ライフサイエンスコーパス: OCD

1 OCD is associated with an increased risk of metabolic an

2 OCD patients exhibited excessive habits that were associ

3 OCD patients had a disorder-specific increase in structu

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 patients with ADHD and 591 controls), and 18 OCD fMRI data sets (287 patients with OCD and 284 contro

8 neuroanatomic changes that are shared by 22 OCD adult and adolescent patients and 25 of their unaffe

9 931 patients with ADHD and 822 controls), 30 OCD VBM data sets (928 patients with OCD and 942 control

10 in 200 children and adolescents (ADHD: N=31; OCD: N=36; ASD: N=71; controls: N=62; mean age range: 10

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

12 performance monitoring were recorded from 45 OCD patients and 39 healthy comparison subjects while pe

13 iduals were diagnosed as having TS/CT; 6191, OCD; and 412, both disorders.

14 We identified 36 788 OCD patients in the Swedish National Patient Register be

15 I response, we conducted a GWAS study in 804 OCD patients with information on SRI response.

16 significant effect of adduction on absolute OCD (slope 1.09 +/- 0.36 mum/degree, P = .0037).

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

18 als of SSRIs or SNRIs in youths with DD, AD, OCD, or PTSD were included.

19 al Disorders, Fifth Edition, which addresses OCD separately from anxiety disorders and contains speci

20 dency of error monitoring by examining adult OCD patients before and after symptom reduction through

21 his is the first longitudinal study in adult OCD patients showing stability of enhanced error monitor

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

23 and in parallel with PCP signaling to affect OCD.

24 symmetry, while risk scores derived from an OCD GWAS were not.

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

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

27 a transdiagnostic endophenotype in ADHD and OCD, were associated with disorder-differential function

28 ties (relative to controls) between ADHD and OCD.

29 losum) as a shared feature of ASD, ADHD, and OCD.

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

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

32 ntrol abnormalities in patients with ASD and OCD.

33 Tourette syndrome/CT and OCD cluster in families.

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

35 yperexcitability of medium spiny neurons and OCD-like behavior.

36 work has shown that Tourette's syndrome and OCD have some degree of shared genetic variation.

37 tion study (GWAS) of Tourette's syndrome and OCD.

38 The OC density (OC amount per unit area, OCD) exhibited a decreasing trend from the south-eastern

39 rapies for neuropsychiatric diseases such as OCD and ASDs with Hoxb8-microglia being the central targ

40 ccurs in neuropsychiatric conditions such as OCD and TS.

41 AS) is comprised of comprehensively assessed OCD patients with an early age of OCD onset.

42 ne, Glu did not differ significantly between OCD and controls in pACC or vPCC.

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

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

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

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

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

48 The combined OCD participants (CBT-only plus waitlist-CBT) also showe

49 TS (29.8%) may be accounted for by comorbid OCD (OR, 3.7; 95% CI, 2.9-4.8; P < .001).

50 0.3-0.9; P = .02) independent from comorbid OCD and ADHD; however, high rates of mood disorders amon

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

52 signaling polarizes renal tubules to control OCD.

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

54 Obsessive-compulsive disorder (OCD) affects 2%-3% of the population worldwide and can c

55 hologies like obsessive-compulsive disorder (OCD) and autism spectrum disorders (ASDs).

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

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

58 rs related to obsessive-compulsive disorder (OCD) and Tourette syndrome (TS).

59 Obsessive-compulsive disorder (OCD) and Tourette's syndrome are highly heritable neurod

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

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

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

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

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

65 patients with obsessive-compulsive disorder (OCD) exhibit an inadequate response to serotonin reuptak

66 patients with obsessive-compulsive disorder (OCD) have symptoms that are refractory to pharmacologic

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

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 condition characterized by intrusi

71 Obsessive-compulsive disorder (OCD) is associated with increased mortality, but the cau

72 ng youth with obsessive-compulsive disorder (OCD) is effective, but many patients remain symptomatic

73 reatments for obsessive-compulsive disorder (OCD) is hampered by a lack of mechanistic understanding

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

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

76 ur underlying obsessive-compulsive disorder (OCD) may be related to abnormalities in decision-making.

77 r (TS/CT) and obsessive-compulsive disorder (OCD) overlap in their phenomenological features and ofte

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

79 le finding in obsessive-compulsive disorder (OCD) research and may be an endophenotype of the disorde

80 er (ADHD) and obsessive-compulsive disorder (OCD) share impaired inhibitory control.

81 der (ASD) and obsessive-compulsive disorder (OCD) share inhibitory control deficits possibly underlyi

82 s involved in obsessive compulsive disorder (OCD), a neuropsychiatric disorder characterized by the e

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

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

85 orders (ADs), obsessive-compulsive disorder (OCD), and posttraumatic stress disorder (PTSD) are commo

86 for pediatric obsessive-compulsive disorder (OCD), but non-response is common.

87 reatments for obsessive-compulsive disorder (OCD), some patients continue to be treatment-refractory

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

89 circuits and obsessive-compulsive disorder (OCD)-like grooming behaviors.

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

91 the case for obsessive-compulsive disorder (OCD).

92 e the risk of obsessive-compulsive disorder (OCD).

93 sociated with obsessive-compulsive disorder (OCD).

94 apy (CBT) for obsessive-compulsive disorder (OCD).

95 of refractory obsessive-compulsive disorder (OCD).

96 urobiology of obsessive-compulsive disorder (OCD).

97 d adults with obsessive-compulsive disorder (OCD).

98 discovery in obsessive-compulsive disorder (OCD).

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

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

101 er [ASD], and obsessive-compulsive disorder [OCD]) share genetic vulnerability and symptom domains.

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

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

104 ers, depression, or substance use disorders, OCD was still associated with increased mortality risk (

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

106 significant peripapillary RPE displacement, OCD, or ONH tilt.

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

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

109 Finally, sufficiency of mGluR5 to drive OCD-like behavior in wild-type mice was tested by potent

110 e underlying molecular signaling that drives OCD-related behaviors remains largely unknown.

111 Twenty-eight OCD patients and thirty-five controls were tested with a

112 years); 17 studies for DD, 10 for AD, 8 for OCD, and 1 for PTSD.

113 lly higher than the familial aggregation for OCD.

114 ars was 9.88% (95% CI, 8.02%-12.16%) and for OCD, 4.01% (95% CI, 2.78%-5.76%).

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

116 tified a significant polygenic component for OCD (p=2x10(-4)), predicting 3.2% of the phenotypic vari

117 orders, Fourth Edition (DSM-IV) criteria for OCD.

118 rs of full siblings that were discordant for OCD.

119 It has been proposed as an endophenotype for OCD because it is heritable and more prevalent in famili

120 hus emerges as a promising endophenotype for OCD.

121 with an mGluR5 antagonist were evaluated for OCD-relevant phenotypes of self-grooming, anxiety-like b

122 ange of potential perinatal risk factors for OCD, controlling for unmeasured factors shared between s

123 uss the circuit hyperactivity hypothesis for OCD, a potential circuitry dysfunction of action termina

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

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

126 tentials for closed-loop neuromodulation for OCD.

127 eening, diagnosis, and treatment options for OCD.

128 een associated with enhanced CBT outcome for OCD among adults but requires evaluation among youth.

129 factors is associated with a higher risk for OCD independent of shared familial confounders, suggesti

130 An increased risk for OCD remained after controlling for shared familial confo

131 ons, whereby an increasingly higher risk for OCD was noted in children with a shorter gestational age

132 In contrast, the sibling RRR for OCD was 4.89 (95% CI, 3.45-6.93).

133 dophenotype that indicates vulnerability for OCD.

134 Furthermore, OCD with co-occurring Tourette's syndrome/chronic tics m

135 In OCD patients, they were enhanced relative to controls.

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

137 gate the process of evidence accumulation in OCD in perceptual discrimination, hypothesizing enhanced

138 ior, suggesting that habit-forming biases in OCD may be a result of impairments in this system, rathe

139 etabolic and cardiovascular complications in OCD patients compared with the general population and un

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

141 stronger recruitment of proactive control in OCD.

142 en and the dorsolateral prefrontal cortex in OCD patients, as well as to symptom severity.

143 al putamen, and anterior cingulate cortex in OCD.

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

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

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

147 ded self-help nor cCBT led to differences in OCD symptoms.

148 chanisms of this important symptom domain in OCD is necessary for development of novel, more globally

149 nterior/posterior hippocampal dysfunction in OCD is warranted.

150 engthen the evidence for rACC dysfunction in OCD, but weigh against an underlying association with ab

151 ecific frontostriatoinsular dysregulation in OCD in the form of poor frontal control over overactive

152 ggest that enhanced information gathering in OCD can be accounted for by a higher decision threshold

153 ng predicted the degree of generalization in OCD patients during reversal, whereas vmPFC safety signa

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

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

156 ork that has been consistently implicated in OCD.

157 d structure and function in BG and insula in OCD patients, but a reduction in ASD patients, presumabl

158 We investigated performance monitoring in OCD with simultaneous recording of electroencephalograph

159 nvolved in altered performance monitoring in OCD.

160 se of LFP for closed-loop neuromodulation in OCD.

161 for impaired decision-formation processes in OCD, with a differential influence of high and low uncer

162 the rostral subdivision of the ACC (rACC) in OCD patients.

163 mechanisms underlying treatment response in OCD, studies with larger sample sizes and detailed infor

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

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

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

167 idespread and severe in ASD and ADHD than in OCD.

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

169 the number of perinatal events and increased OCD risk, with HRs ranging from 1.11 (95% CI, 1.07-1.15)

170 ma capsulotomy for patients with intractable OCD.

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

172 We compared 16 juvenile OCD patients with 16 matched healthy controls whilst the

173 D was associated with a higher burden of non-OCD, non-ADHD comorbid psychiatric disorders (OR, 1.86;

174 y assessed OCD patients with an early age of OCD onset.

175 TS/CT was 0.42% (95% CI, 0.41%-0.43%) and of OCD, 0.84% (95% CI, 0.81%-0.87%).

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

177 cortico-striato-thalamo-cortical circuit of OCD.

178 umbens, an area implicated in development of OCD, display hyperexcitability in PGRN knockout mice.

179 SD) age of individuals at first diagnosis of OCD was 23.4 (6.5) years.

180 The diagnosis of OCD was revised for the Diagnostic and Statistical Manua

181 eneral Hospital) with a primary diagnosis of OCD were randomized in a double-blind fashion to d-cyclo

182 ists and because of the disabling effects of OCD symptoms.

183 Although the etiology of OCD is still unknown, research evidence points toward th

184 heritable and more prevalent in families of OCD patients.

185 ubstantial challenges remain in the field of OCD research and therapeutics.

186 edule-induced polydipsia, an animal model of OCD.

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

188 ta extend major neuropsychological models of OCD by providing a direct link between intrinsically abn

189 rophysiologic findings from animal models of OCD.

190 ng inflammation within the neurocircuitry of OCD.

191 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

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

193 onvergence with the known pathophysiology of OCD and to infer, based on abnormalities in brain activa

194 region implicated in the pathophysiology of OCD, the caudate nucleus.

195 To date, genetic predictors of OCD treatment response have not been systematically inve

196 The presence of OCD was associated with a significantly increased mortal

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

198 l variants associated with increased risk of OCD.

199 l population and unaffected full siblings of OCD individuals.

200 similar in mothers, fathers and siblings of OCD probands, whereas it tended to be higher in mothers

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

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

203 epresent a major advancement in treatment of OCD.

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

205 We identified those with TS/CT and/or OCD.

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

207 y (GWAS) signals from a previously published OCD study identified significant enrichment (P=0.0176).

208 t benefits over the waiting list in reducing OCD symptoms (adjusted mean difference = -1.91, 95% CI -

209 trial (RCT) was conducted with 16 refractory OCD patients allocated to active treatment (n=8) and sha

210 o dorsal anterior cingulotomy for refractory OCD.

211 ical procedure for many treatment-refractory OCD patients.

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

213 urosurgical ablation for treatment-resistant OCD.

214 Thirty-seven OCD patients and 33 healthy comparison subjects learned

215 The majority were experiencing severe OCD.

216 e the risk of mental disorders, specifically OCD and tic disorders, after a streptococcal throat infe

217 METHOD: Assessments for Tourette syndrome, OCD, and ADHD symptoms were conducted in a discovery sam

218 Assessments for Tourette syndrome, OCD, and ADHD symptoms were conducted in a discovery sam

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

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

221 It further emphasizes that OCD patients are sensitive to monetary incentives height

222 rth-western plateau, with the exception that OCD in the swamp meadow was substantially higher than th

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

224 The OCD Collaborative Genetics Association Study (OCGAS) is

225 The OCD group, as a whole, showed hyperactivation in the med

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

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

228 Unlike healthy subjects, participants in the OCD group did not show activation in the left ventral pu

229 r emergence of these subjective costs in the OCD group, also evident in an increased decision thresho

230 pared with the control group, but not in the OCD group.

231 deactivation and Gln/Glu, Glu, or Gln in the OCD group.

232 tion with depressive symptom severity in the OCD group.

233 During navigation, the OCD group, unlike the healthy comparison group, exhibite

234 in the ASD and ADHD groups compared with the OCD group but was not different in ADHD participants com

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

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

237 8 unaffected first-degree relatives of these OCD patients and 49 healthy subjects.

238 glutamate (Glu) signaling may contribute to OCD pathophysiology and moderate CBT outcomes.

239 dding a more biologically valid framework to OCD will help researchers define and test new hypotheses

240 evated frontostriatal activity are linked to OCD, the underlying molecular signaling that drives OCD-

241 risk factors may be in the causal pathway to OCD.

242 bidities may be more biologically related to OCD and/or ADHD rather than to TS.

243 bnormalities and behaviors with relevance to OCD and show the tractability of acute mGluR5 inhibition

244 vioral and circuit abnormalities relevant to OCD.

245 mpared with those without OCD in response to OCD-specific words versus neutral words on the emotional

246 Excessive mGluR5 signaling underlies OCD-like behaviors and striatal circuit abnormalities in

247 its and those cognitive processes underlying OCD symptoms.

248 iolation of reward expectations, unmedicated OCD participants did not and instead over-relied on the

249 Outcomes and Measures: Previously validated OCD codes (International Statistical Classification of D

250 d reduced right BG and insula volumes versus OCD patients.

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

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

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

254 pectroscopy in 51 children with ASD, 29 with OCD, and 53 healthy controls (aged 8-13 years) to invest

255 e was compared in 33 unmedicated adults with OCD and 33 healthy, age-matched comparison subjects duri

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

257 h no SNPs were identified as associated with OCD at genome-wide significance level, follow-up analyse

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

259 erlying genetic susceptibility compared with OCD alone.

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

261 grouped together, showed that, compared with OCD, HC had a significantly deactivation of a widespread

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

263 Twenty-seven participants, 15 diagnosed with OCD and 12 healthy controls (HC), underwent a functional

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

265 he cohort, 17305 persons were diagnosed with OCD.

266 Individuals with OCD and TD/CTD had increased comorbidity with any AD (43

267 Individuals with OCD had a higher risk of any metabolic or cardiovascular

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

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

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

271 Participants with OCD (n = 20) and age-matched healthy control individuals

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

273 In a sample of 30 participants with OCD and 29 age- and sex-matched participants without OCD

274 participants without OCD, participants with OCD displayed significantly reduced rACC deactivation co

275 RI data were collected from 20 patients with OCD and 22 healthy control subjects during a flanker tas

276 and 18 OCD fMRI data sets (287 patients with OCD and 284 controls).

277 ls), 30 OCD VBM data sets (928 patients with OCD and 942 controls), 33 ADHD fMRI data sets (489 patie

278 In addition, both patients with OCD and unaffected siblings showed similar increased thi

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

280 entary motor area was found in patients with OCD compared with healthy controls.

281 c and cardiovascular health in patients with OCD early in the course of the disorder.

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

283 Patients with OCD show significant surface expansion compared with hea

284 Patients with OCD showed disorder-specific reduced function and struct

285 sular-striatal regions whereas patients with OCD showed larger and hyperfunctioning insular-striatal

286 Patients with OCD showed significantly increased ERN amplitudes.

287 1065 families (containing 1406 patients with OCD), combined with population-based samples (resulting

288 llowing errors was observed in patients with OCD.

289 tive response toward errors in patients with OCD.

290 state independent in pediatric patients with OCD.

291 ould be carefully monitored in patients with OCD.

292 Of 10,155 persons with OCD (5935 women and 4220 men with a mean [SD] age of 29.

293 was significantly higher among persons with OCD (MRR, 1.68 [95% CI, 1.31-2.12] for natural causes; M

294 d significantly increased among persons with OCD.

295 in patients with ADHD relative to those with OCD (and controls).

296 benefit relative to placebo among youth with OCD.

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

298 29 age- and sex-matched participants without OCD, participants with OCD displayed significantly reduc

299 ompare persons with OCT with persons without OCD.

300 ACC deactivation compared with those without OCD in response to OCD-specific words versus neutral wor