ライフサイエンスコーパス: narcolepsy

1 ty of pitolisant in treating the symptoms of narcolepsy.

2 mal dominant cerebellar ataxia, deafness and narcolepsy.

3 macogenetic approach for the amelioration of narcolepsy.

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

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

6 olysomnographic findings that are similar to narcolepsy.

7 and reduces cataplexy in two mouse models of narcolepsy.

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

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

10 attention-deficit hyperactivity disorder and narcolepsy.

11 understand the function of HCRT neurons and narcolepsy.

12 e recruited to block the muscle paralysis in narcolepsy.

13 st of CNS autoimmune complications including narcolepsy.

14 tom of the neurodegenerative sleep disorder, narcolepsy.

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

16 tive for detection of Hcrt1 for diagnosis of narcolepsy.

17 sm may contribute to sleep disorders such as narcolepsy.

18 (CeA) triggered cataplexy of sleep disorder narcolepsy.

19 associated with the sleep/arousal disorder, narcolepsy.

20 tes wakefulness and their destruction causes narcolepsy.

21 p-wake regulators and HCRT deficiency causes narcolepsy.

22 aking, is an important diagnostic symptom of narcolepsy.

23 excessive sleepiness in adult patients with narcolepsy.

24 d allow improved management of children with narcolepsy.

25 he hcrt-1 peptide and the pathophysiology of narcolepsy.

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

27 uces a condition similar to canine and human narcolepsy.

28 gulation of sleep and the pathophysiology of narcolepsy.

29 oss of these cells causes the sleep disorder narcolepsy.

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

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

32 sed in most patients with the sleep disorder narcolepsy.

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

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

35 s or mutation of hypocretin receptors causes narcolepsy.

36 uld be of potential value for treating human narcolepsy.

37 or of its receptors causes human and animal narcolepsy.

38 d the safety and efficacy of solriamfetol in narcolepsy.

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

40 nd muscle tone and in the pathophysiology of narcolepsy.

41 transmitter system as a key target for human narcolepsy.

42 stasis; the absence of hypocretin results in narcolepsy.

43 r mechanisms underlying REM disregulation in narcolepsy.

44 Hcrt function results in the sleep disorder narcolepsy.

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

46 he multiple sleep disturbances that occur in narcolepsy.

47 peptides linked to the human sleep disorder narcolepsy.

48 cells in DQ6(+) individuals with and without narcolepsy.

49 ss and excessive sleepiness in patients with narcolepsy.

50 that might explain the metabolic syndrome in narcolepsy.

51 eep apnea, 28% have hypersomnia, and 4% have narcolepsy.

52 ers such as REM sleep behaviour disorder and narcolepsy.

53 tudying the neurobiological underpinnings of narcolepsy.

54 ad beneficial effects in two mouse models of narcolepsy.

55 ave been implicated in Parkinson disease and narcolepsy.

56 radoxical sleep, and cataplexy, hallmarks of narcolepsy.

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

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

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

60 fectors of the immunopathological process in narcolepsy.

61 to the treatment of sleep disorders such as narcolepsy.

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

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

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

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

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

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

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

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

70 This review is focused on EDS due to OSA and narcolepsy and addresses some of the challenges with man

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

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

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

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

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

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

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

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

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

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

81 EDS is a common symptom of both narcolepsy and obstructive sleep apnea (OSA).

82 In addition, narcolepsy and OSA can occur as comorbid disorders.

83 contributing to the complex pathogenesis of narcolepsy and OSRDs.

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

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

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

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

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

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

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

91 1 have high sensitivity for the diagnosis of narcolepsy and that SOREM periods from NREM1 are a marke

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

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

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

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

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

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

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

99 to children and reproductive-age women with narcolepsy, and reviews the negative impact of health-re

100 mitations of current diagnostic criteria for narcolepsy are discussed, and a possible new classificat

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

102 itionally, the psychosocial ramifications of narcolepsy are often neglected.

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

104 s in the symptomatic and causal treatment of narcolepsy are reviewed.

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

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

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

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

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

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

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

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

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

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

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

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

117 ing daytime functioning for individuals with narcolepsy, but side effects and/or lack of efficacy can

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

119 Canine narcolepsy can readily be quantified.

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

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

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

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

124 Narcolepsy-cataplexy is a neurological disorder associat

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

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

127 Narcolepsy-cataplexy, a neurological disorder associated

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

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

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

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

132 In narcolepsy caused by hypocretin/orexin deficiency, catap

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

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

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

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

137 estigation of the autoimmune contribution to narcolepsy development.

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

139 been well established as a gold standard of narcolepsy diagnosis, although some portions of narcolep

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

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

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

143 ts, and the indication for sodium oxybate in narcolepsy has been expanded to include children.

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

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

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

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

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

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

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

151 5% CI, 10.6%-60.8%] of 14) for patients with narcolepsy/hypocretin deficiency vs population-based con

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 Narcolepsy is a chronic sleep disorder caused by a loss

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

170 Narcolepsy is a common cause of chronic sleepiness disti

171 Narcolepsy is a human sleep disorder resulting from the

172 Narcolepsy is a neurological disorder characterized by e

173 Narcolepsy is a neurological disorder of the sleep-wake

174 Narcolepsy is a rare brain disorder that reflects a sele

175 Narcolepsy is a sleep disorder marked by chronic, debili

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

177 also summarize the developing evidence that narcolepsy is an autoimmune disorder that may be caused

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

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

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

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

182 Narcolepsy is caused by loss of the hypothalamic neurons

183 Narcolepsy is caused by selective degeneration of hypoth

184 The discovery about 20 years ago that narcolepsy is caused by selective loss of the neurons pr

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

186 Narcolepsy is characterized by an impaired ability to ma

187 Narcolepsy is characterized by chronic sleepiness and ca

188 Narcolepsy is characterized by chronic sleepiness and ca

189 The sleep disorder narcolepsy is characterized by excessive daytime sleepin

190 Narcolepsy is characterized by excessive sleepiness and

191 Narcolepsy is characterized by the loss of orexin neuron

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

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

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

195 Narcolepsy is the most common neurological cause of chro

196 Narcolepsy is treated with a combination of lifestyle mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 Narcolepsy patients displayed multifaceted immune activa

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

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

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

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

228 Current narcolepsy pharmacotherapeutics include controlled subst

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

230 Pharmacological therapy for narcolepsy primarily aims to increase wakefulness and re

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

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

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

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

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

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

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

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

239 health-related stigma and efforts to address narcolepsy stigma.

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

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

242 Individuals with narcolepsy suffer from abnormal sleep patterns due to lo

243 In most people with narcolepsy, symptom onset occurs between the ages of 10

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

245 further study of TAAR1 agonists as potential narcolepsy therapeutics.

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

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

248 Narcolepsy type 1 (NT1) is characterized by excessive da

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

250 erebrospinal fluid (CSF) are associated with narcolepsy type 1 (NT1).

251 Narcolepsy type 1 is a devastating neurological sleep di

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

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

254 ning the 'narcoleptic borderland', including narcolepsy type 2 (NT2).

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

256 Narcolepsy was first shown to be tightly associated with

257 1N1)pdm09 Pandemrix vaccination and onset of narcolepsy was suggested in Scandinavia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 ands or receptors) causes the sleep disorder narcolepsy with cataplexy in humans and in animal models

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

275 Narcolepsy with cataplexy is a rare and severe sleep dis

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

277 Narcolepsy with cataplexy is caused by a loss of orexin

278 Idiopathic narcolepsy with cataplexy is thought to be an autoimmune

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

280 Narcolepsy with cataplexy, characterized by sleepiness a

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

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

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

284 ocretin system underlies the pathogenesis of narcolepsy with cataplexy.

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

286 s been implicated as the underlying cause of narcolepsy with cataplexy.

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

288 Narcolepsy with hcrt deficiency is now known to be assoc

289 Symptomatic narcolepsy with low hypocretin level has been described

290 Patients with narcolepsy with mean sleep latency <25 minutes on the Ma

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

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

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

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

295 Previous studies found associations of narcolepsy with the human leukocyte antigen (HLA)-DQ6 al

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