

140 Cataplexy is a hallmark of narcolepsy characterized by the sudden uncontrollable on

141 eceptor HCRTR2, which has been implicated in narcolepsy, correlated with sleep disturbance.

142 nergic neurons, which causes acquired murine narcolepsy, delays emergence from anesthesia, without ch

143 hanisms leading to orexin(+) neuron loss and narcolepsy development.

144 lta power in SWS, reproducing, respectively, narcolepsy excessive daytime sleepiness and poor sleep q

145 By contrast, genes conferring risk for narcolepsy function in the immune system.

146 An increased incidence in the sleep-disorder narcolepsy has been associated with the 2009-2010 pandem

147 The sleep disorder narcolepsy has been linked to loss of hypothalamic neuro

148 almost 10-fold increase in the incidence of narcolepsy has been reported following the use of one ty

149 QB1*06:02 allele, the autoimmune etiology of narcolepsy has remained largely hypothetical.

150 r 2, the gene for autosomal recessive canine narcolepsy, has led to the development of a physical map

151 Humans with narcolepsy have decreased numbers of Hcrt neurons and Hc

152 Pathogenetic mechanisms of narcolepsy have so far mainly focused on autoimmunity.

153 ive (57.4% [95% CI, 48.1%-66.3%] of 122) for narcolepsy/hypocretin deficiency (area under the curve,

154 to determine optimal diagnostic cutoffs for narcolepsy/hypocretin deficiency compared with different

155 5% CI, 10.6%-60.8%] of 14) for patients with narcolepsy/hypocretin deficiency vs population-based con

156 Finally, 118 patients with narcolepsy/hypocretin deficiency were compared with 118

157 ison, 516 age- and sex-matched patients with narcolepsy/hypocretin deficiency were selected from 1749

158 f NPSG REML and MSLT as diagnostic tests for narcolepsy/hypocretin deficiency.

159 compared within groups by final diagnosis of narcolepsy/hypocretin deficiency.

160 ised regarding a spike in cases of childhood narcolepsy in 2010 following the 2009 H1N1 pandemic (pH1

161 Hypocretin mutations produce narcolepsy in animal models.

162 ministration of Hcrt can reverse symptoms of narcolepsy in animals, may be effective in treating huma

163 Hcrtr2) gene were identified as the cause of narcolepsy in Dobermans and Labradors.

164 in (Hcrt or orexin) reverses the symptoms of narcolepsy in genetically narcoleptic dogs.

165 The absence of these neurons causes narcolepsy in humans and model organisms.

166 esigner drug (DREADD) technology ameliorated narcolepsy in mice lacking orexin neurons.

167 rotransmission results in the sleep disorder narcolepsy in mice, dogs, and humans.

168 Low CSF hypocretin-1 is most predictive of narcolepsy in patients positive for HLA allele DQB1*0602

169 uenza virus infection in the pathogenesis of narcolepsy in susceptible subjects.

170 ance of this stabilizing role is apparent in narcolepsy, in which an absence of the orexin neurons ca

171 ween human narcoleptics and animal models of narcolepsy, including therapeutic drug use and species d

172 ician suspect the diagnosis.RECENT FINDINGS: Narcolepsy is a chronic rapid eye movement sleep disorde

173 Narcolepsy is a chronic sleep disorder, likely with an a

174 Narcolepsy is a common cause of chronic sleepiness disti

175 Narcolepsy is a disabling sleep disorder affecting human

176 Narcolepsy is a human sleep disorder resulting from the

177 Narcolepsy is a neurological disorder characterized by e

178 Narcolepsy is a sleep disorder affecting animals and hum

179 that the onset of symptoms in canine genetic narcolepsy is accompanied by degenerative changes in for

180 of hypocretin neurons in the human disorder narcolepsy is associated with excessive somnolence, cata

181 Narcolepsy is caused by a lack of orexin (hypocretin), b

182 Narcolepsy is caused by a loss of orexin/hypocretin sign

183 We have determined that canine narcolepsy is caused by disruption of the hypocretin (or

184 he same conclusion: the human sleep disorder narcolepsy is caused by failure of signaling mediated by

185 Narcolepsy is caused by loss of the hypothalamic neurons

186 Narcolepsy is caused by selective degeneration of hypoth

187 Narcolepsy is caused by the loss of hypocretin (orexin)-

188 Narcolepsy is characterized by an impaired ability to ma

189 Narcolepsy is characterized by chronic sleepiness and ca

190 Narcolepsy is characterized by chronic sleepiness and ca

191 The sleep disorder narcolepsy is characterized by excessive daytime sleepin

192 Narcolepsy is characterized by excessive sleepiness and

193 Narcolepsy is characterized by the loss of orexin neuron

194 aracteristics than previously recognized and narcolepsy is common to both.

195 contrast to these animal models, most human narcolepsy is not familial, is discordant in identical t

196 A known triggering factor for narcolepsy is pandemic 2009 influenza H1N1, suggesting a

197 In humans, narcolepsy is rarely due to hypocretin mutations, but th

198 disorders such as insomnia, parasomnias, and narcolepsy is still evolving.

199 gic process that underlies the sleepiness of narcolepsy is unknown.

200 Cataplexy, a symptom associated with narcolepsy, is a waking state in which muscle tone is lo

201 dafinil, a wake-promoting drug used to treat narcolepsy, is increasingly being used as a cognitive en

202 of the hypocretin system, such as occurs in narcolepsy, leads to a disruption of sleep and is often

203 ns and cataplexy-like symptoms, suggesting a narcolepsy-like phenotype.

204 the loss of Hcrt cells may be a cause of the narcolepsy-like symptoms of PD and may be ameliorated by

205 Mice lacking the orexin peptides develop narcolepsy-like symptoms, whereas mice with a selective

206 prising increase in histaminergic neurons in narcolepsy may be a compensatory response to loss of exc

207 nt advances provide compelling evidence that narcolepsy may be a neurodegenerative or autoimmune diso

208 eased histamine cell numbers we see in human narcolepsy may instead be related to the process causing

209 suggest that the triggering events of human narcolepsy may involve a proliferation of histamine-cont

210 ccumulating evidence indicates that signs of narcolepsy may start during childhood.

211 that are dysfunctional in the sleep disorder narcolepsy, may be involved in the expression of the cir

212 f CSF hypocretin-1 concentration to diagnose narcolepsy might be most useful in ambulatory patients w

213 Although hypocretin-1 deficiency in narcolepsy might have therapeutic relevance, additional

214 ompounds reduced body temperature in the two narcolepsy models at the highest doses tested.

215 thognomonic symptom of this disorder, in the narcolepsy models.

216 re, and cataplexy were assessed in two mouse narcolepsy models.

217 n (Hcrt) receptor-2 mutant dogs, and 3 mouse narcolepsy models: Hcrt (orexin) knockouts, ataxin-3-ore

218 rogress has occurred in the understanding of narcolepsy--molecular techniques have identified the lat

219 duction in their activity has been linked to narcolepsy, obesity and depression.

220 ing disorders, reproductive disorders, pain, narcolepsy, obesity, and inflammation.

221 ts with excessive sleepiness associated with narcolepsy, obstructive sleep apnea, and shift-work slee

222 s to REM sleep, a defining characteristic of narcolepsy, occurred frequently.

223 nges are primary to an autoimmune process in narcolepsy or secondary to orexin deficiency, these find

224 no significant differences in the CSF of IH, narcolepsy, or control groups.

225 in-concentrating hormone, and histamine in 7 narcolepsy patients and 12 control subjects using stereo

226 Narcolepsy patients displayed multifaceted immune activa

227 Compared to controls, narcolepsy patients had 94% more histaminergic TMN neuro

228 Additionally, T cells from narcolepsy patients showed increased production of the p

229 This increase was higher in 5 narcolepsy patients with >90% orexin neuron loss than in

230 compared peripheral mononucleated cells from narcolepsy patients with HLA-DQB1*06:02-matched healthy

231 ibit a phenotype strikingly similar to human narcolepsy patients, as well as canarc-1 mutant dogs, th

232 Latency Test (MSLT) raise the possibility of narcolepsy, patients with obstructive sleep apnea (OSA)

233 Current narcolepsy pharmacotherapeutics include controlled subst

234 phagia and severe obesity in addition to the narcolepsy phenotype.

235 rons, or orexin receptors recapitulate human narcolepsy phenotypes, further highlighting a critical r

236 In canine genetic narcolepsy, produced by a mutation of the Hcrtr2 gene, s

237 n ligand is deficient in most cases of human narcolepsy, providing possible diagnostic applications.

238 of orexin (hypocretin) neurons causes human narcolepsy raises the possibility that other acquired di

239 ding excessive daytime sleepiness, insomnia, narcolepsy, rapid eye movement sleep behavior disorder,

240 Thus, the cause of human narcolepsy remains unknown.

241 Cataplexy, a symptom associated with narcolepsy, represents a unique dissociation of behaviou

242 isorders, in particular circadian disorders, narcolepsy, restless-legs syndrome, and OSAS.

243 r subtype P2Y gene, which is associated with narcolepsy (rs2305795, combined P = 6.1 x 10(1), odds ra

244 Among patients being evaluated for possible narcolepsy, short REML (</=15 minutes) at NPSG had high

245 mnia and thus a high pretest probability for narcolepsy, short REML remained highly specific (95.4% [

246 nd may contribute to some of the symptoms of narcolepsy such as preserved consciousness during catapl

247 l loss caused manifestations mimicking human narcolepsy, such as cataplexy and sleep attacks.

248 The genetic contribution of HLA-DQ to narcolepsy susceptibility was also estimated by use of l

249 Despite the known role of orexin neurons in narcolepsy, the precise neural mechanisms downstream of

250 We explored the role of hypocretins in human narcolepsy through histopathology of six narcolepsy brai

251 pealing links for medical histories spanning narcolepsy to axonal neuropathy.

252 ic and environmental factors associated with narcolepsy, together with serologic data, collectively p

253 les, mean age 11 years) with recent onset of narcolepsy type 1 (NT1) were studied with fMRI while vie

254 Narcolepsy type 1 is a devastating neurological sleep di

255 e children and adolescents with recent onset narcolepsy type 1 were investigated.

256 IH, 12 patients (9 males and 3 females) with narcolepsy type 1, and 15 controls (9 males and 6 female

257 y, we searched for autoantibodies related to narcolepsy using a neuroanatomical array: rat brain sect

258 Narcolepsy was first shown to be tightly associated with

259 1N1)pdm09 Pandemrix vaccination and onset of narcolepsy was suggested in Scandinavia.

260 or =8 min and > or =2 SOREMPs (diagnostic of narcolepsy) was observed in 5.9% (males) and 1.1% (femal

261 sed prevalence of HLA-DQB1*0602, a marker of narcolepsy, was observed in males but not in females wit

262 ing orexin knock-out (KO) mice as a model of narcolepsy, we critically tested the three leading hypot

263 histamine levels may be low in patients with narcolepsy, we examined histaminergic neurons in patient

264 Using orexin knock-out mice as a model of narcolepsy, we found that palatable foods, especially ch

265 To identify the neuronal circuits underlying narcolepsy, we produced a mouse model in which a loxP-fl

266 ts with a high pretest probability of having narcolepsy were compared within group by their final dia

267 ia, rapid eye movement sleep disorder and/or narcolepsy were identified in 11 subjects.

268 Relative risks for narcolepsy were next calculated for heterozygous DQB1*06

269 sleep disorders (low pretest probability for narcolepsy) were compared within groups by final diagnos

270 humans is associated with the sleep disorder narcolepsy, which is characterized by excessive daytime

271 Lack of orexin produces narcolepsy, which is characterized by poor maintenance o

272 All these symptoms are present in narcolepsy, which is linked to a selective loss of hypoc

273 to over 100 HLA-associated disorders; thus, narcolepsy will provide new insights on how HLA-TCR inte

274 polysomnography and MSLT, including 25 with narcolepsy with cataplexy (N+C), 41 with narcolepsy with

275 ng with muscle tone cannot be maintained and narcolepsy with cataplexy ensues.

276 ng a waking state because, in their absence, narcolepsy with cataplexy ensues.

277 and Drug Administration for the treatment of narcolepsy with cataplexy in patients aged more than 16

278 Narcolepsy with cataplexy is a rare and severe sleep dis

279 rowing evidence supports the hypothesis that narcolepsy with cataplexy is an autoimmune disease.

280 Narcolepsy with cataplexy is caused by a loss of orexin

281 Idiopathic narcolepsy with cataplexy is thought to be an autoimmune

282 ts with hypersomnolence syndromes (excluding narcolepsy with cataplexy) and evidence for abnormal cer

283 Narcolepsy with cataplexy, characterized by sleepiness a

284 in the number of histamine neurons in human narcolepsy with cataplexy, with no overlap between narco

285 retin/orexin (hcrt) producing neurons causes narcolepsy with cataplexy.

286 entified for both restless legs syndrome and narcolepsy with cataplexy.

287 ocretin system underlies the pathogenesis of narcolepsy with cataplexy.

288 nea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy.

289 nal fluid hypocretin-1 results available) or narcolepsy with documented low (</= 110 pg/mL) cerebrosp

290 Narcolepsy with hcrt deficiency is now known to be assoc

291 Symptomatic narcolepsy with low hypocretin level has been described

292 s with other hypersomnias, and patients with narcolepsy with normal hypocretin levels.

293 Remarkably, narcolepsy with or without cataplexy with low/intermedia

294 report genome-wide association analyses for narcolepsy with replication and fine mapping across thre

295 Given the tight association of narcolepsy with the human leukocyte antigen (HLA) HLA-DQ

296 ith narcolepsy with cataplexy (N+C), 41 with narcolepsy without cataplexy (N-C), 21 with idiopathic h

297 These results suggest a high prevalence of narcolepsy without cataplexy, as defined by the Internat

298 ar clarify heterogeneity among patients with narcolepsy without cataplexy.

299 The diagnosis of narcolepsy without documented cataplexy is based on the

300 t sleep (REM) control and the sleep disorder narcolepsy, yet how they influence sleep-related systems