ライフサイエンスコーパス: PTSD

1 PTSD is associated with high individual and societal cos

2 PTSD is associated with premature mortality and frequent

3 PTSD is characterized by fear overgeneralization involvi

4 PTSD psychotherapy adaptively attenuates functional inte

5 PTSD (CRP -> PTSD: beta = 0.065, p = 0.015; PTSD -> CRP: beta = 0.008, p = 0.009).

6 al regions across both hemispheres from 1379 PTSD patients to 2192 controls without PTSD after data w

7 -48.0%), anxiety 21.0% (95% CI: 4.8%-58.4%), PTSD 19.7% (95% CI 3.2%-64.6%), psychological distress 4

8 depression (patient health questionnaire-8), PTSD (8Q-PCL-5), pain, and functional outcomes (trauma q

9 lood-derived DNA methylation data from 1,896 PTSD cases and trauma-exposed controls.

10 rch aimed at understanding inflammation as a PTSD risk factor or as a pathway linking PTSD with poor

11 During subsequent abstinence, PTSD-like behavior responses, GABAergic synaptic transmi

12 s Inventory (TEI) and Clinician-Administered PTSD Scale (CAPS) were used to measure lifetime trauma b

13 rent findings on these domains in adolescent PTSD.

14 s known about the neurobiology of adolescent PTSD, nor about how current treatments may alter adolesc

15 nding of biological mechanisms of adolescent PTSD, taken in the context of neurodevelopment, is cruci

16 These studies suggest that adolescent PTSD, while phenomenologically similar to adult PTSD, sh

17 aracterize the biology underlying adolescent PTSD.

18 ed to clinical symptom severity in the adult PTSD group.

19 In contrast to adult PTSD, relatively little is known about the neurobiology

20 D, while phenomenologically similar to adult PTSD, shows unique neurodevelopmental substrates that ma

21 ower prefrontal-limbic TSPO availability and PTSD severity.

22 e used to measure lifetime trauma burden and PTSD, respectively.

23 a bidirectional association between CRP and PTSD (CRP -> PTSD: beta = 0.065, p = 0.015; PTSD -> CRP:

24 he trauma, long-term cognitive deficits, and PTSD-associated hippocampal dysfunction.

25 he comorbidity between opioid dependence and PTSD, and they are also pertinent to the use of opioids

26 esting consistent markers related to ELT and PTSD on gray matter structure in trauma-exposed individu

27 idence for distinct CT correlates of ELT and PTSD that are present across adolescents and adults, sug

28 ongest link between regional methylation and PTSD risk and symptoms was observed for NTRK2, which enc

29 evalence for TBI(mild) , TBI(non-mild) , and PTSD was 0.65%, 0.69%, and 5.5%, respectively.

30 66-2.77) for TBI(mild) , TBI(non-mild) , and PTSD, respectively).

31 geted treatment for panic symptoms in PD and PTSD patients.

32 association between re-experiencing PRS and PTSD symptoms observed only among veterans with an insec

33 le may moderate the relation between PRS and PTSD.

34 l features that are associated with PTSD and PTSD comorbidities.

35 the interplay which exists between sleep and PTSD on a biological level.

36 ry consolidation and extinction, stress, and PTSD.

37 determine the burden of trauma symptoms and PTSD in SSA and to identify acceptable and feasible appr

38 Both TBI and PTSD were significantly associated with PD in single-ris

39 PD, TBI, and PTSD were ascertained by validated International Classif

40 Trauma and PTSD have been associated with accelerated cellular agin

41 ur findings suggest that lifetime trauma and PTSD may contribute to a higher epigenetic-based mortali

42 his study evaluated the effect of trauma and PTSD on accelerated GrimAge, an epigenetic predictor of

43 , after controlling for childhood trauma and PTSD severity.

44 ndividual differences in depression/anxiety, PTSD, and motor phenotypes.

45 hat risk for fear-related disorders, such as PTSD, is biased toward females, we examined whether H2A.

46 s and treatment for stress disorders such as PTSD, that result in decreased quality of life and adver

47 tress-related psychiatric disorders, such as PTSD.

48 and risk of stress-induced disorders such as PTSD.

49 tive data from SSA is a barrier to assessing PTSD.

50 a bidirectional genetic association between PTSD and CRP, also suggesting a potential role of SES in

51 lyses suggested that the association between PTSD symptoms and attachment style is bidirectional.

52 termining the direction of causality between PTSD and inflammation.

53 Despite the large comorbidity between PTSD and opioid use disorders, as well as the common tre

54 differences may help to distinguish between PTSD cases and trauma-exposed controls.

55 alcium channel, have been implicated in both PTSD and highly comorbid neuropsychiatric conditions, su

56 leukin (IL) 1beta and IL-6 concentrations by PTSD symptom trajectory class.

57 ividuals most at risk for developing chronic PTSD in the aftermath of trauma.

58 e not associated with development of chronic PTSD.

59 ficantly lower in individuals in the chronic PTSD class compared with those in the recovery and resil

60 positive interaction observed with comorbid PTSD/TBI in dual-risk factor analyses, with significant

61 Relative to veteran controls, PTSD subjects exhibited a stronger neural response assoc

62 re-exposure to all trauma-related cues cures PTSD-like hypermnesia.

63 Lifetime trauma burden (p = 0.03), current PTSD (p = 0.02) and lifetime PTSD (p = 0.005) were assoc

64 D history who are not categorized as current PTSD cases.

65 study included 218 individuals with current PTSD, 427 trauma-exposed controls without any history of

66 ers (ARBs), may be associated with decreased PTSD symptoms.

67 o Afghanistan for predicting post-deployment PTSD status.

68 gests that genetic influences on depression, PTSD, and suicidal ideation/self-harm are at least parti

69 hree major psychiatric outcomes (depression, PTSD, and suicidal ideation and/or self-harm) were score

70 ion PRSs significantly predicted depression, PTSD, and suicidal ideation/self-harm and explained up t

71 trauma survivors are more likely to develop PTSD, mood, and anxiety disorders and demonstrate endocr

72 tic event are at greater risk for developing PTSD; highlighting that sleep potentially plays a role i

73 may contribute to greater risk of developing PTSD after experiencing trauma and/or serve as a mechani

74 s with 8-week posttraumatic stress disorder (PTSD) adjusting for pre-MVC PTSD and mediated by peritra

75 pression, and posttraumatic stress disorder (PTSD) after injury and their association with long-term

76 rat model of posttraumatic stress disorder (PTSD) and identified predictors and biomarkers of comorb

77 subtypes of post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) on the basis o

78 for treating posttraumatic stress disorder (PTSD) and related syndromes, which develop in a subset o

79 ociated with post-traumatic stress disorder (PTSD) and traumatic experiences, but the underlying mech

80 herapies" for posttraumatic stress disorder (PTSD) and treatment-resistant depression, respectively.

81 inction in a post-traumatic stress disorder (PTSD) animal model and was related to reducing PTSD symp

82 ry (TBI) and post-traumatic stress disorder (PTSD) are risk factors for Parkinson's disease (PD).

83 exposure and posttraumatic stress disorder (PTSD) both affect neural structure, which predicts a var

84 k of not only posttraumatic stress disorder (PTSD) but also other mental health comorbidities.

85 r developing post-traumatic stress disorder (PTSD) compared with the general population.

86 Posttraumatic stress disorder (PTSD) has increasingly been linked to heightened systemi

87 Post-traumatic stress disorder (PTSD) impacts many veterans and active duty soldiers, bu

88 Posttraumatic stress disorder (PTSD) in adolescents is common and debilitating.

89 Post-traumatic stress disorder (PTSD) is a common, debilitating condition with limited t

90 Post-traumatic stress disorder (PTSD) is a debilitating disorder that develops in some p

91 Post-traumatic stress disorder (PTSD) is a heterogeneous condition evidenced by the abse

92 Post-traumatic stress disorder (PTSD) is characterized by emotional hypermnesia on which

93 Post-traumatic stress disorder (PTSD) is characterized by persistent fear memory of remo

94 Posttraumatic stress disorder (PTSD) may develop when mechanisms for making accurate di

95 on studies of posttraumatic stress disorder (PTSD) may inform risk for this disorder.

96 atients with post-traumatic stress disorder (PTSD) show heightened amygdala activity; elevated levels

97 revalence of post-traumatic stress disorder (PTSD) that is observed in women may involve sex differen

98 prevalence of posttraumatic stress disorder (PTSD) was 31.46% (95% CI 24.43-38.5), the prevalence of

99 epression or post-traumatic stress disorder (PTSD)(2-4).

100 positive for posttraumatic stress disorder (PTSD), all SF-12 physical health subdomain scores were s

101 on, anxiety, post-traumatic stress disorder (PTSD), and suicidal behaviour.

102 treatment for posttraumatic stress disorder (PTSD), but its mechanisms are poorly understood.

103 gy, including posttraumatic stress disorder (PTSD), depression, and alcohol-use disorders, in associa

104 flammation in posttraumatic stress disorder (PTSD), few studies have assessed whether inflammatory ma

105 ders, such as posttraumatic stress disorder (PTSD), is a prominent example where inconsistent effects

106 orrelates of post-traumatic stress disorder (PTSD), little is known about its molecular determinants.

107 gies, such as posttraumatic stress disorder (PTSD), that are characterized by unwanted memories of di

108 activation in posttraumatic stress disorder (PTSD), there are no studies of brain immunologic regulat

109 reatment for post-traumatic stress disorder (PTSD).

110 d symptoms of posttraumatic stress disorder (PTSD).

111 rders such as posttraumatic stress disorder (PTSD).

112 symptoms in post-traumatic stress disorder (PTSD).

113 ased risk for posttraumatic stress disorder (PTSD).

114 der (PD) and post-traumatic stress disorder (PTSD).

115 rs, including posttraumatic stress disorder (PTSD).

116 e and current posttraumatic stress disorder (PTSD).

117 phobias and post-traumatic stress disorder (PTSD).

118 anxiety, and Post Traumatic Stress Disorder (PTSD).

119 sorders like post-traumatic stress disorder (PTSD).

120 creening for post-traumatic stress disorder (PTSD); new functional limitations; return to work; and p

121 ave identified the relationship between ELT, PTSD, development, and brain structure using cortical th

122 and biomarkers of comorbid alcohol (ethanol)/PTSD-like symptoms in these animals.

123 al treatments are effective for single-event PTSD, it is not known if people who have experienced com

124 xamine relationship between combat exposure, PTSD, and prior head injuries on cortical thickness (Mon

125 Associations between trauma exposure, PTSD, cortical thickness, and GrimAge acceleration were

126 markers serve as prospective biomarkers for PTSD risk.

127 f two novel distinct epigenetic biotypes for PTSD may have future utility in understanding biological

128 be a sex-specific epigenetic risk factor for PTSD susceptibility, with implications for developing se

129 conferring significant genetic liability for PTSD.

130 ress-enhanced fear learning (SEFL) model for PTSD, we characterized the impact of chronic opioid regi

131 t, 66 patients (12.4%) screened negative for PTSD but positive for depression and/or anxiety.

132 ng as a potential intermediate phenotype for PTSD risk.

133 any MHD: of those who screened positive for PTSD (7.9%, N = 42), all had co-morbid depression and/or

134 rval (CI) 1.08-4.87], to screen positive for PTSD (adjusted OR 3.06, 95% CI 1.42-6.58), and had signi

135 h no MHD, patients who screened positive for PTSD were more likely to have chronic pain {odds ratio (

136 rted daily pain, 53.2% screened positive for PTSD, 38.7% reported a new functional limitation in an a

137 rial, mechanisms proposed to be relevant for PTSD development.

138 chment style may moderate polygenic risk for PTSD symptoms, and a novel locus implicated in synaptic

139 In the search for PTSD diagnostic biomarkers, we ascertained over one mill

140 al to facilitate fear extinction therapy for PTSD.

141 ss responsive to psychotherapy treatment for PTSD and failed to respond to an antidepressant medicati

142 mary evidence-based behavioral treatment for PTSD, has only partial efficacy.

143 form interpersonally oriented treatments for PTSD for individuals with high polygenic risk for this d

144 hological and pharmacological treatments for PTSD symptoms in people exposed to complex traumatic eve

145 related dissociative symptoms, distinct from PTSD and childhood trauma, can be estimated on the basis

146 c structural correlates distinct to ELT from PTSD.

147 cent neurodevelopment to allow recovery from PTSD.

148 3p, was significantly elevated in serum from PTSD military veterans, relative to combat-exposed contr

149 nal association between CRP and PTSD (CRP -> PTSD: beta = 0.065, p = 0.015; PTSD -> CRP: beta = 0.008

150 suggest that peripheral immune activation in PTSD is associated with deficient brain microglial activ

151 e a relationship between cortical atrophy in PTSD-relevant brain regions and shorter predicted lifesp

152 i were significantly smaller, on average, in PTSD patients than controls (standardized coefficients =

153 lly diagnosed with PTSD (N = 26), changes in PTSD symptom severity were correlated with AgeAccelGrim

154 impairing extinction-retention, a deficit in PTSD, by (1) altering class IIa histone deacetylases (HD

155 Given known sex differences in PTSD prevalence and cardiovascular disease, here we test

156 as a contributor to immune dysregulation in PTSD.

157 is the first study to assess DNAm GrimAge in PTSD patients.

158 ing biological and clinical heterogeneity in PTSD and potential applications in risk assessment for a

159 t contextual amnesia is causally involved in PTSD-like memory formation, and that treating the amnesi

160 e comparisons, with lower DNA methylation in PTSD cases relative to controls.

161 ypothesized based on clinical observation in PTSD, but the neural mechanisms remain unexplored.

162 ntified two distinct SDs highly prevalent in PTSD; insomnia and nightmares.

163 The primary outcome was reduction in PTSD symptoms.

164 s were associated with greater reductions in PTSD and depression symptoms and improved sleep quality.

165 pathophysiological processes which result in PTSD, as well as emphasising the importance of specifica

166 hting that sleep potentially plays a role in PTSD's pathology.

167 r physiological markers are related to SD in PTSD.

168 ation were related to the severity of SDs in PTSD.

169 e findings indicate that cortical volumes in PTSD patients are smaller in prefrontal regulatory regio

170 G2 biotype was associated with an increased PTSD risk and had higher polygenic risk scores and a gre

171 military veterans (n = 46) were grouped into PTSD (n = 23) and non-PTSD (n = 23).

172 tal connectivity were associated with larger PTSD symptom reductions.

173 dataset with genotype data from the largest PTSD genome-wide association study identified the intern

174 0.03), current PTSD (p = 0.02) and lifetime PTSD (p = 0.005) were associated with GrimAge accelerati

175 story of PTSD and 209 subjects with lifetime PTSD history who are not categorized as current PTSD cas

176 The association with lifetime PTSD was replicated in an independent cohort (p = 0.04).

177 g trauma and/or serve as a mechanism linking PTSD to adverse physical health outcomes.

178 s a PTSD risk factor or as a pathway linking PTSD with poor health.

179 = 0.89, specificity = 0.79) and longitudinal PTSD symptom trajectories identified with latent growth

180 ost effective treatment package for managing PTSD in complex trauma.

181 nterventions are most effective for managing PTSD in this population.

182 nges of shared DEGs associated with maternal PTSD and paternal PTSD were in opposite directions, whil

183 The Modified PTSD Symptom Scale (M-PSS) was administered and ACE-I/AR

184 of opioid treatments to subsequently modify PTSD-related behavior has not been well studied.

185 stress disorder (PTSD) adjusting for pre-MVC PTSD and mediated by peritraumatic symptoms and 2-week a

186 Using data from the VA National PTSD Brain Bank (n = 117), we found that rs9315202 inter

187 46) were grouped into PTSD (n = 23) and non-PTSD (n = 23).

188 the largest DNA methylation meta-analysis of PTSD to date.

189 mice as a potential diagnostic biomarker of PTSD.

190 Three distinct classes of PTSD symptom trajectories were identified: chronic (N=28

191 ure modeling was used to identify classes of PTSD symptom trajectories.

192 eview, we highlight prevailing constructs of PTSD and current findings on these domains in adolescent

193 r influence on the subsequent development of PTSD are largely unknown.

194 method exists to predict the development of PTSD symptoms upon ED admission after trauma(5).

195 l mechanisms that lead to the development of PTSD, it is first imperative to understand the interplay

196 e would predict later chronic development of PTSD.

197 ed a significant multivariate main effect of PTSD symptom trajectory class membership on proinflammat

198 d memory after accounting for the effects of PTSD and prior head injury.

199 outcomes were point prevalence estimates of PTSD across all studies, and then within subgroups.

200 y was present in the prevalence estimates of PTSD, depression, and anxiety, and limited covariates we

201 auma-exposed controls without any history of PTSD and 209 subjects with lifetime PTSD history who are

202 an-administered settings, and improvement of PTSD diagnostic markers.

203 Fewer studies evaluate the influence of PTSD on subsequent inflammation levels, and findings are

204 ay a potential role as epigenetic markers of PTSD.

205 tress-enhanced fear learning (SEFL) model of PTSD, as well as associated changes in pain sensitivity.

206 ex that contribute to the pathophysiology of PTSD in humans.

207 or the diagnosis and prognosis prediction of PTSD in recently traumatized individuals.

208 earning in the generation and progression of PTSD, these findings are of direct translational relevan

209 ARB medication associated with lower rate of PTSD diagnosis (p < 0.001).

210 um seekers have high and persistent rates of PTSD and depression, and the results of this review high

211 egions, this review cannot speak to rates of PTSD in any regions not included in this review.

212 ism that could contribute to higher rates of PTSD in women.

213 approach for promoting durable remission of PTSD, particularly in patients with CACNA1C mutations or

214 or intervening to prevent and reduce risk of PTSD.

215 ng all cortical regions in a large sample of PTSD and control subjects can potentially provide new in

216 ived from a genome-wide association study of PTSD re-experiencing symptoms (N = 146,660) in the Milli

217 ort the efficacy of MDMA in the treatment of PTSD and psilocybin in the treatment of depression and c

218 l therapeutic candidate for the treatment of PTSD.

219 sults indicated that the ACE-I/ARB effect on PTSD may be driven more by ARBs (e.g., Losartan) than by

220 prior studies almost exclusively focused on PTSD.

221 d whether the effects of ACE-I/ARB status on PTSD differ by sex.

222 ctive effects of PRS and attachment style on PTSD symptoms in a nationally representative sample of t

223 es current prevalence estimates for not only PTSD but also depression, anxiety, and psychosis.

224 s associated with maternal PTSD and paternal PTSD were in opposite directions, while fold changes of

225 This manuscript sought to calculate pooled PTSD prevalence estimates from nationally and regionally

226 Individuals with a primary PTSD diagnosis (N = 66) participated in a randomized cli

227 Yet, they are often resistant to primary PTSD therapies.

228 (SEFL) paradigm in inbred mice that produces PTSD-like characteristics in a subset of mice, including

229 loyment symptom trajectories and provisional PTSD diagnosis based on pre-deployment data achieved hig

230 achine-learning models predicted provisional PTSD diagnosis 90-180 days post deployment (random fores

231 owed that psychological interventions reduce PTSD symptoms more than inactive control (k = 46; n = 3,

232 Resolving SDs will not only reduce PTSD symptom severity and improve quality of life but wi

233 xposure were the most effective for reducing PTSD symptoms (k = 17; n = 1,077; mean difference = -37.

234 SD) animal model and was related to reducing PTSD symptom development in humans.

235 elates of biological aging in combat-related PTSD, which may help explain the increased medical morbi

236 and reduce bias in diagnosing combat-related PTSD.

237 to mitigate the risk for deployment-related PTSD.

238 predominantly associated with memory-related PTSD symptoms, and because they seem to precede traumati

239 In a discovery cohort of 83 warzone-related PTSD cases and 82 warzone-exposed controls, we identifie

240 nt of chronic anxiety in treatment-resistant PTSD.

241 i-inflammatory effects of BHB using a rodent PTSD model, induced by single prolonged stress (SPS).

242 In this study, PTSD symptoms consistent with a probable diagnosis were

243 ally targeting sleep as part of a successful PTSD intervention strategy.

244 icity during extinction learning to suppress PTSD-like fear responses.

245 robabilistic sampling methods and systematic PTSD assessments; and included >= 450 participants who w

246 We found that PTSD was associated with an enhanced neural response in

247 so, few studies address the possibility that PTSD abnormalities may be confounded by comorbid depress

248 Prior studies suggest that PTSD may be a systemic illness, affecting not just the b

249 However, if the PTSD-inflammation relation is correlational, it may not

250 AgeAccelGrim was significantly higher in the PTSD group compared to the control group (N = 162, 1.26

251 Prefrontal-limbic TSPO availability in the PTSD group was negatively associated with PTSD symptom s

252 ith GAD, the risk genotype identified in the PTSD literature (rs2267735, CC genotype) was associated

253 udies rigorously assess the direction of the PTSD-inflammation relation.

254 After adjusting for depression symptoms, the PTSD findings in left and right LOFG remained significan

255 on biological diversity observed within the PTSD group observed following epigenome-wide analysis of

256 iles identified two PTSD biotypes within the PTSD+ group, G1 and G2, associated with 34 clinical feat

257 tial miRNA expression was found according to PTSD diagnosis in two composite marker groups.

258 functions in nontraumatized subjects and to PTSD risk and symptoms in traumatized populations.

259 n the composite marker groups contributed to PTSD symptom severity, which may be explained by differe

260 ter injury is significant and not limited to PTSD.

261 assess the longitudinal evidence related to PTSD and inflammation to understand more clearly the dir

262 nnectivity changes and their relationship to PTSD symptom improvements.

263 t and inflammatory processes with respect to PTSD risk.

264 s, may render individuals more vulnerable to PTSD.

265 A methylation (DNAm) profiles identified two PTSD biotypes within the PTSD+ group, G1 and G2, associa

266 stinct biological risk profiles underpinning PTSD.

267 sus 2.17-fold and 2.80-fold excess risk when PTSD was absent.

268 TBI(non-mild) versus those without TBI when PTSD was present versus 2.17-fold and 2.80-fold excess r

269 the cortical surface to investigate whether PTSD and ELT exposure uniquely affect CT, controlling fo

270 ar gyrus in both adolescents and adults with PTSD.

271 bon receptor repressor (AHRR) associate with PTSD after adjustment for multiple comparisons, with low

272 4 clinical features that are associated with PTSD and PTSD comorbidities.

273 ditioned responses have been associated with PTSD in adults, with increased fear-potentiated startle

274 he PTSD group was negatively associated with PTSD symptom severity and was significantly lower than i

275 ent style were independently associated with PTSD symptoms.

276 ng mir-135b-5p, and proteins associated with PTSD-like heightened fear expression.

277 ost significant gene network associated with PTSD.

278 renin-angiotensin system is associated with PTSD.

279 iate with smoking, the AHRR association with PTSD is most pronounced in non-smokers, suggesting the r

280 erated biological aging in both cohorts with PTSD.

281 tudy of individuals initially diagnosed with PTSD (N = 26), changes in PTSD symptom severity were cor

282 marker, was conducted in 23 individuals with PTSD and 26 healthy individuals-with or without trauma e

283 of 48 recently traumatized individuals with PTSD and 47 healthy individuals.

284 n the molecular profiles of individuals with PTSD and major depressive disorder despite their high co

285 able therapeutic target for individuals with PTSD and related disorders.

286 n immunologic regulation in individuals with PTSD.

287 17), we found that rs9315202 interacted with PTSD to predict advanced epigenetic age in motor cortex

288 The rs9315202 SNP interacted with PTSD to predict decreased KL expression via DNAm age res

289 netic correlations of CRP were observed with PTSD (rg = 0.16, p = 0.026) and traits related to trauma

290 halography in four datasets of patients with PTSD and MDD, and show that the subtypes are transferabl

291 egions from postmortem tissue of people with PTSD demonstrate extensive remodeling of the transcripto

292 levels, which are lower among subjects with PTSD.

293 upports epigenetic differences in those with PTSD and suggests a role for decreased kynurenine as a c

294 and lifetime healthcare costs for those with PTSD.

295 ting of 83 male combat exposed veterans with PTSD, and 83 combat veterans without PTSD in order to id

296 1-month, in a sample of fifty veterans with PTSD, using a crossover design.

297 rauma-exposed male veterans with and without PTSD using cross-sectional and longitudinal data from tw

298 ned positive for depression/anxiety (without PTSD) were more likely to have chronic pain [OR: 5.06 (9

299 1379 PTSD patients to 2192 controls without PTSD after data were processed by 32 international labor

300 ns with PTSD, and 83 combat veterans without PTSD in order to identify patterns that might distinguis