ライフサイエンスコーパス: OCD

1 OCD and mood were assessed with standardized scales and

2 OCD is the key example of the 'obsessive-compulsive and

3 OCD neuroimaging studies have consistently shown abnorma

4 OCD polygenic risk scores were significantly associated

5 OCD youth-in a randomized rater-blinded trial-were re-sc

6 between 1940 and 2007, we identified 30 082 OCD and 7279 TD/CTD cases in the National Patient Regist

7 We performed whole-exome sequencing in 222 OCD parent-child trios (184 trios after quality control)

8 er GWAS meta-analysis of 3495 AN cases, 2688 OCD cases, and 18,013 controls.

9 vo measures of functional connectivity in 44 OCD patients and 43 healthy comparison subjects.

10 Among them, 54 OCD patients were treated with SSRIs for 16 weeks, resul

11 tmortem brain tissue were compared between 6 OCD and 8 control cases.

12 At 11 centers, 99 OCD patients were randomly allocated to treatment with e

13 Diagnostic information about OCD was obtained using the Swedish National Patient Regi

14 s), and placebo for the treatment of DD, AD, OCD, and PTSD in children and adolescents.

15 In addition, OCD is an important example of a neuropsychiatric disord

16 ry therapies should be investigated in adult OCD, rather than solely childhood OCD, particularly in c

17 and in parallel with PCP signaling to affect OCD.

18 Although OCD is a relatively homogenous disorder with similar sym

19 utations displayed OCD and self-grooming (an OCD-like behavior in mice), respectively.

20 dium spiny neurons were most enriched for AN-OCD risk, consistent with neurobiological findings for b

21 er tested whether shared genetic risk for AN/OCD was associated with particular tissue or cell-type g

22 ith ASD (structural MRI: 911; fMRI: 188) and OCD (structural MRI: 928; fMRI: 247) and control subject

23 ents with ADHD (N=2,271), ASD (N=1,777), and OCD (N=2,323) from 151 cohorts worldwide were analyzed u

24 ed a high genetic correlation between AN and OCD (r(g) = 0.49 +/- 0.13, p = 9.07 x 10(-7)) and a siza

25 gical findings of shared risk between AN and OCD and suggest that larger GWASs are warranted.

26 ow-up analyses revealed that although AN and OCD overlap heavily in their shared risk with other psyc

27 ased glutamate both in children with ASD and OCD compared with controls (p=0.007), but no differences

28 ent findings confirm overlap between ASD and OCD in terms of glutamate involvement.

29 ntrol abnormalities in patients with ASD and OCD.

30 ss different age groups among ADHD, ASD, and OCD.

31 rom eight pairs of unaffected comparison and OCD subjects.

32 ionships between functional connectivity and OCD symptoms pre- and post-CBT were examined using longi

33 hermore, the risk of any mental disorder and OCD was more elevated after a streptococcal throat infec

34 MDD and OCD both involve deficits in cognitive control.

35 ccurs in neuropsychiatric conditions such as OCD and TS.

36 o Streptococcus-related conditions) and both OCD and TD/CTD.

37 C), a structure known to be involved in both OCD and depression.

38 ions of hyperactivity in pre-SMA/SMA in both OCD and Tourette syndrome, and evidence that pre-SMA is

39 ptake inhibitor medication-for managing both OCD and non-OCD anxiety disorders in clinical settings.

40 e cortex (vPCC)-regions possibly affected by OCD-at baseline.

41 d in adult OCD, rather than solely childhood OCD, particularly in cases with prominent distress when

42 In the combined OCD group, within vPCC, lower pre-CBT Glu predicted grea

43 Primary comparisons concerned OCD symptoms, measured using the Yale-Brown Obsessive Co

44 lanar cell polarity (PCP) signaling controls OCD and CE in other contexts, leading to the hypothesis

45 ALIC-NAcc-DBS significantly decreased OCD symptoms (mean Yale-Brown Obsessive Compulsive Scale

46 sorder (ASD), obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD)

47 behaviors in obsessive-compulsive disorder (OCD) and related illnesses, but it is unclear whether th

48 ns related to obsessive-compulsive disorder (OCD) and the role of TNFalpha and related signaling path

49 evelopment of obsessive-compulsive disorder (OCD) and tic disorders, a concept termed pediatric autoi

50 ation between obsessive-compulsive disorder (OCD) and Tourette's/chronic tic disorders (TD/CTD) with

51 criteria for obsessive-compulsive disorder (OCD) and various types of anxiety disorders, but phenome

52 d behavior in obsessive-compulsive disorder (OCD) are caused by impaired frontostriatal function.

53 er (ASD), and obsessive-compulsive disorder (OCD) are common neurodevelopmental disorders that freque

54 vosa (AN) and obsessive-compulsive disorder (OCD) are often comorbid and likely to share genetic risk

55 rs (ASDs) and obsessive compulsive disorder (OCD) are often comorbid with the overlap based on compul

56 nt-refractory obsessive-compulsive disorder (OCD) can be considered an established therapy.

57 Patients with obsessive-compulsive disorder (OCD) can be described as cautious and hesitant, manifest

58 percentage of obsessive-compulsive disorder (OCD) cases exhibiting additional neuropsychiatric sympto

59 patients with obsessive-compulsive disorder (OCD) during both processes.

60 nt refractory obsessive-compulsive disorder (OCD) has not been examined.

61 toms (OCS) or Obsessive Compulsive Disorder (OCD) in the context of schizophrenia or related disorder

62 activation in Obsessive Compulsive Disorder (OCD) in the transition between a resting and a non-rest

63 ders (DSM-5), obsessive-compulsive disorder (OCD) included a new "tic-related" specifier.

64 Obsessive-compulsive disorder (OCD) is a chronic and disabling condition that often res

65 Obsessive-compulsive disorder (OCD) is a debilitating neuropsychiatric disorder with a

66 Obsessive-compulsive disorder (OCD) is a disabling condition, often associated with a c

67 Obsessive-compulsive disorder (OCD) is a highly prevalent and chronic condition that is

68 Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder associated with sign

69 a are limited.Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder with symptoms includ

70 Obsessive-compulsive disorder (OCD) is a psychiatric disorder characterized by obsessio

71 Obsessive compulsive disorder (OCD) is a severe illness that affects 2-3% of people wor

72 Obsessive-compulsive disorder (OCD) is a severe, chronic neuropsychiatric disorder with

73 Obsessive-compulsive disorder (OCD) is associated with high risk of suicide.

74 Obsessive-compulsive disorder (OCD) is commonly associated with alterations in cortico-

75 ividuals with obsessive-compulsive disorder (OCD) is largely unknown.

76 Obsessive-compulsive disorder (OCD) is prevalent and without adequate treatment usually

77 e networks in obsessive-compulsive disorder (OCD) may provide clues to the pathophysiology of this ne

78 patients, 13 obsessive-compulsive disorder (OCD) patients, 18 unaffected first-degree relatives of t

79 ma samples of obsessive-compulsive disorder (OCD) patients.

80 nt-refractory obsessive-compulsive disorder (OCD) patients.

81 Pediatric obsessive-compulsive disorder (OCD) sometimes appears rapidly, even overnight, often af

82 reatments for obsessive-compulsive disorder (OCD) tend to be of mixed efficacy but include psychologi

83 g symptoms of obsessive-compulsive disorder (OCD) that have proven refractory to extensive, appropria

84 tte syndrome, obsessive-compulsive disorder (OCD), and attention deficit hyperactivity disorder (ADHD

85 ng symptom in obsessive-compulsive disorder (OCD), and is associated with worse functional impairment

86 treatment for obsessive-compulsive disorder (OCD), but only some patients achieve minimal symptoms fo

87 the risk for obsessive-compulsive disorder (OCD), there is also evidence that there are maternal com

88 nic nature of obsessive-compulsive disorder (OCD), where compulsive actions are recognized as disprop

89 the Sapap3-KO obsessive-compulsive disorder (OCD)-relevant mouse model, with M2 inputs strengthened b

90 mans with the obsessive-compulsive disorder (OCD)-spectrum disorder, trichotillomania.

91 th refractory obsessive-compulsive disorder (OCD).

92 opathology of obsessive compulsive disorder (OCD).

93 ent-resistant obsessive-compulsive disorder (OCD).

94 nt for severe obsessive-compulsive disorder (OCD).

95 ion (MDD) and obsessive-compulsive disorder (OCD).

96 for treating obsessive-compulsive disorder (OCD).

97 d by anxiety, Obsessive Compulsive Disorder (OCD).

98 r EAAC1, with obsessive-compulsive disorder (OCD).

99 symptoms and obsessive compulsive disorder (OCD).

100 nt-refractory obsessive-compulsive disorder (OCD).

101 disorders, schizophrenia, anxiety disorder, OCD, and most affective disorders also showed mean disso

102 ster for a diagnosis of any mental disorder, OCD, or tic disorders.

103 observed in obsessive compulsive disorders (OCD).

104 terior or posterior) optic cup displacement (OCD) averaged 41 +/- 7 mum in 30-degree adduction.

105 tients and mice with GRN mutations displayed OCD and self-grooming (an OCD-like behavior in mice), re

106 Oriented cell division (OCD) and convergent extension (CE) shape developing rena

107 h a dramatic loss of oriented cell division (OCD).

108 ross 37 datasets participating in the ENIGMA-OCD Working Group, we calculated intra-individual brain

109 when the groups were matched by age at first OCD diagnosis and after various sensitivity analyses.

110 and diagnostic and treatment approaches for OCD among adults (>/=18 years), published between Januar

111 to make a clear statement on whether DBS for OCD is established therapy.

112 However, clinical experience with DBS for OCD remains limited.

113 -reviewed articles reporting ABL and DBS for OCD was performed in January 2018.

114 kdrop that gamma knife capsulotomy (GKC) for OCD was developed.

115 hough less than streptococcal infections for OCD and any mental disorder, which could also support im

116 s first-line pharmacologic interventions for OCD; however, more recent data support the adjunctive us

117 d promising last-resort treatment option for OCD.

118 6.9%-8.3%) of the total variance in risk for OCD for the best model, and direct additive genetics acc

119 tic maternal effects as influencing risk for OCD in offspring.

120 ct genetic and maternal effects, on risk for OCD.

121 traits is markedly stronger for AN than for OCD.

122 Effective treatments for OCD include serotonin reuptake inhibitors and cognitive-

123 A total of 102 medication-free OCD patients and 101 matched healthy control (HC) subjec

124 of variance revealed a main effect of group (OCD < CONT; F([1,87]) = 5.3; P = 0.024) upon fractional

125 Compared to HCs, OCD patients exhibited significantly larger FC between t

126 s, serotonergic dysfunction in heterogeneous OCD patients should be investigated for precision medici

127 rior cingulate cortex significantly improved OCD symptoms and may be considered as a potential interv

128 In OCD, TSPO VT was significantly elevated in these brain r

129 of most serotonergic neurons, was altered in OCD patients and could predict the SSRI response.

130 rtical-striatal-thalamic-cortical circuit in OCD, and a previous feasibility study indicated benefici

131 Reduced connectivity in OCD relative to HC participants was detected between def

132 ty structure of the functional connectome in OCD patients as nodes within the basal ganglia and cereb

133 nstrated clinically significant decreases in OCD symptoms when conducted by trained therapists.

134 CC dysfunction contributing to depression in OCD, particularly involving intracingulate connectivity

135 logical mechanisms of comorbid depression in OCD, we examined effective connectivity and neurochemica

136 pathway toward systematic gene discovery in OCD via identification of DN damaging variants.

137 e also show that additive genetic effects in OCD are overestimated when maternal effects are not mode

138 d damaging missense variants are enriched in OCD probands (rate ratio, 1.52; p = .0005) and contribut

139 ertainty and distrust of past experiences in OCD.

140 iatum, a brain region that is hyperactive in OCD.

141 We tested this hypothesis in OCD patients and control subjects by relating measures o

142 in brain regions consistently implicated in OCD human imaging studies.

143 of the functional neuroanatomy implicated in OCD, has resulted in improved clinical efficacy for an a

144 le signature of altered brain morphometry in OCD, while the hub findings point to OCD-related alterat

145 ization of structural covariance networks in OCD, and reorganization of brain hubs.

146 recruitment of PFC has also been observed in OCD patients during paradigms assessing cognitive flexib

147 Skin conductance responses in OCD patients (n = 43) failed to differentiate during rev

148 ship emphasized lower network segregation in OCD compared to healthy controls.

149 h did not correlate with symptom severity in OCD.

150 veal an absence of vmPFC safety signaling in OCD, undermining flexible threat updating and explicit c

151 registers to estimate the risk of suicide in OCD and identify the risk and protective factors associa

152 anscranial magnetic stimulation treatment in OCD, these results support further dissection of the rol

153 ower (rank-transformed) centrality values in OCD for volume of caudate nucleus and thalamus, and surf

154 ore, genes harboring DN damaging variants in OCD are enriched for those reported in neurodevelopmenta

155 estimate that 34% of DN damaging variants in OCD contribute to risk and that DN damaging variants in

156 -related hyperconnectivity with the vmPFC in OCD, consistent with biased processing of the CS+.

157 et for the surgical treatment of intractable OCD.

158 Youths aged 7-17 years with DSM-IV OCD and typically developing controls underwent 3 T prot

159 s of OCD parent-child trios will reveal more OCD risk genes and will provide needed insights into und

160 No OCD-specific differences were observed across different

161 tor medication-for managing both OCD and non-OCD anxiety disorders in clinical settings.

162 ately 335 genes contribute to risk in 22% of OCD cases.

163 behaviours, and the genetic architecture of OCD is increasingly understood.

164 de new information on the molecular basis of OCD and suggest new avenues for its treatment.

165 tal factors to the familial coaggregation of OCD and suicidal behavior.

166 Familial coaggregation of OCD and suicide attempts was explained by additive genet

167 Sequencing larger cohorts of OCD parent-child trios will reveal more OCD risk genes a

168 s, and collected register-based diagnoses of OCD, suicide attempts, and deaths by suicide and followe

169 er 31, 1990, and followed for a diagnosis of OCD through December 31, 2013.

170 support for the glutamatergic hypothesis of OCD, particularly for the increased EAAT3 function, and

171 l regions may represent neural mechanisms of OCD.

172 pap3, Slitrk5 and Shank3, reported models of OCD and autism spectrum disorders (ASDs).

173 Psychophysical models of OCD propose that anxiety (amygdala) and habits (dorsolat

174 ay result not only from direct modulation of OCD neural pathways but also from enhanced efficacy of p

175 level, the structural covariance networks of OCD showed lower clustering (P < 0.0001), lower modulari

176 ng inflammation within the neurocircuitry of OCD.

177 rs/transporters occurred primarily in OFC of OCD subjects.

178 5% CI, 1.15-1.21; P < .001), particularly of OCD (n = 556; IRR, 1.51; 95% CI, 1.28-1.77; P < .001) an

179 lu may be involved in the pathophysiology of OCD and may moderate response to CBT.

180 ated understanding of the pathophysiology of OCD are considered in the context of dimensional psychia

181 an important role in the pathophysiology of OCD.

182 The observed familial patterns of OCD in relation to tics were not seen in relation to oth

183 n perseveration challenges preconceptions of OCD as a disorder of inflexibility.

184 among second- and third-degree relatives of OCD and TD/CTD probands.

185 CD was considerably greater than the risk of OCD in relatives of individuals with non-tic-related OCD

186 aHR) were calculated to estimate the risk of OCD in relatives of individuals with OCD with and withou

187 However, the risk of OCD in relatives of individuals with tic-related OCD was

188 dications as well as biological specimens of OCD patients.

189 t not significantly different in striatum of OCD subjects.

190 largest brain structural covariance study of OCD to date, point to a less segregated organization of

191 ing tic-related OCD as a distinct subtype of OCD is lacking.

192 ed OCD is a particularly familial subtype of OCD.

193 the autoimmune/neuroinflammatory theories of OCD should extend beyond the basal ganglia to include th

194 bitors or as monotherapy in the treatment of OCD, although their efficacy has not yet been establishe

195 Treatment of OCD-like grooming behavior in Slitrk5, SAPAP3, and laser

196 epresent a major advancement in treatment of OCD.

197 reflect the neurobiological underpinning of OCD and could aid future precision medicine as a differe

198 therapy, reflecting a floor effect of DBS on OCD.

199 pproaches could further advance knowledge on OCD and improve clinical outcomes.

200 and nucleus accumbens region (ALIC-NAcc) on OCD symptoms, executive functions, and personality trait

201 pathophysiology in children with rapid-onset OCD symptoms, and perhaps in other conditions.

202 l measures in 176 children with ASD, ADHD or OCD with complete data that passed quality control.

203 n of PCP signaling interferes with CE and/or OCD to produce PKD.

204 ated risks of mental disorders, particularly OCD and tic disorders.

205 dard treatments is recommended for pediatric OCD and anxiety disorders, young patients often remain s

206 al markers of cognitive control in pediatric OCD and anxiety disorders, including before and after tr

207 tive and task-negative networks in pediatric OCD may contribute to the impaired control over intrusiv

208 networks across the whole brain in pediatric OCD or how patterns of connectivity associate with treat

209 ons may predict response to CBT in pediatric OCD, highlighting the clinical relevance of these networ

210 may be relevant for understanding pediatric OCD and anxiety disorders is cognitive control, given th

211 site significantly and equivalently reduced OCD symptoms with little additional gain following combi

212 elected cases of otherwise highly refractory OCD.

213 imulation for otherwise treatment refractory OCD using a multipolar electrode implanted in the ventra

214 ure clinical trials for treatment refractory OCD.

215 Six patients with treatment-refractory OCD (5 men; Yale-Brown Obsessive Compulsive Scale score

216 vALIC for patients with treatment-refractory OCD in a regular clinical setting.

217 ctive and tolerable for treatment-refractory OCD in the long term and improves functioning and overal

218 ical procedure for many treatment-refractory OCD patients.

219 ith severely disabling, treatment-refractory OCD received bilateral lesions in the ventral portion of

220 ty patients with severe treatment-refractory OCD received DBS of the ventral part of the anterior lim

221 tive targets for severe treatment-refractory OCD.

222 in an open study of patients with refractory OCD.

223 elatives of individuals with non-tic-related OCD (e.g., risk for full siblings: aHR = 10.63 [95% CI,

224 d 2007 (n = 4,085,367; 1257 with tic-related OCD and 20,975 with non-tic-related OCD), we identified

225 ever, strong evidence supporting tic-related OCD as a distinct subtype of OCD is lacking.

226 hether, at the population level, tic-related OCD has a stronger familial load than non-tic-related OC

227 Tic-related OCD is a particularly familial subtype of OCD.

228 in relatives of individuals with tic-related OCD was considerably greater than the risk of OCD in rel

229 -related OCD and 20,975 with non-tic-related OCD), we identified all twins, full siblings, maternal a

230 stronger familial load than non-tic-related OCD.

231 urosurgical ablation for treatment-resistant OCD.

232 ically targeted treatments to better resolve OCD and anxiety symptoms, the identification of neural c

233 nt loss of S6K1 in Tsc1-mutant mice restores OCD but does not decrease hyperproliferation, leading to

234 The majority were experiencing severe OCD.

235 Relative to unaffected comparison subjects, OCD subjects had significantly lower levels of several t

236 enic load associated with Tourette syndrome, OCD, and ADHD were estimated.

237 nal stimulation in the DLS elicits long term OCD-like behavior in mice associated with circuitry chan

238 ct additional Tourette syndrome (rather than OCD) genetic liability that is not captured by tradition

239 We find that OCD distortion is intrinsically due to S6 kinase 1 (S6K1

240 We found that OCD is a familial disorder, regardless of comorbid tic d

241 Concluding, the present study found that OCD patients had difficulties with the deactivation of D

242 llectively, these observations indicate that OCD and suicidal behaviors coaggregate in families large

243 RN as a seed region was compared between the OCD and HC groups, as well as between SSRI responders an

244 In the OCD and healthy groups, the mean (SD) ages were 27.4 (7.

245 he right pACC was significantly lower in the OCD group and showed significant correlation with depres

246 tion with depressive symptom severity in the OCD group.

247 pole predicted better response to CBT in the OCD group.

248 Within the OCD cohort, a previous suicide attempt was the strongest

249 Therefore, OCD patients develop an accurate, internal model of the

250 8 unaffected first-degree relatives of these OCD patients and 49 healthy subjects.

251 ermine how mPFC hyperactivity contributes to OCD-relevant cognitive dysfunction.

252 stimated the contribution of DN mutations to OCD risk and the number of genes involved.

253 etry in OCD, while the hub findings point to OCD-related alterations in trajectories of brain develop

254 bances and cognitive functioning relevant to OCD, Sapap3 knockout mice (KOs) and littermate controls

255 rlie corticostriatal dysfunction relevant to OCD, we used the Sapap3 knock-out (Sapap3-KO) mouse mode

256 e striatum and contribute in various ways to OCD pathophysiology.

257 scribe cognitive impairments in a transgenic OCD-relevant model, and demonstrate pronounced heterogen

258 everal neurobiological mechanisms underlying OCD have been identified, including specific brain circu

259 luding specific brain circuits that underpin OCD.

260 At long-term follow-up, OCD symptoms decreased by 39% (p < .001), and half of th

261 ed posterior cingulate deactivation, whereas OCD patients showed temporoparietal underactivation.

262 This study examined whether OCD is associated with an increased risk of metabolic an

263 It is yet unknown whether OCD and suicidal behaviors coaggregate in families and,

264 While OCD patients (like controls) correctly updated their con

265 reatment-naive children and adolescents with OCD (12.8 +/- 2.9 years) and 23 matched healthy control

266 ulum bundle could distinguish 48 adults with OCD (mean age [SD] = 23.3 [4.5] years; F/M = 30/18) from

267 nance spectroscopy (MRS) was associated with OCD and/or CBT response.

268 ell as other brain areas was associated with OCD illness duration, suggesting greater involvement of

269 /or rare variants previously associated with OCD that were differentially expressed or part of a leas

270 in the 3 circuit CSTC model associated with OCD.

271 human brain tissue have been associated with OCD.

272 Forty-nine children with OCD (mean age 12.2+/-2.9 years) and 29 controls (13.2+/-

273 Results showed that HC, when compared with OCD, had a significant deactivation in two anterior node

274 Individuals diagnosed with OCD (n = 25,415) were identified from a cohort of 12,497

275 empted suicide in individuals diagnosed with OCD, compared with matched general population controls (

276 the birth cohort (0.87%) were diagnosed with OCD.

277 RI scans acquired from 1616 individuals with OCD and 1463 healthy controls across 37 datasets partici

278 In unadjusted models, individuals with OCD had an increased risk of both dying by suicide (odds

279 risk of OCD in relatives of individuals with OCD with and without comorbid tics, compared with relati

280 ved across all relatives of individuals with OCD, increasing proportionally to the degree of genetic

281 of a broad range of ADs in individuals with OCD, individuals with TD/CTD and their biological relati

282 of 40 ADs was evaluated in individuals with OCD, individuals with TD/CTD and their first- (siblings,

283 1.80; 95% CI 1.43-2.26) of individuals with OCD.

284 S) data were obtained from participants with OCD (n=49) and healthy individuals of equivalent age and

285 11.0 +/- 3.3 years) before participants with OCD completed a course of cognitive-behavioral therapy (

286 From 2010 to 2016, 20 patients with OCD (10 men/10 women) were included in a single-centre t

287 error processing analysis, 239 patients with OCD (120 male; 79 medicated) and 229 HCs (129 male) were

288 control analysis included 245 patients with OCD (120 male; 91 medicated) and 239 HCs (135 male).

289 tom improvement with EX/RP for patients with OCD (false discovery rate-corrected P < 0.05).

290 Unmedicated adult patients with OCD (n = 36) and healthy participants (n = 33) completed

291 t-maps from studies comparing patients with OCD and healthy control subjects (HCs) during error proc

292 We conclude that patients with OCD are at a substantial risk of suicide.

293 We found that patients with OCD outperformed healthy controls, winning significantly

294 one of the largest samples of patients with OCD treated with DBS thus far support the results of pre

295 Patients with OCD, relative to HCs, showed longer inhibitory control r

296 ould be carefully monitored in patients with OCD.

297 nts that augment the ability of persons with OCD to resolve cognitive conflict and thereby facilitate

298 Children with ADHD compared with those with OCD had smaller hippocampal volumes, possibly influenced

299 volume than control subjects and those with OCD or ASD.

300 Within OCD subjects, a treatment-by-scan interaction (p=0.034)