ライフサイエンスコーパス: schizophrenia

1 al computational dysfunction prototypical of schizophrenia.

2 ess in identifying genetic risk variants for schizophrenia.

3 ine whether the ARP2/3 complex is altered in schizophrenia.

4 ions of which are associated with autism and schizophrenia.

5 nteers and compared them with the effects of schizophrenia.

6 g phenotypes relevant to the pathobiology of schizophrenia.

7 ypofunction to predictive coding deficits in schizophrenia.

8 genic mechanism of cognitive deficiencies in schizophrenia.

9 ntribute to subcortical hyperdopaminergia in schizophrenia.

10 odevelopmental psychiatric disorders such as schizophrenia.

11 e than 20-fold increased risk for developing schizophrenia.

12 le as indicators of the genetic liability of schizophrenia.

13 y represent a novel therapeutic strategy for schizophrenia.

14 flexibility, and inhibition, are impaired in schizophrenia.

15 and proteomic findings are still lacking for schizophrenia.

16 antipsychotic monotherapy among adults with schizophrenia.

17 association between cannabis use and risk of schizophrenia.

18 moking cessation, in smokers with or without schizophrenia.

19 ve disorder, consistent with observations in schizophrenia.

20 sed in cortical networks in association with schizophrenia.

21 rmal brain development and increased risk of schizophrenia.

22 deficit/hyperactivity disorder, autism, and schizophrenia.

23 D), bipolar disorder, anxiety disorders, and schizophrenia.

24 between autism spectrum disorders (ASD) and schizophrenia.

25 s selectively reduced in the early stages of schizophrenia.

26 interrupt the program in young adults cause schizophrenia.

27 el that can now be explored in patients with schizophrenia.

28 ptor antibody affects behavioral outcomes in schizophrenia.

29 rect both positive and cognitive symptoms of schizophrenia.

30 re abnormal in psychiatric illnesses such as schizophrenia.

31 cognitive remediation effort for people with schizophrenia.

32 ated symptoms, such as cognitive deficits in schizophrenia.

33 ions (CNVs) on Autism spectrum disorders and schizophrenia.

34 , has been implicated in the pathobiology of schizophrenia.

35 lism is implicated in the pathophysiology of schizophrenia.

36 negative symptoms and cognitive deficits in schizophrenia.

37 networks that are disrupted in patients with schizophrenia.

38 nd Top3beta gene deletion has been linked to schizophrenia.

39 ensitivity and specificity in the context of schizophrenia.

40 Parkinson's disease, Alzheimer's disease and schizophrenia.

41 tivity contribute to auditory dysfunction in schizophrenia.

42 cline associated with Alzheimer's disease or schizophrenia.

43 vide new insight into the pathophysiology of schizophrenia.

44 utoimmune disorders that have been linked to schizophrenia.

45 rs, including both bipolar disorder (BD) and schizophrenia.

46 he highest rates of prevention of relapse in schizophrenia.

47 Proteins including DISC1 (disrupted in schizophrenia 1) and dysbindin-1B are found in insoluble

48 nts have shown that mutants for Disrupted-In-Schizophrenia-1 (DISC1), a well-accepted genetic risk fa

49 on using serum from 10 people diagnosed with schizophrenia, a mental health disorder that is increasi

50 receptor ErbB4 are associated with risk for schizophrenia, a neurodevelopmental disorder characteriz

51 red in neuropsychiatric disorders, including schizophrenia-a disorder that can be accompanied by heav

52 ysis of epigenetic variation associated with schizophrenia across multiple brain regions and highligh

53 f 2,370 individuals with treatment-resistant schizophrenia after Jan.

54 made in identifying the biologic effects of schizophrenia alleles to identify novel mechanisms prote

55 Consequently, in schizophrenia, alterations in the expression of gene pro

56 nce for a substantial polygenic component to schizophrenia, although the neurobiological mechanisms u

57 nd 196 control subjects) and hippocampus (83 schizophrenia and 187 control subjects).

58 dorsolateral prefrontal cortex (DLPFC) (144 schizophrenia and 196 control subjects) and hippocampus

59 nd mediodorsal thalamus may be 1) reduced in schizophrenia and 2) related to deficits in executive fu

60 independent post-mortem DLPFC data set (182 schizophrenia and 212 control subjects), although notabl

61 nts (1272 [32.6%] female) with first-episode schizophrenia and 4040 controls (1613 [39.9%] female) we

62 an unbiased link between polygenic risk for schizophrenia and a lower risk of psychosis in AD.

63 chiatric and neurological disorders, such as schizophrenia and Alzheimer's disease.

64 plicated neurophysiological abnormalities in schizophrenia and are linked to underlying dysfunction o

65 Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits

66 l delays in childhood and risk of developing schizophrenia and autism.

67 inked to a higher risk of converting to both schizophrenia and bipolar disorder.

68 licated in the underlying pathophysiology of schizophrenia and bipolar disorder.

69 ng protein 804A (ZNF804A) is associated with schizophrenia and bipolar disorder.

70 cases having a greater genetic overlap with schizophrenia and bipolar disorder.

71 The path to new therapies for schizophrenia and bipolar illness.

72 ciation studies, 21 loci jointly influencing schizophrenia and cognitive traits were identified: 2 lo

73 ylated in brain tissue between patients with schizophrenia and controls.

74 ariation associated with both a diagnosis of schizophrenia and elevated polygenic risk burden for the

75 nd reaction time, and 14 loci shared between schizophrenia and general cognitive function.

76 brain volumes in patients with first-episode schizophrenia and healthy controls by using magnetic res

77 ion mechanisms were similar in patients with schizophrenia and in healthy volunteers.

78 tors (NMDARs) in both the pathophysiology of schizophrenia and in neuronal plasticity suggests that f

79 ct is notably stronger in patients with both schizophrenia and intellectual disability, it is also se

80 gets show increased human genetic burden for schizophrenia and intellectual disability.

81 lamic connectivity in the pathophysiology of schizophrenia and mechanisms of cognitive impairment.

82 ATEMENT The AKT1 gene has been implicated in schizophrenia and psychosis.

83 s well recognized and has been implicated in schizophrenia and psychosis.

84 l-numerical reasoning, 6 loci shared between schizophrenia and reaction time, and 14 loci shared betw

85 lood-brain barrier structure and function in schizophrenia and related psychoses.

86 thylazoxymethanol acetate (MAM) rat model of schizophrenia and saline-treated control (SHAM) rats, in

87 Genetic overlap between schizophrenia and social communication difficulties, by

88 gical mechanism leading to PVI impairment in schizophrenia and some forms of autism.

89 ese results suggest that comorbidity between schizophrenia and substance use disorder is partially at

90 asing evidence of a blurred boundary between schizophrenia and substance use disorder.

91 onsisting of Japanese patients with sporadic schizophrenia and their parents.

92 CCB) in cognitive impairment associated with schizophrenia and to examine which demographic, clinical

93 ble dendritic pathologies among persons with schizophrenia and to some extent among those with bipola

94 tex tissue sections from 20 matched pairs of schizophrenia and unaffected comparison subjects were im

95 der, major depressive disorder, neuroticism, schizophrenia and verbal-numerical reasoning (absolute r

96 raits were identified: 2 loci shared between schizophrenia and verbal-numerical reasoning, 6 loci sha

97 lthy first-degree relatives of patients with schizophrenia, and 24 healthy nonrelatives.

98 sorders, including autism spectrum disorder, schizophrenia, and Alzheimer's disease.

99 en neuronal circuit function and symptoms of schizophrenia, and as a consequence generate new hypothe

100 thalamic volume is consistently observed in schizophrenia, and correlates with cognitive impairment.

101 ials in patients with acute exacerbations of schizophrenia, and they investigate which trial characte

102 s strongest in autism spectrum disorders and schizophrenia, and weakest in bipolar illness.

103 ive disorders, feeding and eating disorders, schizophrenia, anxiety disorder, OCD, and most affective

104 suggesting that altered GABAergic systems in schizophrenia are associated with either disease state o

105 investigated whether CNVs from patients with schizophrenia are enriched for genes expressed during th

106 Brain dynamic changes associated with schizophrenia are largely equivocal, with interpretation

107 ppocampal pathology (Alzheimer's disease and schizophrenia) are more enriched with normal hippocampal

108 ychotic drugs, originally developed to treat schizophrenia, are used to treat psychosis, agitation an

109 ould provide new insights into the nature of schizophrenia as a neurodevelopmental disorder.

110 rol status and to predict the development of schizophrenia as opposed to other psychoses.

111 ps between the normal development of-and the schizophrenia-associated alterations in-the DLPFC circui

112 ated genes in schizophrenia GWAS loci and in schizophrenia-associated biological pathways.

113 The schizophrenia-associated BRD1 gene encodes a transcripti

114 tudy assessed the transcriptional drive of a schizophrenia-associated BRD1 risk variant in vitro.

115 Carriers of schizophrenia-associated CNVs and of the group of 41 oth

116 A schizophrenia-associated rare sequence variant in TGEF1

117 ampal meQTLs and eQTLs significantly overlap schizophrenia-associated SNPs.

118 ome 19p13.2 were found to be associated with schizophrenia at the suggestive significance level of 5

119 ion did not have an established diagnosis of schizophrenia at the time of assessment.

120 trategy can be recommended for patients with schizophrenia based on the current meta-analytic literat

121 ogical and psychiatric conditions, including schizophrenia, bipolar disorder, Tourette's syndrome, de

122 s and 5,493 patients with various disorders (schizophrenia, bipolar or unipolar depression, anxiety d

123 eotide exchange factor, upregulated in human schizophrenia brain tissue.

124 In schizophrenia, brain-wide alterations have been identifi

125 the most promising medications for managing schizophrenia but it is under-utilized because of the ch

126 valent in neuropsychiatric disorders such as schizophrenia, but it is unclear whether these abnormali

127 id supplementation confers modest benefit in schizophrenia, but its effectiveness is influenced by co

128 in considered declining course a hallmark of schizophrenia, but others have suggested that outcomes u

129 ionally associated with an increased risk of schizophrenia, but whether the relationship is causal is

130 In a sample of 11 917 schizophrenia cases and 16 416 controls, we investigated

131 ine methyltransferase COMT that is linked to schizophrenia, cause deafness.

132 served RL value learning in individuals with schizophrenia compared with control subjects.

133 d Treatment Research to Improve Cognition in Schizophrenia Consensus Cognitive Battery (MCCB) in cogn

134 rongly associated with functional outcome in schizophrenia, current treatment strategies largely fail

135 These results suggest that, in schizophrenia, current well-powered GWAS results can rel

136 well as in psychiatric disorders, including schizophrenia, depression, attention-deficit hyperactivi

137 assessing the coaggregation between them and schizophrenia, depression, attention-deficit/hyperactivi

138 estry case subjects who went on to acquire a schizophrenia diagnosis from those who developed other p

139 likely to be differentially involved in the schizophrenia disease process and likely determine the s

140 ood, whereas most symptoms characteristic of schizophrenia do not appear before early adulthood.

141 wered GWAS results can reliably detect known schizophrenia drugs and thus may hold considerable poten

142 METHOD: The Recovery After an Initial Schizophrenia Episode-Early Treatment Program (RAISE-ETP

143 estigate whether patients with first-episode schizophrenia exhibit greater variability of regional br

144 ed risk of schizophrenia (odds ratio (OR) of schizophrenia for users vs nonusers of cannabis: 1.37; 9

145 Future November 1946: The Genetic Theory of Schizophrenia Franz Kallmann's influential twin study of

146 13.18 [1.08] x 10-3 min-1; P = .002) and the schizophrenia group (mean [SD], 12.94 [0.79] x 10-3 min-

147 For rare exonic deletions, the schizophrenia group had, on average, more genes overlapp

148 As a preliminary analysis, the schizophrenia group was subdivided by (1) treatment stat

149 om clozapine-treated and clozapine-untreated schizophrenia groups are well correlated to centralized

150 ce in striatal Kicer between the bipolar and schizophrenia groups.

151 nrichments of haloperidol-regulated genes in schizophrenia GWAS loci and in schizophrenia-associated

152 First, patients with schizophrenia had dysfunctional delta rhythms between 1-

153 Patients with schizophrenia had reduced cortical GABA compared with he

154 Schizophrenia has been associated with impaired predicti

155 Research in schizophrenia has established correlations among measure

156 Volume deficits of the hippocampus in schizophrenia have been consistently reported.

157 However, recent studies in people at risk of schizophrenia have found elevated striatal dopamine synt

158 Genome-wide association studies (GWAS) for schizophrenia have identified over 100 loci encoding >50

159 vents (eg, insomnia, akathisia, worsening of schizophrenia, headache, anxiety) were reported in 123 (

160 thways may contribute to the pathogenesis of schizophrenia, highlighting metabolic systems as importa

161 h these CNVs confer risk for the symptoms of schizophrenia, however, remains unclear.

162 , except 298A and 298B) and narrowly defined schizophrenia (ICD-9 code 295 and ICD-10 code F20).

163 A previous Free Water Imaging study in schizophrenia identified significantly greater extracell

164 a Franz Kallmann's influential twin study of schizophrenia in 691 twin pairs was the largest in the f

165 al impairments, implicated as antecedents to schizophrenia in high-risk, developmental studies, might

166 historical candidate gene polymorphisms for schizophrenia in the largest genome-wide association stu

167 at cognitive abnormalities in disorders like schizophrenia in which gluatamatergic signalling is impl

168 l association between smoking initiation and schizophrenia, in either direction.

169 sregulation of systems typically affected in schizophrenia, including glutamatergic, dopaminergic, im

170 ssociated with core pathological features of schizophrenia, increasing confidence that P50 inhibitory

171 homeostasis is altered from illness onset in schizophrenia, indicating that patients are at increased

172 Since schizophrenia is a developmental disorder, we examined t

173 m synaptic plasticity.SIGNIFICANCE STATEMENT Schizophrenia is a profoundly disabling psychiatric illn

174 Schizophrenia is associated with an increased risk of ty

175 Schizophrenia is associated with cognitive deficits that

176 evidence that abnormal WM microstructure in schizophrenia is associated with genes that are likely i

177 Schizophrenia is characterized by a multiplicity of symp

178 The pathogenesis of schizophrenia is considered to be multi-factorial, with

179 A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds rat

180 ption that central low-grade inflammation in schizophrenia is mirrored by increased TSPO expression o

181 ce and findings in patients with established schizophrenia, it was unclear what role dopamine played

182 variants in patients with autism (S1415L) or schizophrenia (L1424F and S1452F) (S1413L, L1422F, and S

183 their preclinical effectiveness for treating schizophrenia-like behaviors.

184 nvestigate whether people with circumscribed schizophrenia-like illnesses have such antibodies-especi

185 d treatment research to improve cognition in schizophrenia (MATRICS) consensus cognitive battery (MCC

186 sychiatric conditions, such as addiction and schizophrenia, may arise in part from dysregulated activ

187 obtained from Data set 1: 155 patients with schizophrenia (mean duration of illness of 7 years) and

188 m the latest Psychiatric Genomics Consortium schizophrenia meta-analysis.

189 ding molecular changes in the brain of a new schizophrenia model that incorporates genetic risk at th

190 tests of carriers of 12 CNVs associated with schizophrenia (n = 1087) and of carriers of another 41 n

191 ts with psychotic disorders from the Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP

192 s were observed between anorexia nervosa and schizophrenia, neuroticism, educational attainment, and

193 e among individuals with treatment-resistant schizophrenia not treated with clozapine compared with c

194 Furthermore, schizophrenia occurs in 30% of individuals with 22q11 de

195 nnabis was associated with increased risk of schizophrenia (odds ratio (OR) of schizophrenia for user

196 no evidence for pleiotropy in the effect of schizophrenia on smoking initiation (intercept OR 1.01,

197 le evidence in support of a causal effect of schizophrenia on smoking initiation (OR 1.01, 95% CI 0.9

198 ductions in fractional anisotropy emerged in schizophrenia only after age 35, and the rate of fractio

199 ed 1415 unrelated outpatients diagnosed with schizophrenia or schizoaffective disorder (mean [SD] age

200 Individuals with schizophrenia or schizoaffective disorders were included

201 waist circumference in men (P=1.1 x 10(-9)), schizophrenia (P=1.6 x 10(-9)), cognitive decline (P=5.3

202 not only in inflammation-related models for schizophrenia pathogenesis, but also in neurodevelopment

203 d similar deficits in organoids derived from schizophrenia patient induced pluripotent stem cells (iP

204 and Data set 2: an independent cohort of 46 schizophrenia patients (mean duration of illness of 18 y

205 ere acquired on a 3-T system from 26 chronic schizophrenia patients and 26 matched healthy control su

206 he case-control study, N1 amplitudes from 34 schizophrenia patients and 33 healthy control volunteers

207 by comparing post-mortem brain material from schizophrenia patients and control individuals.

208 in the striatal associative loop in chronic schizophrenia patients and healthy control subjects.

209 mean and radial diffusivity was observed for schizophrenia patients compared with controls.

210 anisotropy and fewer streamlines in chronic schizophrenia patients for all four tracts, both segrega

211 017) transplant human glial progenitors from schizophrenia patients into mouse brains, which develop

212 ields were found in the more chronic and ill schizophrenia patients of Data set 2.

213 der did not differ significantly from either schizophrenia patients or healthy controls, and it was i

214 As expected, schizophrenia patients showed highly significant, large

215 Also, male schizophrenia patients showed worse cognition than femal

216 anner similar to the dysfunction observed in schizophrenia patients, consistent with the theorized co

217 ive symptomatic improvement in this study of schizophrenia patients, warranting larger clinical trial

218 decreased MD-PFC connectivity is observed in schizophrenia patients.

219 and problem solving, and social cognition in schizophrenia patients.

220 ced prefrontal cortical thickness in chronic schizophrenia patients; however, this theory needs to be

221 'normalized' PPI in antipsychotic-medicated schizophrenia patients; no concurrent acute neurocogniti

222 The schizophrenia polygenic risk scores also predicted socia

223 a to be 14.3% (7.05-21.6; P=1 x 10(-4)) with schizophrenia polygenic risk scores explaining up to 0.1

224 l-D-aspartate receptor hypofunction model of schizophrenia predicts dysfunction in both glutamatergic

225 contribute to aberrant cortical thinning in schizophrenia prodromes and reduced prefrontal cortical

226 nt loss of gray matter volume was evident in schizophrenia, progressively worsening with age to a max

227 using hypothesis of cognitive dysfunction in schizophrenia proposes that people with schizophrenia (P

228 n in schizophrenia proposes that people with schizophrenia (PSZ) tend to concentrate processing resou

229 ective loss of dysbindin-1A and investigated schizophrenia-related phenotypes in both males and femal

230 The slope of this line was 60% steeper in schizophrenia relative to comparison subjects, indicatin

231 d integrative genomic analyses with focus on schizophrenia-relevant parameters.

232 re whether these changes in individuals with schizophrenia remain stable, are accelerated, or are dim

233 The role of the immune system in schizophrenia remains controversial despite numerous stu

234 ensively reported in Parkinson's disease and schizophrenia research.

235 ociated with autism, Parkinson's disease and schizophrenia, respectively.

236 ith a causal effect of smoking initiation on schizophrenia risk (OR 1.73, 95% CI 1.30-2.25, p < 0.001

237 One possibility is that schizophrenia risk CNVs impact basic associative learnin

238 affecting striated muscle and may also be a schizophrenia risk gene.

239 own (e.g., GRM7, 15q13.3, 16p12.2) and novel schizophrenia risk genes and loci.

240 nsive chromatin interactome is enriched with schizophrenia risk genes.

241 ntially mediated at least in part by CRP) on schizophrenia risk.

242 ffect (if any) of inflammatory biomarkers on schizophrenia risk.

243 sample of post-mortem brain of patients with schizophrenia: RNA sequencing was performed to assess th

244 with catatonic signs in a deeply phenotyped schizophrenia sample (n = 1095).

245 ne-induced dopamine release in subjects with schizophrenia (SCH) relative to healthy control subjects

246 re mental illness as a clinical diagnosis of schizophrenia, schizoaffective disorder, bipolar disorde

247 cebo-controlled trial included patients with schizophrenia, schizoaffective disorder, or a mood disor

248 e dyskinesia in participants with underlying schizophrenia, schizoaffective disorder, or mood disorde

249 Although the pathogenesis of schizophrenia (SCZ) is proposed to involve alterations o

250 Schizophrenia (SCZ), bipolar disorder (BD) and recurrent

251 pkins syndrome, intellectual disability, and schizophrenia (SCZ).

252 on deficit hyperactivity disorder (ADHD) and schizophrenia (SCZ).

253 8 to 65 years, had a clinical diagnosis of a schizophrenia spectrum (ICD10 F20-29) or affective disor

254 Patients with a schizophrenia spectrum disorder and bipolar disorder sho

255 social functioning from 485 respondents with schizophrenia spectrum disorders and psychotic mood diso

256 rders, including psychopathy, and autism and schizophrenia spectrum disorders, have been linked with

257 n of Diseases codes for bipolar disorder and schizophrenia spectrum disorders.

258 dded to clozapine or olanzapine treatment of schizophrenia spectrum disorders.

259 s with a diagnosis of severe mental illness (schizophrenia spectrum or bipolar disorder) with 574 018

260 aged 12-17 years with a diagnosis of ICD-10 schizophrenia-spectrum disorder, delusional disorder, or

261 olar disorder, major depressive disorder and schizophrenia (standardised beta's had absolute values<0

262 vGLUT2 levels were similar between medicated schizophrenia subjects and controls.

263 In contrast, unmedicated schizophrenia subjects had higher vGLUT2 levels than con

264 bnormalities in certain clinical features of schizophrenia, such as working memory impairments, depen

265 reorganization of expression of synaptic and schizophrenia-susceptibility genes.

266 are also at high risk for the development of schizophrenia symptoms, including psychosis, later in li

267 tion of cortico-thalamo-cortical circuits in schizophrenia (SZ) and bipolar disorder (BD).

268 People with schizophrenia (SZ) experience abnormal visual perception

269 determined using 5090 exomes from the Sweden-Schizophrenia (SZ) Population-Based Case-Control Exome S

270 etic and environmental factors contribute to schizophrenia (SZ) risk.

271 to play a critical role in vulnerability to schizophrenia (SZ), but the pathogenic impact of SZ-risk

272 ing memory) are typically most pronounced in schizophrenia (SZ), intermediate in bipolar disorder, an

273 hibit similar, subtle symptoms to those with schizophrenia (SZ).

274 netic loci that significantly associate with schizophrenia (SZ).

275 mpirical support for use in the treatment of schizophrenia (SZ).

276 s study also reveals significant pathways in schizophrenia that were not identified previously, and p

277 In schizophrenia, the density of cartridges detectable by g

278 has been implicated in the neuropathology of schizophrenia, the transcript structure of GAD1 in the h

279 This study has established that, as in schizophrenia, there is a therapeutic window of D2/3 rec

280 bnormalities and behaviors characteristic of schizophrenia, thereby suggesting a primary role for gli

281 d appear to be significantly associated with schizophrenia, these genes were not particularly notewor

282 h neurological disorders, such as autism and schizophrenia, this signaling cascade offers new avenues

283 etic variation in the molecular aetiology of schizophrenia, this study aimed to identify epigenetic v

284 Syndrome Scale (PANSS) >60) individuals with schizophrenia to 3 monthly infusions of 8 mg/kg tocilizu

285 mate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P=1 x 10(-4)) with

286 tes mechanisms underlying MMN impairments in schizophrenia using event-related potential, event-relat

287 unction (Stroop) task in 28 individuals with schizophrenia using functional magnetic resonance imagin

288 ate the genetic relationship between ALS and schizophrenia using genome-wide association study data f

289 mate concentrations in vivo in patients with schizophrenia using proton magnetic resonance spectrosco

290 c risk factors for cognitive dysfunction and schizophrenia, we found that goal-oriented learning in w

291 For example, candidates for schizophrenia were enriched for antipsychotics, while th

292 rs to contribute to cognitive dysfunction in schizophrenia, whereas psychosis is associated with exce

293 In patients with schizophrenia who also have intellectual disability, thi

294 disability, it is also seen in patients with schizophrenia who do not have intellectual disability.

295 7T was performed in 21 patients with chronic schizophrenia who were taking medication, 23 healthy fir

296 frontal gyrus of patients with recent-onset schizophrenia, who were previously shown to display incr

297 he need to interpret altered TSPO binding in schizophrenia with caution, especially when measures of

298 d genome-wide effects of genetic variants in schizophrenia with significant predictive power.

299 nts contribute significantly to the risk for schizophrenia, with the 22q11.2 locus consistently impli

300 In schizophrenia, working memory deficit was mostly account