ライフサイエンスコーパス: antipsychotic

1 ne prior to treatment with second-generation antipsychotics.

2 ted response to treatment with glutamatergic antipsychotics.

3 ity could also be restored by application of antipsychotics.

4 ts occurring in placebo-controlled trials of antipsychotics.

5 randomised controlled trials and compared 32 antipsychotics.

6 , as well as with response to treatment with antipsychotics.

7 use of valproate, and growing use of modern antipsychotics.

8 wo-week washout period from standard of care antipsychotics.

9 ychosis show a better subsequent response to antipsychotics.

10 ced by dopamine receptor blockers, including antipsychotics.

11 ols neuronal gene expression is regulated by antipsychotics.

12 expression is associated with treatment with antipsychotics.

13 ivity at the 5-HT2C receptor with respect to antipsychotic activity.

14 erogeneity in antipsychotic dosing, route of antipsychotic administration, assessment of outcomes, an

15 by the Veterans Affairs Risk Score-CVD, and antipsychotic and anticonvulsant/mood stabilizer medicat

16 ogic profile is consistent with the observed antipsychotic and antidepressant effects.

17 ing in cells was differentially regulated by antipsychotic and antiparkinsonian drugs.

18 for bipolar disorder were enriched for both antipsychotics and antidepressants.

19 onfounds of illness chronicity or the use of antipsychotics and illicit substances.

20 of the evidence, recommend reserving use of antipsychotics and other sedating medications for treatm

21 d, randomised controlled trials comparing 18 antipsychotics and placebo in acute treatment of schizop

22 Differences in efficacy between antipsychotics and placebo in schizophrenia trials have

23 r to fully understand the difference between antipsychotics and placebo.

24 esearch should focus on development of safer antipsychotics and specific therapies for the different

25 opamine signaling involved in treatment with antipsychotics and the transcriptional regulation mechan

26 ption until 22 May 2020 to investigate which antipsychotics and/or mood stabilizers are better for pa

27 od stabilizers, first- and second-generation antipsychotics, and antidepressants among psychiatrist v

28 d glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resista

29 (1.63%) to 862 (2.02%) of 42 600 patients on antipsychotics, and in 343 (1.37%) to 419 (1.67%) of 25

30 s differently to clozapine relative to other antipsychotics, and whether greater efficacy of clozapin

31 oplastics, antiretrovirals, antidepressants, antipsychotics, anticonvulsants, and immunosuppressants

32 acologic profile that may be relevant to the antipsychotic, antidepressant, and side effect profiles

33 ntidementia drugs, alone and in combination, antipsychotics, antidepressants, anxiolytics, and hypnot

34 In antipsychotic (AP)-medicated schizophrenia patients, amp

35 Antipsychotics are commonly used; however, the associate

36 haracteristics of DD and schizophrenia (SZ), antipsychotics are deemed equally effective pharmaceutic

37 Although antipsychotics are effective in treating mania, few anti

38 ly used to treat pathologies for which other antipsychotics are indicated because it displays fewer s

39 Hence, clinicians should be aware that antipsychotics are potentially toxic, particularly when

40 erventions, although stimulants and atypical antipsychotics are sometimes used, especially in individ

41 Antipsychotics are used to prevent delirium, but their b

42 d-release bupropion; or augmentation with an antipsychotic-aripiprazole.

43 Antipsychotics blocked synaptic vesicle release during e

44 There are some efficacy differences between antipsychotics, but most of them are gradual rather than

45 We aimed to compare and rank antipsychotics by quantifying information from randomise

46 ained by theta power changes, head movement, antipsychotics, cannabis use, or IQ, and is not found in

47 We found evidence that antipsychotics cause short-term somatic serious adverse

48 Antipsychotic clinical response occurred at a threshold

49 Use of the atypical antipsychotic clozapine is associated with life-threaten

50 Chronic treatment with the antipsychotic clozapine led to a decrease in mouse front

51 The antipsychotic clozapine, the only licensed medication fo

52 readily reversible by administration of the antipsychotics clozapine and risperidone suggesting that

53 se-dependent manner, similar to the atypical antipsychotic, clozapine.

54 second included studies on second-generation antipsychotic combination therapies (SGAs) (i.e., aripip

55 erior responses of first-episode patients to antipsychotics compared with patients with chronic illne

56 l K(i)(cer) values and time to relapse after antipsychotic discontinuation (R(2) = 0.518, p = 0.018).

57 METHOD: In the Antipsychotic Discontinuation in Alzheimer's Disease tri

58 on might precipitate psychotic relapse after antipsychotic discontinuation in FEP.

59 EPs remain remitted even without medication, antipsychotic discontinuation is regarded as the most co

60 the patients showed psychotic relapse after antipsychotic discontinuation.

61 e prevention of psychotic relapse related to antipsychotic discontinuation.

62 as BP(ND) using [(11)C]raclopride PET after antipsychotic discontinuation.

63 ing [(18)F]DOPA PET before and 6 weeks after antipsychotic discontinuation.

64 for psychotic relapse during 12 weeks after antipsychotic discontinuation.

65 possible mechanisms underlying relapse after antipsychotic discontinuation.

66 Antipsychotic dosages were not correlated with ERG param

67 duration (t = -0.167, df = 277, P = 0.868), antipsychotic dose (t = -0.439, df = 210, P = 0.521), ag

68 nglia and internal capsule, not explained by antipsychotic dose.

69 as increased conformity was seen with higher antipsychotic dose.

70 There was significant heterogeneity in antipsychotic dosing, route of antipsychotic administrat

71 Haloperidol is a typical antipsychotic drug (APD) associated with an increased ri

72 Clinical research has shown that chronic antipsychotic drug (APD) treatment further decreases cor

73 We also investigated the effects of antipsychotic drug administration on SV2A levels in Spra

74 of a formal structural hybridization of the antipsychotic drug aripiprazole and the heterocyclic cat

75 Aripiprazole is an antipsychotic drug characterized by partial agonist acti

76 dy raises the possibility of repurposing the antipsychotic drug chlorpromazine for treatment of neuro

77 eurotransmission is a prioritized target for antipsychotic drug development.

78 ein levels in schizophrenia in vivo and that antipsychotic drug exposure is unlikely to account for t

79 -blocking effect of the mGluR2/3 agonist and antipsychotic drug in development LY404039.

80 nce strategy, a late-stage deuteration of an antipsychotic drug is described.

81 receptor in its inactive state bound to the antipsychotic drug nemonapride, with resolutions up to 1

82 ferentially methylated genes and 49 genes as antipsychotic drug targets.

83 hibition of the dopamine transporter rescued antipsychotic drug treatment outcomes, supporting the hy

84 phrenia tended to have less improvement with antipsychotic drug treatment.

85 imprinting of an electroactive aripiprazole antipsychotic drug were herein designed and synthesized.

86 renia, SEP-363856, a non-D2-receptor-binding antipsychotic drug, resulted in a greater reduction from

87 Antipsychotic drugs (AP) are used to treat a multitude o

88 Most clinically available antipsychotic drugs (APDs) bind dopamine D2 receptors (D

89 Second-generation antipsychotic drugs (SGAs) are essential in the treatmen

90 ay be useful in the preclinical screening of antipsychotic drugs acting to correct altered epigenetic

91 Of note, currently used antipsychotic drugs ameliorate psychosis, but they are n

92 ose-finding studies for 20 second-generation antipsychotic drugs and haloperidol (oral and long-actin

93 the dopamine transporter is a main target of antipsychotic drugs and predicting that dopamine transpo

94 Although antipsychotic drugs are effective for relieving the psyc

95 Antipsychotic drugs are effective interventions in schiz

96 Antipsychotic drugs are its treatment of choice, but the

97 tified several diphenylbutylpiperidine-class antipsychotic drugs as agents that decreased PRL-induced

98 level of occupancy is lower than most other antipsychotic drugs at their efficacious doses and likel

99 The dose-response relationships of antipsychotic drugs for schizophrenia are not well defin

100 Antipsychotic drugs have been proven to alleviate acute

101 Traditional D(2) antagonist antipsychotic drugs have been shown previously to reduce

102 Antipsychotic drugs might cause acutely occurring, serio

103 Considering the actions of antipsychotic drugs on presynaptic and postsynaptic dopa

104 e repeated in monkeys chronically exposed to antipsychotic drugs to determine their effect on mitocho

105 D2 receptor (D2R) levels and the failure of antipsychotic drugs to rescue adult behavioral defects.

106 The prescription of antipsychotic drugs was not significantly different betw

107 peutic target for Parkinson's disease(1) and antipsychotic drugs(2).

108 macological treatments for delirium (such as antipsychotic drugs) are not effective, reflecting subst

109 for a scientific commentary on this article.Antipsychotic drugs, originally developed to treat schiz

110 Some antipsychotic drugs, such as aripiprazole, are less effi

111 Antipsychotic drugs, such as penfluridol, block PRL sign

112 n in patients with SCZ before treatment with antipsychotic drugs.

113 erebrovascular disease and use anxiolytic or antipsychotic drugs.

114 ses in dopamine target areas declined during antipsychotic efficacy and showed potentiation during fa

115 However, antipsychotic efficacy associated with high D(2)RO is of

116 ITI-007, a dose that previously demonstrated antipsychotic efficacy in a controlled trial, administer

117 er PRSs for schizophrenia were predictive of antipsychotic efficacy in four independent cohorts of pa

118 We report that antipsychotic efficacy in rat models declines in concert

119 Furthermore, it is unknown whether antipsychotic efficacy is linked to reductions in dopami

120 The antipsychotic efficacy of olanzapine plus samidorphan wa

121 The primary aims were to confirm that the antipsychotic efficacy of olanzapine plus samidorphan wa

122 The antipsychotic efficacy of the combination treatment was

123 Antipsychotic efficacy was associated with a suppression

124 Antipsychotic efficacy, as assessed by total score on th

125 neuron firing, which was not observed during antipsychotic efficacy.

126 renia and unaffected comparison subjects, 2) antipsychotic-exposed monkeys, and 3) adult mice exposed

127 In schizophrenia subjects, but not antipsychotic-exposed monkeys, we found higher messenger

128 lying the potential repercussion of previous antipsychotic exposure on the therapeutic performance of

129 Antipsychotic failure coincided with reduced dopamine ne

130 in patients treated with clozapine and other antipsychotics for both treatment-resistant schizophreni

131 tine use of haloperidol or second-generation antipsychotics for prevention of delirium.

132 the phenomenon of decreasing effect size of antipsychotics for schizophrenia over time and should he

133 eptor (D(2)R) is a key therapeutic target of antipsychotics for the treatment of schizophrenia.

134 ogic harms associated with short-term use of antipsychotics for treating delirium in adult inpatients

135 Thirty-one schizophrenia patients (n = 10 antipsychotic free) and twenty-nine matched healthy cont

136 Compared with controls, BP(ND) was lower in antipsychotic-free (n = 6), but not in medicated, ROS pa

137 11)C]Ro15-4513 V(T) and total PANSS score in antipsychotic-free patients (r = 0.72; p = 0.044).

138 The results suggest that antipsychotic-free patients with schizophrenia have lowe

139 er [11C]Ro15-4513 V(T) in the hippocampus of antipsychotic-free patients, but not in medicated patien

140 nvestigated alpha5-GABA(A)Rs availability in antipsychotic-free schizophrenia patients and antipsycho

141 acological treatment and medicated only with antipsychotics had increased GLU compared to FEP with sh

142 nd the prescription of potentially hazardous antipsychotics halved after the introduction of national

143 chotics are effective in treating mania, few antipsychotics have proven to be effective in bipolar de

144 Pharmacogenomic studies of antipsychotics have typically examined effects of indivi

145 d methionil (POM), showed promise as a novel antipsychotic in preclinical research but failed to show

146 ised controlled trials comparing placebo and antipsychotics in acute treatment of schizophrenia liste

147 Clozapine was superior to other antipsychotics in improving total symptoms in both TRS (

148 er the past 20 years, with second-generation antipsychotics in large measure supplanting traditional

149 rolled trials comparing clozapine with other antipsychotics in patients with schizophrenia were ident

150 Marked differences exist between antipsychotics in terms of metabolic side-effects, with

151 er significantly between clozapine and other antipsychotics in TRS studies (VR = 1.84; 95%CI, 0.85-4.

152 thylamines, cathinones, antidepressants, and antipsychotics, in neat oral fluid was carried out using

153 thnicity are predictors of susceptibility to antipsychotic-induced metabolic change, and improvements

154 physiological and demographic predictors of antipsychotic-induced metabolic dysregulation, and inves

155 tion of striatal structure and function with antipsychotic-induced weight gain.

156 Clozapine is more effective than other antipsychotics irrespective of treatment-resistance, arg

157 lterations occur in treatment with different antipsychotics is unclear.

158 In particular, second generation antipsychotics, like first generation agents, are associ

159 t investigations revealed that 12c displayed antipsychotic-like activity by significantly inhibiting

160 M(4) to inhibit dopamine release and induce antipsychotic-like effects in animal models is dependent

161 ive allosteric modulator (PAM) exerts robust antipsychotic-like effects through an endocannabinoid-de

162 sts have pro-cognitive, antidepressant-, and antipsychotic-like properties in both rodents and non-hu

163 e is limited evidence that second-generation antipsychotics may lower delirium incidence in the posto

164 e is limited evidence that second-generation antipsychotics may lower the incidence of delirium in po

165 ntipsychotic-free schizophrenia patients and antipsychotic-medicated schizophrenia patients using [(1

166 Experimental Medicine use of amphetamine in antipsychotic-medicated schizophrenia patients were dete

167 Patients were predominantly antipsychotic-medicated.

168 n the study, 17 of whom were concordant with antipsychotic medication at therapeutic doses.

169 ippocampal subfields from our SZ ON- and OFF-antipsychotic medication cohort.

170 metabolism abnormalities before significant antipsychotic medication exposure.

171 udy subjects received initial treatment with antipsychotic medication for first-episode psychosis, an

172 the efficacy and tolerability of continuing antipsychotic medication for patients with psychotic dep

173 so examine changes in gene expression due to antipsychotic medication in the hippocampal subfields fr

174 The effects of antipsychotic medication on dopamine synthesis capacity

175 ique pattern of subfield-specific effects by antipsychotic medication on gene expression levels with

176 in the lack of full efficacy of conventional antipsychotic medication on SZ symptomatology.

177 It is frequently postulated that antipsychotic medication possibly alters functional mech

178 We previously proposed that long-term antipsychotic medication restricted the therapeutic effe

179 as a new diagnosis of psychosis for which an antipsychotic medication was prescribed during the first

180 The association of antipsychotic medication with abnormal brain morphometry

181 code for psychosis and a prescription for an antipsychotic medication) in the matched populations (2.

182 ecule chlorpromazine (CH), widely used as an antipsychotic medication, binds to the isolated PAS doma

183 There were two groups of participants: an antipsychotic medication-naive psychosis risk group (n =

184 reflect our patients' relative wellbeing on antipsychotic medication.

185 s, indicating that they were unlikely due to antipsychotic medication.

186 hrenia independent from potential effects of antipsychotic medication.

187 de of psychosis who have not been exposed to antipsychotic medication.

188 ss phenotype and the confounds introduced by antipsychotic medication.

189 th SZ and 45 with BP-balanced for their main antipsychotic medication.

190 even after balancing patients for their main antipsychotic medication.

191 d for gender, occupational status, race, and antipsychotic medication.

192 e striatum, where D2 receptors are abundant, antipsychotic medications may affect neural function in

193 heral D(2)-like receptors by drugs including antipsychotic medications may significantly contribute t

194 Failure of antipsychotic medications to resolve symptoms in patient

195 amine D2 receptors, which are antagonized by antipsychotic medications, plays a key role in the human

196 past cannabis exposure or current intake of antipsychotic medications.

197 ) is a key feature of all currently approved antipsychotic medications.

198 sed mental health program that provided free antipsychotic medications.

199 ndication for using immunotherapy instead of antipsychotic medications.

200 n modules, and DEGs were not attributable to antipsychotic medications.

201 Antipsychotic medicine (k = 5; n = 364; SMD = -0.45; -0.

202 These outcomes remained similar in antipsychotic naive sensitivity analyses.

203 nts with first-episode psychosis (14 of them antipsychotic naive) and 20 healthy volunteers underwent

204 lanine positron emission tomography study in antipsychotic naive/free people with first-episode psych

205 We recruited 42 schizophrenia patients (30 antipsychotic-naive and 12 currently untreated) and 42 m

206 in young schizophrenia subjects (N = 36, 19 antipsychotic-naive and 17 antipsychotic-treated) and he

207 We enrolled 66 antipsychotic-naive first-episode psychosis (FEP) patien

208 .35, p = .039), i.e., increased glutamate in antipsychotic-naive patients (d = 0.46 [95% CI, 0.08 to

209 d lower variability in cortical glutamate in antipsychotic-naive patients as a possible key factor re

210 The whole group of antipsychotic-naive patients had lower levels of GABA in

211 In total, 56 antipsychotic-naive patients with schizophrenia or psych

212 Finally in antipsychotic-naive patients, NAA was reduced in right f

213 as not been investigated in a large group of antipsychotic-naive patients.

214 to the hypothesis that there is a subtype of antipsychotic non-responsive schizophrenia.

215 We aimed to compare and rank antipsychotics on the basis of their metabolic side-effe

216 tion fills for antidepressants, anxiolytics, antipsychotics, opioids, and antiepileptics among commun

217 tions in NDEL1 activity after treatment with antipsychotics or psychostimulants may suggest a possibl

218 in terms of dose and administration route of antipsychotics, outcomes, and measurement instruments.

219 ains unsatisfactory but includes some modern antipsychotics (particularly lurasidone, olanzapine + fl

220 investigation, as it has implications beyond antipsychotic prescribing.

221 Finally, FEP patients treated only with antipsychotics presented higher Glx compared to those wi

222 AC inhibitor SAHA (vorinostat) preserved the antipsychotic profile of LY379268 and frontal cortex mGl

223 ilitate the process is readily reversible by antipsychotics, providing conceptual links to particular

224 ast 20 years, with several second-generation antipsychotics receiving regulatory approval in the 1990

225 Effect size estimates suggested all antipsychotics reduced overall symptoms more than placeb

226 which displays behavioural deterioration on antipsychotic reduction that prevents discontinuation; p

227 Chronic clozapine treatment blunted the antipsychotic-related behavioral effects of LY379268, an

228 action of antipsychotics, and development of antipsychotic resistance.

229 city has been implicated in the etiology and antipsychotic response in psychotic illness.

230 Lower variability in antipsychotic-response relative to placebo was associate

231 e pathology and their modulation by atypical antipsychotic risperidone treatment in rats with neonata

232 However, the choice of antipsychotic should be made on an individual basis, con

233 ute or dysphoric mania is provided by modern antipsychotics, some anticonvulsants (divalproex and car

234 Addition of the antipsychotics, spiperone or haloperidol, resulted in re

235 Atypical antipsychotics such as olanzapine often induce excessive

236 ublications demonstrated that DRD2-targeting antipsychotics such as thioridazine induce proliferation

237 in adhesion, while inhibition of 5-HT(2A) by antipsychotics, such as risperidone, olanzapine or chlor

238 in daily functioning tend to persist despite antipsychotic therapy but their neural basis is less cle

239 t comparisons of different second-generation antipsychotics, there was no difference in mortality and

240 tine use of haloperidol or second-generation antipsychotics to treat delirium in adult inpatients.

241 dividual patient dataset (N = 522 patients), antipsychotic treated patients did not show significantl

242 Antipsychotic-treated and naive patients (vs HC) had sim

243 ve variability of symptomatic improvement in antipsychotic-treated individuals compared to placebo-tr

244 on over 5 years, 26 illness duration-matched antipsychotic-treated patients and 24 demographically-ma

245 us and bilateral putamen/caudate relative to antipsychotic-treated patients and controls.

246 Compared with placebo, antipsychotic-treated patients demonstrated greater tota

247 Both never-treated and antipsychotic-treated schizophrenia patient groups showe

248 However, creatine was higher in antipsychotic-treated vs HC's in a larger left hemispher

249 jects (N = 36, 19 antipsychotic-naive and 17 antipsychotic-treated) and healthy controls (HC, N = 29)

250 curacy 78.6%) and predict their responses to antipsychotic treatment (accuracy 82.5%) at an individua

251 ively correlated with subsequent response to antipsychotic treatment (r = -0.38; p = 0.049).

252 p = 0.03) and poorer subsequent response to antipsychotic treatment (r = 0.40; p = 0.01).

253 ckers may be an adjunct treatment to reverse antipsychotic treatment failure.

254 ing, GAF) occurred at baseline and following antipsychotic treatment for a minimum of 4 weeks.

255 d weight gain over the course of 12 weeks of antipsychotic treatment in 81 patients with early-phase

256 dence for a relatively homogeneous effect of antipsychotic treatment in improving symptoms of schizop

257 vity and clinical response after 24-weeks of antipsychotic treatment in patients with schizophrenia (

258 easured before and after at least 5 weeks of antipsychotic treatment in people with first-episode psy

259 The response to antipsychotic treatment in schizophrenia appears to vary

260 Antipsychotic treatment is associated with metabolic dis

261 he subgroup of patients in whom conventional antipsychotic treatment is ineffective and offer alterna

262 Here we show that this maladaptive effect of antipsychotic treatment is mediated mostly via histone d

263 heir role in psychosis onset and response to antipsychotic treatment is unclear.

264 usually has an acute or subacute onset, and antipsychotic treatment may be ineffective and associate

265 han treated patients suggests that long-term antipsychotic treatment may partially protect or enhance

266 unction indexed as K(i)(cer) differs between antipsychotic treatment responders and non-responders.

267 on and established its utility in predicting antipsychotic treatment response, clinical stratificatio

268 FSA scores was significantly associated with antipsychotic treatment response.

269 Compared to placebo, antipsychotic treatment shows greater improvement and lo

270 Dopamine synthesis capacity is unaltered by antipsychotic treatment, and therapeutic effects are not

271 nt and/or function, which is counteracted by antipsychotic treatment.

272 toms and change in metabolic parameters with antipsychotic treatment.

273 ople with first-episode psychosis commencing antipsychotic treatment.

274 raphy scan to measure DSC (Ki(cer)) prior to antipsychotic treatment.

275 ocognitive functioning following 12 weeks of antipsychotic treatment.

276 asures at baseline and following 12 weeks of antipsychotic treatment.

277 alid criteria to predict who will respond to antipsychotic treatment.

278 occ;30-60) value) within 1 month of starting antipsychotic treatment.

279 establish possible correlations with chronic antipsychotic treatments.

280 tional Institute of Mental Health's Clinical Antipsychotic Trials of Intervention Effectiveness (CATI

281 ymptoms (t = 0.151, df = 289, P = 0.879), or antipsychotic type (chi-square = 6.670, df = 3, P = 0.08

282 long-term treatment with typical or atypical antipsychotics, under conditions in which SCZ-like pheno

283 is <2 years, minimally or never treated with antipsychotics) undergoing initial treatment with amisul

284 47, 75% of studies), duration (67, 34%), and antipsychotic use (42, 22%) were most commonly reported.

285 ardiac effects occurred more frequently with antipsychotic use.

286 hotics, with insufficient or no evidence for antipsychotics versus placebo.

287 ty between haloperidol and second-generation antipsychotics versus placebo.

288 re is little evidence that short-term use of antipsychotics was associated with neurologic harms.

289 ore sedatives, whereas doses of morphine and antipsychotics were equal.

290 Antipsychotics were increasingly more commonly prescribe

291 However, antipsychotics were nearly as efficacious as antiparkins

292 in astrocytes and secreted via exosomes, and antipsychotics were shown to control its cellular and ex

293 Current treatments comprise antipsychotics which act solely symptomatic, are limited

294 ndidates for schizophrenia were enriched for antipsychotics, while those for bipolar disorder were en

295 tial multiple-assignment randomized trial of antipsychotics with high dropout rates.

296 (spi) should be of value for designing novel antipsychotics with improved safety and efficacy.

297 ed trials (RCTs) comparing second-generation antipsychotics with placebo.

298 orld effectiveness and tolerability of newer antipsychotics with those of traditional mood stabilizer

299 OE) for haloperidol versus second-generation antipsychotics, with insufficient or no evidence for ant

300 predictions of future treatment responses to antipsychotics would be of great value, but there has be