ライフサイエンスコーパス: schizophrenia

1 on, insomnia, intelligence, neuroticism, and schizophrenia).

2 l mechanisms in persons at familial risk for schizophrenia.

3 reas the baseline gamma power is enhanced in schizophrenia.

4 rain is associated with an increased risk of schizophrenia.

5 genome-wide association studies, emphasizing schizophrenia.

6 lume, including Alzheimer's disease (AD) and schizophrenia.

7 e concentration in unmedicated patients with schizophrenia.

8 ing gamma-band ASSR network abnormalities in schizophrenia.

9 g of regional and cellular neuropathology in schizophrenia.

10 with recent onset (ROS) and established (ES) schizophrenia.

11 lar disorder, major depressive disorder, and schizophrenia.

12 n neurological disorders, such as autism and schizophrenia.

13 rmid syndrome, autism spectrum disorder, and schizophrenia.

14 ar neuroanatomic abnormalities to idiopathic schizophrenia.

15 en white matter and cognitive performance in schizophrenia.

16 ortico-thalamic intrinsic dysconnectivity in schizophrenia.

17 ic or that it reflects a more severe form of schizophrenia.

18 he association between BMI and Hcy levels in schizophrenia.

19 l prefrontal cortex (DLPFC) of patients with schizophrenia.

20 eatment of positive symptoms associated with schizophrenia.

21 elucidate the neurodevelopmental aspects of schizophrenia.

22 arget of antipsychotics for the treatment of schizophrenia.

23 risk genotype with very high penetrance for schizophrenia.

24 eveloping neuropsychiatric disorders such as schizophrenia.

25 in neuroimaging studies of individuals with schizophrenia.

26 opic agent for the treatment of psychosis in schizophrenia.

27 quence PCM1 in two human cohorts with severe schizophrenia.

28 henotypes and known genetic risk factors for schizophrenia.

29 alpha5-GABA(A)Rs protein and mRNA levels in schizophrenia.

30 esity is common comorbidity in patients with schizophrenia.

31 the molecular basis of synaptic pathology in schizophrenia.

32 were not found for polygenic risk for ASD or schizophrenia.

33 memory (WM) impairment are core features of schizophrenia.

34 eatment of positive and negative symptoms of schizophrenia.

35 mptomatology, including major depression and schizophrenia.

36 rk further disentangles the heterogeneity in schizophrenia.

37 c overlap of subicular subfield volumes with schizophrenia.

38 ional attainment, risk-taking behaviors, and schizophrenia.

39 pecific CNVs increase the risk of developing schizophrenia.

40 22q11DS) is associated with a 20-25% risk of schizophrenia.

41 ological studies of brain gene expression in schizophrenia.

42 d cortico-basal ganglia-thalamic circuits in schizophrenia.

43 ey role in hierarchical Bayesian theories of schizophrenia.

44 we show those of reduced mGluR5 signaling in schizophrenia.

45 ain's cognitive and reward circuits underlie schizophrenia.

46 and the immune system in the pathogenesis of schizophrenia.

47 hat mimics multiple symptoms associated with schizophrenia.

48 rted that homocysteine (Hcy) is increased in schizophrenia.

49 identified in GWASs of bipolar disorder and schizophrenia.

50 e underlying individual genetic liability to schizophrenia.

51 ging from GWAS: the role of glycosylation in schizophrenia.

52 ggested that infections increase the risk of schizophrenia.

53 orders, such as Phelan-McDermid syndrome and schizophrenia.

54 rders including autism spectrum disorder and schizophrenia.

55 rain that contributes to the pathogenesis of schizophrenia.

56 variants, particularly those associated with schizophrenia.

57 revailing hypothesis for the pathogenesis of schizophrenia.

58 TG may be critical to the pathophysiology of schizophrenia.

59 er structural brain features and with AD and schizophrenia.

60 tional anisotropy (FA), across the course of schizophrenia.

61 11 control subjects and 144 individuals with schizophrenia.

62 we assign direction of expression changes in schizophrenia.

63 itive control engagement in individuals with schizophrenia.

64 rontal information updating in patients with schizophrenia.

65 prefrontal cortex, striatum, and thalamus in schizophrenia.

66 ed with intellectual disability, autism, and schizophrenia.

67 onal psychopathology and in genetic risk for schizophrenia.

68 in the striatum predictive of conversion to schizophrenia.

69 rodevelopmental disorders such as autism and schizophrenia.

70 ltiple neuropsychiatric disorders, including schizophrenia.

71 ted MDD, recurrent MDD, bipolar disorder and schizophrenia.

72 ties are established core characteristics of schizophrenia.

73 for PCM1 in some individuals diagnosed with schizophrenia.

74 etiological and therapeutic implications for schizophrenia.

75 is also genome-wide associated with risk for schizophrenia.

76 istent large-scale brain imaging findings in schizophrenia.

77 in a sample of 133 individuals with chronic schizophrenia (48 women, mean age 34.7 +/- 12.9 years) a

78 of 130 genome-wide significant variants for schizophrenia, 5 of 40 for major depression, 3 of 11 for

79 of a C4 isoform has recently been linked to schizophrenia, a C4 inhibitor and structural characteriz

80 Diagnoses that are psychiatric (e.g. schizophrenia), acute rather than chronic, or benefittin

81 t nine times more women than men(1), whereas schizophrenia affects men with greater frequency and sev

82 Only hepatitis predicted conversion to schizophrenia after substance-induced psychosis (hazard

83 d in many neuro-psychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum diso

84 in mRNAs compared to both "low inflammation" schizophrenia and "low inflammation" control subgroups.

85 tron emission tomography in 18 patients with schizophrenia and 18 controls.

86 ent for 33 patients with treatment-resistant schizophrenia and 31 controls, and processed using the l

87 natures of various brain diseases, including schizophrenia and Alzheimer's disease, have also been id

88 ntrol are implicated in the etiopathology of schizophrenia and are attractive drug targets for indivi

89 Stress exacerbates symptoms of schizophrenia and attention-deficit/hyperactivity disord

90 evelopmental psychiatric conditions, such as schizophrenia and autism, in the offspring.

91 eases, both linked to hypofunctional NMDARs: schizophrenia and autoimmune anti-NMDAR encephalitis.

92 We also show that differences between schizophrenia and bipolar disorder are concentrated in e

93 Schizophrenia and bipolar disorder do not appear to shar

94 ferences in the body of the corpus callosum; schizophrenia and bipolar disorder featured comparable c

95 While schizophrenia and bipolar disorder may have similar path

96 ies, detailed cellular mechanisms underlying schizophrenia and bipolar disorder remain poorly underst

97 an is under development for the treatment of schizophrenia and bipolar I disorder.

98 d model of the neurodevelopmental aspects of schizophrenia and can be used to elucidate the etiology

99 ies novel genes not previously implicated in schizophrenia and corroborates a number of predicted tar

100 in the pathophysiology of disorders such as schizophrenia and drug addiction.

101 argets for GIN-associated disorders, such as schizophrenia and epilepsy.

102 types with two polygenic scores, derived for schizophrenia and intelligence, and evaluated their use

103 high-risk CNVs are not only associated with schizophrenia and other neurodevelopmental disorders, bu

104 role in the etiology and pathophysiology of schizophrenia and other psychiatric disorders with devel

105 Schizophrenia and other psychotic disorders are highly d

106 red functional capacity is a core feature of schizophrenia and presents even in first-episode psychos

107 BAergic levels in dorsal ACC are involved in schizophrenia and psychotic disorder, whereas increased

108 tantial portion of epigenetic alterations in schizophrenia and related disorders may be acquired thro

109 al immune challenges may elevate the risk of schizophrenia and related psychoses in offspring, yet th

110 inical findings of epigenetic alterations in schizophrenia and relevant disease models and discuss th

111 M (methylazoxymethanol acetate) rat model of schizophrenia and saline-treated control animals, we inv

112 t in SLC39A8 is convincingly associated with schizophrenia and several additional phenotypes.

113 r central nervous system disorders including schizophrenia and substance use disorders.

114 at brain volume loss is a general feature of schizophrenia and suggest differential aetiologies.

115 odel of the dopamine pathophysiology seen in schizophrenia and test approaches to reverse the dopamin

116 The emergence of prodromal symptoms of schizophrenia and their evolution into overt psychosis m

117 y, bipolar, borderline personality disorder, schizophrenia, and autism.

118 nsular cortex dysfunction, including autism, schizophrenia, and fronto-temporal dementia.

119 These include Parkinson's disease, ADHD, schizophrenia, and mood disorders, which show stark diff

120 een 22q11DS-associated psychosis, idiopathic schizophrenia, and other severe neuropsychiatric illness

121 ads to behavioral phenotypes associated with schizophrenia, and postmortem evidence indicates lower h

122 personality, posttraumatic stress disorder, schizophrenia, and psychotic disorders) not diagnosed du

123 ategories as genes with mutations de novo in schizophrenia, and studies of induced pluripotent stem c

124 ssive Disorder (MDD), Bipolar Disorder (BD), Schizophrenia, anxiety, and Post Traumatic Stress Disord

125 PRSs for bipolar disorder and schizophrenia are associated with risk for progression t

126 Eating disorders and schizophrenia are both moderately to highly heritable an

127 variants that are associated with autism and schizophrenia are colocalized with distinct classes of a

128 ions in parvalbumin-positive interneurons in schizophrenia are the consequence of a deficient signali

129 atric disorders, particularly depression and schizophrenia, are associated with increased risk of the

130 Psychosis-related illnesses, including schizophrenia, are increasingly viewed as existing along

131 ights from the DG-GCL, which identified many schizophrenia-associated genetic signals not found in tr

132 We also highlight a subset of schizophrenia-associated proteins critically modified by

133 plex neurodevelopmental disorders, including schizophrenia, autism and epilepsy.

134 Top3beta mutations have been linked to schizophrenia, autism, epilepsy, and cognitive impairmen

135 In contrast, <10% of the causal variants for schizophrenia, bipolar disorder and attention-deficit/hy

136 In comparison with HCS, we found that schizophrenia, bipolar disorder, and autism spectrum dis

137 e observe differential volume alterations in schizophrenia, bipolar disorder, multiple sclerosis, mil

138 tients with psychiatric disorders (including schizophrenia, bipolar or unipolar depression, anxiety,

139 ncoding VE-cadherin and ICAM1 were higher in schizophrenia brain.

140 arenchyma in over 40% of "high inflammation" schizophrenia brains.

141 argets for improving memory consolidation in schizophrenia, but enhancing spindles is not enough.

142 natomic brain networks have been reported in schizophrenia, but their characterization across patient

143 pretation of social signals in depression or schizophrenia by providing the missing link between body

144 rstanding of functional capacity deficits in schizophrenia by specifying the underlying neural correl

145 were generated from exome sequencing of 4913 schizophrenia cases and 6188 control subjects from Swede

146 yze high-coverage WGS data from 1162 Swedish schizophrenia cases and 936 ancestry-matched population

147 nic, single-gene deletions were validated in schizophrenia cases and none in control subjects (p = .0

148 subgroups across polygenic scores (PGSs) for schizophrenia, cognition, educational attainment, and at

149 for CNS indications, such as depression and schizophrenia, constitute a major challenge for the drug

150 = .03), and the subgroup of patients with a schizophrenia diagnosis had higher glutamate levels in t

151 -related susceptibility factor, Disrupted in schizophrenia (DISC1), is involved in host immune respon

152 Nineteen patients with schizophrenia during remission of psychotic symptoms and

153 Two animal models for the study of schizophrenia endophenotypes, namely the phencyclidine (

154 C dysfunction to neural disorders, including schizophrenia, epilepsy, and autism spectrum disorder (A

155 various neurological disorders like AD, PD, schizophrenia, epilepsy, brain cancer, CNS infection (vi

156 objective is to evaluate the contribution to schizophrenia etiology from a variety of genetic variant

157 (excitatory), major depression (inhibitory), schizophrenia (excitatory and gamma-aminobutyric acid (G

158 he human CYFIP1, a gene linked to autism and schizophrenia, exhibit mitochondrial hyperactivity and a

159 = 1,100), FSA distinguished individuals with schizophrenia from healthy controls with an accuracy exc

160 tions of this approach to toxicogenomics and schizophrenia gene expression data sets.

161 three cognitive trajectory subgroups in the schizophrenia group: preadolescent cognitive impairment

162 plied TS and other comparable methods to the schizophrenia GWAS data and type 2 diabetes (T2D) GWAS m

163 The strongest coding variant in schizophrenia GWAS is a missense mutation in the mangane

164 Schizophrenia has been studied from the perspective of c

165 heir contribution to cognitive impairment in schizophrenia has not been investigated.

166 Schizophrenia has recently been associated with widespre

167 Genome-wide association studies of schizophrenia have demonstrated that variations in nonco

168 nitive classifier was relatively specific to schizophrenia (HC-clinically isolated syndrome for multi

169 itory neurons are significantly enriched for schizophrenia heritability with maximal enrichment in co

170 been linked to a greater risk of developing schizophrenia; however, it is not known whether C4 plays

171 .90); mania, bipolar disorder, psychosis, or schizophrenia (HR = 2.70, 95%CI 1.14-6.37); and substanc

172 s proposed to drive deficits consistent with schizophrenia in adults.

173 Optimisation of Treatment and Management of Schizophrenia in Europe (OPTiMiSE) programme, we conduct

174 (Optimization of Treatment and Management of Schizophrenia in Europe) trial (ClinicalTrials.gov numbe

175 s adversely influenced by polygenic risk for schizophrenia in healthy subjects.

176 cies of brexpiprazole in adult subjects with schizophrenia in order to identify the in vivo pharmacol

177 ctivity contributes to tissue volume loss in schizophrenia in the same manner remains unknown.

178 The likelihood of having schizophrenia in those with AN or OED and their relative

179 the 12 copy number variants associated with schizophrenia in UK Biobank and 9063 individuals who did

180 re lower synaptic terminal protein levels in schizophrenia in vivo and that antipsychotic drug exposu

181 ld be most marked in patients with "residual schizophrenia", in whom an early stage with positive psy

182 identify genetic factors that contribute to schizophrenia, in addition to the ~20-fold increased ris

183 tic framework for understanding psychosis in schizophrenia including heterogeneity in clinical presen

184 or future research into major depression and schizophrenia, including studies of the mechanism(s) of

185 ol associates with a decreased likelihood of schizophrenia-independent of intelligence-and, hence, ma

186 otential contribution of single-gene CNVs to schizophrenia, indicate that the utility of exome sequen

187 kingly, we show that white matter changes in schizophrenia involve dynamic interactions between neuro

188 ugh the critical brain nodes remain unknown, schizophrenia involves networks with broad abnormalities

189 Schizophrenia is a complex genetic disorder, the non-Men

190 Schizophrenia is a highly heritable disorder for which a

191 Schizophrenia is a highly polygenic disorder with import

192 Schizophrenia is a severe neurodevelopmental psychiatric

193 tangling psychopathological heterogeneity in schizophrenia is challenging, and previous results remai

194 Schizophrenia is characterized by reduced spindle activi

195 emonstrates that brain tissue volume loss in schizophrenia is conditioned by structural and functiona

196 ts indicate that mPFC-mTL dysconnectivity in schizophrenia is due to a loss of theta phase coupling,

197 Schizophrenia is genetically highly heterogeneous, invol

198 he pleiotropy between years of schooling and schizophrenia is horizontal and likely confounded by a t

199 sociated with higher TSPO but a diagnosis of schizophrenia is not.

200 Neurobiological heterogeneity in schizophrenia is poorly understood and confounds current

201 t windows, increased anxiety-, despair-, and schizophrenia-like behavior in adulthood.

202 on in the dentate gyrus (DG), accompanied by schizophrenia-like behavior in the adult offspring.

203 immune activation (MIA) may present distinct schizophrenia-like phenotypes in progeny.

204 he role of MDD, we demonstrate that ADHD and schizophrenia likely play a role in the aetiology of sel

205 en FMRP binding and genetic association with schizophrenia, major depressive disorder and bipolar dis

206 history of depression or anxiety, psychosis, schizophrenia, mania, or bipolar disorder, personality d

207 tional association between breast cancer and schizophrenia may partly be explained by the genetic ove

208 Different cognitive development histories in schizophrenia may reflect variation across dimensions of

209 egree of A(2A)R-D(2)R heteromer formation in schizophrenia might constitute a hallmark of the illness

210 orders, where dysfunction was most severe in schizophrenia, milder in bipolar disorder, and indisting

211 In a rodent schizophrenia model characterized by impaired glutathion

212 etic variants play a role in the etiology of schizophrenia, most of the currently explained liability

213 ral MRI and clinical measures in established schizophrenia (n = 307) and healthy controls (n = 364) w

214 n subjects (HCS; N = 1506) and patients with schizophrenia (N = 696), bipolar disorder (N = 211), aut

215 of antipsychotic treatment in patients with schizophrenia (n = 95) using integrated multivariate ana

216 this review, we present some of what Bipolar-Schizophrenia Network for Intermediate Phenotypes (B-SNI

217 Participants recruited by the Bipolar and Schizophrenia Network for Intermediate Phenotypes consor

218 lygenic risk scores for depressive symptoms, schizophrenia, neuroticism, and subjective well-being to

219 of WM structure occur in an early course of schizophrenia onset.

220 OR MRS) AND (glutamate OR glut* OR GLX) AND (schizophrenia OR psychosis OR schizophren*).

221 ers aiming to identify biological markers of schizophrenia or psychosis.

222 total, 56 antipsychotic-naive patients with schizophrenia or psychotic disorder and 51 healthy contr

223 disorders involving GAD dysfunction such as schizophrenia or vitamin B6 deficiency.

224 ive function (P <= 1 x 10(-5)), and risk for schizophrenia (P <= 1 x 10(-10)) and bipolar disorder (P

225 nction is hypothesised to play a key role in schizophrenia pathogenesis, but this has not been tested

226 ns recapitulated group-average brain maps of schizophrenia pathology.

227 in cortical interneurons has been linked to schizophrenia pathophysiology.

228 levels in thalamus seem to be implicated in schizophrenia pathophysiology.

229 entified the first-episode drug-naive (FEDN) schizophrenia patients (accuracy 78.6%) and predict thei

230 sychosis: healthy control subjects (n = 46), schizophrenia patients (n = 25), and bipolar disorder pa

231 measures of auditory discrimination in both schizophrenia patients (WIN) and HS (WIN and QuickSIN),

232 The authors studied 66 schizophrenia patients and 143 healthy control subjects

233 ng findings of smaller hippocampal volume in schizophrenia patients and further our understanding of

234 s obtained from 293 healthy subjects and 427 schizophrenia patients who underwent ASSR testing.

235 nessed to compensate for STGp dysfunction in schizophrenia patients with hallucinations.

236 s, were impaired, reminiscent of findings in schizophrenia patients.

237 as auditory frequency modulation learning in schizophrenia patients.

238 vity, which mirror neuropathologies found in schizophrenia patients.

239 evidence for connectome-wide associations of schizophrenia polygenic risk at the systems level and su

240 Schizophrenia polygenic risk is plausibly manifested by

241 biological ontologies, for association with schizophrenia polygenic risk scores (PRSs) and with diag

242 11, 95% CI=1.03, 1.21), and only the PRS for schizophrenia predicted progression to psychotic disorde

243 The schizophrenia PRS shows promise in enhancing risk predic

244 We conclude that anatomical loci of schizophrenia-related changes are highly heterogeneous a

245 pared with other psychotic disorders such as schizophrenia, relatively few studies on the neurobiolog

246 y number variants (CNVs) are associated with schizophrenia risk and affect cognition in healthy popul

247 Schizophrenia risk is associated with both genetic and e

248 Recent findings suggest that certain schizophrenia risk loci can influence stochastic variati

249 h increased risk of depression in HD, as was schizophrenia risk score with psychosis and irritability

250 rders, enabling identification of functional schizophrenia risk variants and their cis-target genes.

251 ts and may capture individual differences in schizophrenia risk.

252 Although schizophrenia's pathophysiology is still unclear, postmo

253 ve development trajectory subgroups within a schizophrenia sample and profiled the subgroups across p

254 s measured in the plasma of 78 patients with schizophrenia/schizoaffective disorder and 73 healthy co

255 pharmacodynamics of ASP4345 in patients with schizophrenia/schizoaffective disorder.

256 Schizophrenia (SCZ) and bipolar disorder (BD) are severe

257 derived neuronal cultures from patients with schizophrenia (SCZ) and bipolar disorder (BD).

258 ptor gene expression and their relevance for schizophrenia (SCZ) and bipolar disorder (BD).

259 Multiple schizophrenia (SCZ) risk loci may be involved in gene co

260 ons (cINs)-which are known to be affected in schizophrenia (SCZ) when matured-from induced pluripoten

261 Schizophrenia (SCZ), bipolar disorder (BD), and major de

262 ers from the Psychiatric Genomics Consortium-schizophrenia (SCZ), bipolar disorder (BIP), major depre

263 , are thought of as risk factors for ASD and schizophrenia (SCZ).

264 lving patients with an acute exacerbation of schizophrenia, SEP-363856, a non-D2-receptor-binding ant

265 Medicated and unmedicated patients with schizophrenia showed impaired performance.

266 olescence that may serve as risk factors for schizophrenia spectrum disorders.

267 Clinically stable psychosis probands (Schizophrenia spectrum, n = 79; Psychotic Bipolar disord

268 Individuals at risk for schizophrenia-spectrum disorders display abnormalities r

269 powered to detect CNV effects in the Swedish Schizophrenia Study and the Taiwan Biobank.

270 The "high inflammation" schizophrenia subgroup had lower ABCG2 and higher ICAM1,

271 e dimensional (1)H-MRS was acquired in young schizophrenia subjects (N = 36, 19 antipsychotic-naive a

272 Schizophrenia subjects had lower Glx in the left superio

273 probands with psychotic disorders (107 with schizophrenia (SZ), 87 with schizoaffective disorder (SA

274 igh risk for Autism Spectrum Disorder (ASD), schizophrenia (SZ), and Attention-Deficit-Hyperactivity-

275 ult individuals diagnosed with autism (ASD), schizophrenia (SZ), and Down syndrome (DS).

276 Abnormal neurotransmission is central to schizophrenia (SZ).

277 der (ASD), intellectual disability (ID), and schizophrenia (SZ).

278 ing pathophysiological mechanisms related to schizophrenia that exceed those caused by NMDAR interneu

279 According to the adenosine hypothesis of schizophrenia, the classically associated hyperdopaminer

280 e for treatments effective in depression and schizophrenia to be used to treat depression and psychot

281 almefene, and buprenorphine in patients with schizophrenia to determine whether opioid antagonists ha

282 novo variants (DNVs) in a new sample of 613 schizophrenia trios and combined this with published dat

283 Higher volumes of depression and schizophrenia tweets were associated with higher numbers

284 crobiota plays a role in the pathogenesis of schizophrenia via the microbiota-gut-brain axis.

285 ve control that are selectively disrupted in schizophrenia, we trained male monkeys to perform a vari

286 The genetic liabilities for MDD and schizophrenia were associated with self-harm independent

287 Genes whose expression correlate with schizophrenia were enriched for those involved in abnorm

288 with major depression, bipolar psychosis and schizophrenia were evaluated.

289 e with other antipsychotics in patients with schizophrenia were identified using five databases.

290 s led to circuit deficits that recapitulates schizophrenia, whereas adult stress induced a depression

291 ars of schooling increases the likelihood of schizophrenia, whereas higher intelligence distinctly an

292 get for pharmacotherapy in disorders such as schizophrenia which involve aberrant increases in cortic

293 questions are whether there is a subtype of schizophrenia which responds differently to clozapine re

294 ponse prediction in first-episode drug-naive schizophrenia, which could complement other biomarkers i

295 theses are tested in a longitudinal study of schizophrenia with 2,137 observations spanning from chil

296 e frontal and anterior cingulate cortices in schizophrenia with large effect sizes (Cohen's d = 0.8-0

297 disorder, obsessive-compulsive disorder and schizophrenia within the putamen and white matter module

298 ressive disorder (MDD), bipolar disorder and schizophrenia would enhance statistical power to identif

299 We hypothesized that patients with stable schizophrenia would exhibit a reduction in glutathione,

300 ychiatric Genomics Consortium (PGC) study of schizophrenia yielded seven newly genome-wide significan