ライフサイエンスコーパス: psychosis

1 impact on population levels of first-episode psychosis.

2 hological mechanism driving the emergence of psychosis.

3 anistically informed early interventions for psychosis.

4 ntify biological markers of schizophrenia or psychosis.

5 or up to 2 years to assess for conversion to psychosis.

6 hierarchical perceptual-inference models of psychosis.

7 only PTSD but also depression, anxiety, and psychosis.

8 y deficits, and computational performance in psychosis.

9 ent sample of 24 patients with first episode psychosis.

10 l perception is involved in the aetiology of psychosis.

11 ficits linked to the risk and development of psychosis.

12 h CHR individuals are most likely to develop psychosis.

13 between impaired structural connectivity and psychosis.

14 ed with different types of substance-induced psychosis.

15 ns with increased inflammatory activation in psychosis.

16 markers have been reported in patients with psychosis.

17 and is predictive of conversion to syndromal psychosis.

18 ay inform the treatment for people at CHR of psychosis.

19 l atrophy predicted progression to syndromal psychosis.

20 atter (WM) are reported in youth at-risk for psychosis.

21 isk and treatment of cognitive impairment in psychosis.

22 of salience to irrelevant stimuli leading to psychosis.

23 well as role expectations, play in risk for psychosis.

24 ucture may play in mental illnesses, such as psychosis.

25 and nominally associated with sub-threshold psychosis.

26 tion processing speed, and family history of psychosis.

27 hypothesis of an immunological component to psychosis.

28 rence and contributes to the pathogenesis of psychosis.

29 er characterize the pathophysiology of early psychosis.

30 f the progression from being at CHR to frank psychosis.

31 pared with participants with 22q11DS without psychosis.

32 els in unaffected subjects and patients with psychosis.

33 l high risk who subsequently developed frank psychosis.

34 anoids from monozygotic twins discordant for psychosis.

35 focused on novel drug development for early psychosis.

36 dysfunction of the nigrostriatal pathway in psychosis.

37 95 (0.69-1.30) among those with a history of psychosis.

38 to investigate the crosstalk between AD and psychosis.

39 ients and individuals at risk for developing psychosis.

40 -II and 42.6% of our sample had a history of psychosis.

41 gnificantly increased in the early stages of psychosis.

42 th CNS changes and symptoms in first episode psychosis.

43 ic treatment in 81 patients with early-phase psychosis.

44 ith consciousness threshold, particularly in psychosis.

45 nefits learning in health and is impaired in psychosis.

46 y target of cannabis, has been implicated in psychosis.

47 n in the dACC of subjects with first-episode psychosis.

48 During 1-year follow-up, 23 CHRs developed psychosis.

49 amine and contributes to the pathogenesis of psychosis.

50 (CHR) relative to findings in patients with psychosis.

51 tigate WM abnormalities in youth at-risk for psychosis.

52 th (n = 17) and without (n = 9) a history of psychosis.

53 ns were associated with positive symptoms of psychosis.

54 notyping and their analyses to understanding psychosis.

55 the contexts of prevention and treatment of psychosis.

56 ical conditions that range from addiction to psychosis(1).

57 y, comprising 35 subjects with first-episode psychosis (11 DD, 12 SZ, 12 other psychotic disorders) a

58 (14 patients, 15 controls), in first-episode psychosis (16 patients, 16 controls), and in Parkinson d

59 y n = 74: 20 participants with first-episode psychosis, 30 healthy controls and 24 participants with

60 Forty patients with psychosis across two independent cohorts underwent (18)F

61 d cognitive decline than AD patients without psychosis (AD-P).

62 ficantly more likely than females to develop psychosis after maternal exposure to any bacterial infec

63 p-seeking individuals at risk for developing psychosis, aiming at predicting and possibly preventing

64 analysis on 188 subjects with first episode psychosis, all of whom were subsequently treated with am

65 demonstrate that the exosomal secretion of a psychosis-altered and glial-enriched miRNA that controls

66 risk prediction in persons at high risk for psychosis, although its potential utility is limited by

67 scents and young adults without a history of psychosis and 0.95 (0.69-1.30) among those with a histor

68 254 subjects at clinical high risk (CHR) for psychosis and 116 healthy volunteers were tested for ant

69 ubjects (51 people at clinical high risk for psychosis and 19 healthy controls).

70 or insula) of 20 patients with first-episode psychosis and 20 healthy control subjects.

71 , n = 71), including 49 at clinical risk for psychosis and 22 with a frank psychotic disorder.

72 cterize thalamic structural abnormalities in psychosis and a neurodevelopmental cohort, and to determ

73 episode defined as a new diagnosis code for psychosis and a prescription for an antipsychotic medica

74 the thalamus before the onset of full-blown psychosis and are associated with symptom severity, thus

75 ficits as vulnerability markers for emerging psychosis and as indicators of future outcomes.

76 rbed by dopaminergic modulation, impaired in psychosis and associated with task performance and schiz

77 e activity in blood of treated first episode psychosis and chronic schizophrenia (SCZ) compared to he

78 s, DG, CA3, and CA1 from individuals with SZ psychosis and controls to elucidate subfield-relevant mo

79 in HD, as was schizophrenia risk score with psychosis and irritability.

80 in network organization precede the onset of psychosis and may drive psychosis development in at-risk

81 te association nuclei in the pathogenesis of psychosis and mechanisms of cognitive impairment.

82 (i) encephalopathies (n = 10) with delirium/psychosis and no distinct MRI or CSF abnormalities, and

83 me 22-is associated with an elevated risk of psychosis and other developmental brain disorders.

84 erved between participants with 22q11DS with psychosis and participants with schizophrenia, bipolar d

85 o 12 weeks and met criteria for remission of psychosis and remission or near-remission of depressive

86 d individuals with major depression, bipolar psychosis and schizophrenia were evaluated.

87 t dopamine (DA) dysregulation, a hallmark of psychosis and SCZ, had not been tested.

88 lipidomic abnormalities predate the onset of psychosis and that blood lipidomic measures may be usefu

89 abis use associated with the highest odds of psychosis and the correlation between such patterns and

90 ntal mechanisms that impart vulnerability to psychosis and the possibility of interventions that capi

91 nvestigations of plasma amino acids in early psychosis and their unaffected siblings are rare.

92 s biology may critically enhance research on psychosis and thus our understanding of the disorder.

93 with measures of cognition in subjects with psychosis and unaffected subjects.

94 table because deficits predict conversion to psychosis and/or CHR-P remission.

95 the upper limbs, (2) cerebellar ataxia, (3) psychosis and/or severe mood disorder (only in the TS pa

96 oss-sectional sample of 472 adults (293 with psychosis) and the Philadelphia Neurodevelopmental Cohor

97 tions increase the risk of substance-induced psychosis, and 2) whether infections increase the risk o

98 pressive symptoms, autism spectrum disorder, psychosis, and alcohol use disorder compared with the co

99 volume in treatment-responsive patients with psychosis, and compared them to treatment non-responsive

100 Persecutory delusions are core symptoms of psychosis, and social cognition is particularly impaired

101 function in people at clinical high risk for psychosis, and to assess the association with the develo

102 is; patients with recent-onset depression or psychosis; and healthy volunteers.

103 tween cannabis use and acute or long-lasting psychosis are not completely understood.

104 Delusions, a core symptom of psychosis, are false beliefs that are rigidly held with

105 r aberrations and specific manifestations of psychosis as envisioned by the precision medicine agenda

106 as electrophysiological markers of risk for psychosis, as target engagement measures for clinical tr

107 ields in individuals with schizophrenia (SZ) psychosis associated with hippocampal excitability.

108 SCZ and BD patients with positive history of psychosis at the time of death and was inversely associa

109 Paranoia is the most common symptom of psychosis but paranoid concerns occur throughout the gen

110 ce, are central to the pathogenesis of major psychosis, but the molecular origins are unclear.

111 urrently used antipsychotic drugs ameliorate psychosis, but they are not very effective in reversing

112 eeking individuals at clinical high risk for psychosis by identifying covariant longitudinal patterns

113 ent of individuals at clinical high risk for psychosis (CHR) is that it is difficult to predict their

114 rmalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with ps

115 vary among youths at clinical high risk for psychosis (CHR-P), with approximately 20% progressing to

116 or Cognitive Impairment in Psychiatry in the psychosis cohort and the Penn Computerized Neurocognitiv

117 ychotic naive/free people with first-episode psychosis commencing antipsychotic treatment.

118 hyperdopaminergic state thought to underlie psychosis, compared to SAL rats, using in vivo, anesthet

119 young adults at Clinical High Risk (CHR) for psychosis, conducted at the Shanghai Mental Health Cente

120 deficits align on the nonclinical end of the psychosis continuum.

121 psychotic disorders support the notion of a psychosis continuum.

122 significantly by group and was higher in the psychosis converter group compared with both the nonconv

123 The PRS discriminates psychosis converters from nonconverters and modestly imp

124 prior drug exposure or duration of untreated psychosis correlated with baseline BMI.

125 ess of a collaborative shared care model for psychosis delivered by TFH and primary health-care provi

126 infection, poor mental health (suicidality, psychosis, depression, and violence), and increased risk

127 precede the onset of psychosis and may drive psychosis development in at-risk youth.

128 When psychosis develops in NMDA receptor (NMDAR) antibody enc

129 ngly clear that longer duration of untreated psychosis (DUP) is associated with adverse clinical outc

130 ospitalization, a long duration of untreated psychosis (DUP) predicts illness severity and worse trea

131 d relatives and controls (N = 3428) from the Psychosis Endophenotypes International Consortium (PEIC)

132 ough only CHR patients who develop syndromal psychosis exhibit focal hippocampal atrophy.

133 Recently, it has been proposed that psychosis exists on a continuum; however, there is confl

134 se findings support the validity of studying psychosis experiences during development in a way that c

135 In a new psychosis family study, we investigated the effects of C

136 oninergic neurotransmitters in first-episode psychosis (FEP) patients (n = 166), unaffected siblings

137 nrolled 66 antipsychotic-naive first-episode psychosis (FEP) patients and 45 matched healthy controls

138 zophrenia and presents even in first-episode psychosis (FEP) patients.

139 in a minority of patients with first-episode psychosis (FEP), but their role in psychosis onset and r

140 ving the psychotic symptoms of first-episode psychosis (FEP), psychotic relapse is common during the

141 tary-adrenal (HPA) systems) in first-episode psychosis (FEP).

142 cohort of medication-naive youth at risk for psychosis from the Shanghai At Risk for Psychosis (SHARP

143 The psychosis group had smaller pulvinar, mediodorsal, and,

144 g robust markers for predicting the onset of psychosis has been a key challenge for early detection r

145 A broader dimensional examination of psychosis has been applied to population-based studies o

146 neurological autoimmune (NNAI) disorders and psychosis has been widely reported but not yet subjected

147 ng specific thalamic nuclei abnormalities in psychosis has implications for early detection of psycho

148 tion increased the risk of substance-induced psychosis (hazard ratio=1.30, 95% CI=1.22-1.39).

149 ion to schizophrenia after substance-induced psychosis (hazard ratio=1.87, 95% CI=1.07- 3.26).

150 t strongly associated with substance-induced psychosis (hazard ratio=3.42, 95% CI=2.47-4.74).

151 humans of either sex with varying degrees of psychosis: healthy control subjects (n = 46), schizophre

152 were analysed across three sites of PHENOM (Psychosis Heterogeneity Evaluated via Dimensional Neuroi

153 Persons meeting research criteria for psychosis high risk (N=764) and unaffected individuals (

154 gnificant overlap between 22q11DS-associated psychosis, idiopathic schizophrenia, and other severe ne

155 Thalamus models of psychosis implicate association nuclei in the pathogenes

156 neurobehavioral measures relevant to ASD and psychosis in 106 22q11.2 deletion carriers, 38 22q11.2 d

157 neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of va

158 r without CBD) worsened negative symptoms of psychosis in a single study (SMD 0.36 [95% CI 0.10 to 0.

159 itamin D was associated with delayed time to psychosis in AD patients and Vitamin D was used more by

160 wo studies provided epidemiological data for psychosis in conflict-affected populations, existing Glo

161 alterations as well as genetic liability for psychosis in individuals experiencing psychotic symptoms

162 rovide care to a large number of people with psychosis in many sub-Saharan African countries but they

163 uring pregnancy was strongly associated with psychosis in offspring (adjusted odds ratio=1.8, 95% CI=

164 ic risk score (PRS) prediction of subsequent psychosis in persons at high risk and to determine the i

165 The 2-year risk of psychosis in persons who meet research criteria for a hi

166 the NM-MRI signal correlated to severity of psychosis in schizophrenia and individuals at risk for s

167 ovide a holistic framework for understanding psychosis in schizophrenia including heterogeneity in cl

168 s of psychotropic agent for the treatment of psychosis in schizophrenia.

169 ent in a way that can chart the emergence of psychosis in the context of general psychopathology.

170 ther evidence for the idea of a continuum of psychosis in the healthy, nonclinical population.SIGNIFI

171 al dopaminergic dysfunction, which underlies psychosis in the majority of patients who respond to tre

172 ormality associated with psychosis, risk for psychosis in youths, and cognitive impairment.

173 ease categories, including schizophrenia and psychosis, in phenome-wide association studies.

174 ivity in three prior case-control studies of psychosis: in total, n = 185 cases and n = 227 controls.

175 populations included increased prevalence of psychosis, increased perceived risk of violence, increas

176 g pathway abnormality is related to risk for psychosis, independent of disease expression and treatme

177 This first study of brain FAAH in psychosis indicates that FAAH may represent a biomarker

178 the neural basis of affective impairments in psychosis, informing prediction models and interventions

179 Our findings reveal that PBD with psychosis is associated with significant widespread chan

180 Psychosis is strongly related to increased striatal dopa

181 has been hypothesized that lengthy untreated psychosis is toxic or that it reflects a more severe for

182 Furthermore, we examined psychosis-like behaviors and pathological memory process

183 association with hippocampal physiology and psychosis-like behaviors.

184 -based cohort study using the semistructured Psychosis-Like Symptoms Interview at ages 12, 18, and 24

185 o (neuro)monitor clinical outcome defined as psychosis-likeness change after 10-hours of CCT in recen

186 nge during CCT is associated with individual psychosis-likeness change and cognitive gains after CCT.

187 ectory phenotypes: sub-threshold symptoms of psychosis, low baseline intellectual functioning and cog

188 Sera from 387 patients with FEP (duration of psychosis <2 years, minimally or never treated with anti

189 er according to the prominence and timing of psychosis, mania, and depression.

190 ck of effect is that study participants with psychosis may display aberrant brain responses to neutra

191 It has been argued that psychosis may emerge because of a failure to learn senso

192 Hierarchical perceptual-inference models of psychosis may provide a holistic framework for understan

193 cular profiles of the DG, CA3, and CA1 in SZ psychosis may serve to identify further potential hippoc

194 schizophrenia and their evolution into overt psychosis may stem from an aberrant functional reorganiz

195 l model systems may serve as targets to test psychosis mechanisms related to hippocampus and assess p

196 onegative patients but a shorter duration of psychosis (median 1.5 vs. 4.0 months; p = .031).

197 CHR subjects who subsequently developed psychosis (n = 50) were distinguished from those that di

198 disorder (n = 37), or bipolar disorder with psychosis (n = 72), and identified neuroimaging features

199 l N = 449 depression, N = 137; AUD, N = 175; psychosis, N = 95; epilepsy, N = 42).

200 erall association between NNAI disorders and psychosis (odds ratio [OR] = 1.26; 95% confidence interv

201 cused on identifying biomarkers that precede psychosis onset and enhance the accuracy of clinical out

202 t-episode psychosis (FEP), but their role in psychosis onset and response to antipsychotic treatment

203 changes serve to increase the likelihood of psychosis onset during this period, while others may buf

204 ychosocial function was analyzed relative to psychosis onset, DUP did not predict illness course.

205 rmalities in connectome organization precede psychosis onset, we performed a functional connectome an

206 derstanding pathogenic mechanisms underlying psychosis onset, which may support the development of me

207 lopment, and subsequently potentially impact psychosis onset.

208 to the needs and capabilities of people with psychosis or bipolar disorder, and the staff who support

209 health interventions for people affected by psychosis or bipolar disorder.

210 tion adherence, but not baseline symptoms of psychosis or depression, significantly predicted injurio

211 it is unknown if FAAH is altered in vivo in psychosis or related to positive psychotic symptoms.

212 amate OR glut* OR GLX) AND (schizophrenia OR psychosis OR schizophren*).

213 nown if they are present before the onset of psychosis or whether they are associated with particular

214 nts will develop psychotic symptoms (AD with Psychosis, or AD + P) and these patients will experience

215 95%CI 3.97-11.90); mania, bipolar disorder, psychosis, or schizophrenia (HR = 2.70, 95%CI 1.14-6.37)

216 approximately 20% progressing to full-blown psychosis over 2 to 3 years and 30% achieving remission.

217 t rs165940 principally associates within the psychosis (p = 0.025, OR = 1.18, 95% CI: 1.07-1.30) and

218 nt in CHR subjects relative to patients with psychosis, particularly in reward processing.

219 on is particularly impaired in first-episode psychosis patients and individuals at risk for developin

220 no difference in V(ND) between first-episode psychosis patients and their controls, and the administr

221 Psychosis patients showed deficits in working memory, ph

222 patients with clinical high-risk states for psychosis; patients with recent-onset depression or psyc

223 m to large effect) and duration of untreated psychosis predicted lower FAAH (F(1,26.95) = 6.03, p = .

224 Clinically stable psychosis probands (Schizophrenia spectrum, n = 79; Psyc

225 , VEGF, and CRP were significantly higher in psychosis probands compared to HCs, and there were marke

226 Preclinical models of psychosis propose that hippocampal glutamatergic neuron

227 atal dopamine, a molecular hallmark of human psychosis, providing an unprecedented opportunity for st

228 ine study n = 59) and in patients with early psychosis (psychosis study n = 74: 20 participants with

229 of hyperdopaminergia, which display abnormal psychosis-related behaviors, including hyperlocomotion a

230 I) networks with proteins encoded by AD- and psychosis-related genes and Vitamin D-perturbed genes.

231 Psychosis-related illnesses, including schizophrenia, ar

232 tially modulate intellectual functioning and psychosis-related symptomatology but converge on broad A

233 ructure, cognition, and clinical features of psychosis remain unclear.

234 osis has implications for early detection of psychosis risk and treatment of cognitive impairment in

235 nsequences of increased striatal dopamine in psychosis risk are still not fully understood.

236 lation being studied, here assuming a 2-year psychosis risk between 10% and 30%) for Europeans varied

237 Variables in the psychosis risk calculator included stressful life events

238 ed psychosis risk prediction when added to a psychosis risk calculator.

239 of adding the PRS to a previously validated psychosis risk calculator.

240 nal bacterial infection during pregnancy and psychosis risk over the subsequent 40 years, stratified

241 verters and modestly improves individualized psychosis risk prediction when added to a psychosis risk

242 interview as having subthreshold persistent psychosis risk symptoms (n = 46), and were compared to h

243 Compared to TD, youth with persistent psychosis risk symptoms had lower whole-brain WM fractio

244 s are present early in youth with persistent psychosis risk symptoms, however, there is little eviden

245 urodevelopmental abnormality associated with psychosis, risk for psychosis in youths, and cognitive i

246 individuals with attenuated positive symptom psychosis-risk syndrome as defined by the Structured Int

247 interviews and the structured interview for psychosis-risk syndromes (SIPS).

248 e as defined by the Structured Interview for Psychosis-risk Syndromes.

249 change after 10-hours of CCT in recent onset psychosis (ROP) patients.

250 ined this question in a solely first-episode psychosis sample.

251 Patients with psychosis (schizophrenia and bipolar disorder with psych

252 f surgery, history of depression or anxiety, psychosis, schizophrenia, mania, or bipolar disorder, pe

253 disorders, e.g. 22q11.2DS-related ASD and/or psychosis/schizophrenia.

254 s should be cared for within a first-episode psychosis service, when such a service exists.

255 for psychosis from the Shanghai At Risk for Psychosis (SHARP) study.

256 Patients at clinical high-risk (CHR) for psychosis show elevations in [(18)F]DOPA uptake, an esti

257 Participants with 22q11DS with psychosis showed lower ICV and hippocampus, amygdala, an

258 m this pattern, would be elevated across the psychosis spectrum and associated with cognition and bra

259 ment of amygdala connectivity in youths with psychosis spectrum disorders may help us better understa

260 ly developing youth as well as in those with psychosis spectrum disorders.

261 h adverse clinical outcomes in patients with psychosis spectrum disorders.

262 hy control group (HC, analyzed n = 36) and a psychosis spectrum group (PSY, n = 71), including 49 at

263 la-occipital connectivity were unique to the psychosis spectrum group and were not observed in the ot

264 la connectivity and positive symptoms in the psychosis spectrum group.

265 Youths with psychosis spectrum symptoms also had smaller pulvinar vo

266 (PNC), consisting of 1,393 youths (398 with psychosis spectrum symptoms and 609 with other psychopat

267 discuss neurodevelopmental underpinnings of psychosis spectrum symptoms and review brain morphometri

268 at clinical high risk based on subthreshold psychosis spectrum symptoms, and criteria have been arti

269 alyses have been extended across the broader psychosis spectrum, or spectrums, and what we have learn

270 t baseline showed improved attention despite psychosis status on the SVM hyperplane at follow-up (p <

271 = 59) and in patients with early psychosis (psychosis study n = 74: 20 participants with first-episo

272 in the healthy controls (or patients) in the psychosis study.

273 cognitive impairment, mood disturbances, or psychosis, such as Alzheimer's disease or schizophrenia.

274 gical differences between different types of psychosis, such as between delusional disorder (DD) and

275 pathogenic effects on the natural history of psychosis, suggest a biological mechanism underlying thi

276 symptoms, 6.4-point reduction [d = 0.43] in psychosis symptoms, 7.2-point reduction [d = 0.58] in de

277 bust deficits in individuals with persistent psychosis symptoms.

278 post-mortem tissue studies in schizophrenic psychosis (SzP), have demonstrated functional and molecu

279 people, but not patients with first-episode psychosis, take into account the precision of the enviro

280 ne use was associated with a greater risk of psychosis than methylphenidate.

281 ened credibility to support the continuum of psychosis that extends into the nonclinical population.

282 he dopaminergic alterations in patients with psychosis, that this requires activation of midbrain dop

283 erall association between NNAI disorders and psychosis, this was not consistent across all NNAI disor

284 in subjects at clinical high risk (CHR) for psychosis to further characterize the pathophysiology of

285 Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophre

286 he risk of converting from substance-induced psychosis to schizophrenia.

287 ndent cohorts of patients with first-episode psychosis (total N=510).

288 om the National Patient Register) because of psychosis, using the International Classification of Dis

289 % (95% CI 6.75-15.43), and the prevalence of psychosis was 1.51% (95% CI 0.63-2.40).

290 Psychosis was associated with globally reduced morphomet

291 tional health-care providers for people with psychosis was effective and cost-effective.

292 te initiation was 17 years, and a history of psychosis was reported in 479 (2.0%) participants.

293 e treatment of heart disease, impotency, and psychosis) was found to be an effective inhibitor of mul

294 estimated pooled 1 year prevalence rates for psychosis were 6.2% (95% CI 4.0-8.6), 16.0% (11.7-20.8)

295 CHRs who would go on to develop psychosis were found to show abnormal modular connectome

296 om 3,618 cases of incident substance-induced psychosis were recorded.

297 ularly striking in the study of religion and psychosis, where we and others have shown that cultural

298 Here, we test an aberrant saliency model of psychosis, which posits that dysregulated dynamic cross-

299 e levels may underlie acute cannabis-induced psychosis while lower baseline levels may be a marker of

300 There were 343 episodes of psychosis (with an episode defined as a new diagnosis co