ライフサイエンスコーパス: antipsychotics

1 ols neuronal gene expression is regulated by antipsychotics.

2 regardless of whether they were also taking antipsychotics.

3 or antagonists, such as typical and atypical antipsychotics.

4 both first-generation and second-generation antipsychotics.

5 n Registry provided data on prescriptions of antipsychotics.

6 sorder, and 85.5% were receiving concomitant antipsychotics.

7 little difference between second-generation antipsychotics.

8 fects in schizophrenia patients treated with antipsychotics.

9 zapine compared with other second-generation antipsychotics.

10 er there are significant differences between antipsychotics.

11 atients unlikely to respond to non-clozapine antipsychotics.

12 the motor-reducing and cataleptic effects of antipsychotics.

13 ide-effect profile compared with established antipsychotics.

14 + levels on antipsychotics compared with off antipsychotics.

15 led positive symptoms despite treatment with antipsychotics.

16 that is the current target of most effective antipsychotics.

17 s) between active drugs and placebo added to antipsychotics.

18 expression is associated with treatment with antipsychotics.

19 patients treated only with second-generation antipsychotics.

20 ing memory and also modulate the response to antipsychotics.

21 ereotypical behaviors, which are relieved by antipsychotics.

22 he same subjects and from monkeys exposed to antipsychotics.

23 leads to a novel approach to potent atypical antipsychotics.

24 e of the escalating prescription of atypical antipsychotics.

25 ent is an important moderator of response to antipsychotics.

26 e interval, 2.49-3.02) for second-generation antipsychotics.

27 y of auditory thalamocortical projections to antipsychotics.

28 months) and treatment with second-generation antipsychotics.

29 ncertainty about the longer term benefits of antipsychotics.

30 isk of stroke than the use of other types of antipsychotics.

31 n and death after adjustment for exposure to antipsychotics.

32 is patients was normalized by treatment with antipsychotics.

33 first 5 years of the disease who are taking antipsychotics.

34 to structurally diverse typical and atypical antipsychotics.

35 group had less exposure to second-generation antipsychotics.

36 ity could also be restored by application of antipsychotics.

37 d known neurotransmitter receptor targets of antipsychotics.

38 ne prior to treatment with second-generation antipsychotics.

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

40 ted response to treatment with glutamatergic antipsychotics.

41 ts occurring in placebo-controlled trials of antipsychotics.

42 randomised controlled trials and compared 32 antipsychotics.

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

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

45 ychosis show a better subsequent response to antipsychotics.

46 ced by dopamine receptor blockers, including antipsychotics.

47 r (1.24 [1.11-1.39]), psychotropic drug use (antipsychotics 1.51 [1.35-1.69], antidepressants 1.15 [1

48 (95% confidence interval, 2.37-2.68) for any antipsychotics, 2.32 (95% confidence interval, 2.17-2.47

49 106 genes, p=0.00046, pcorrected =0.024) and antipsychotics (347 genes, p=0.00078, pcorrected=0.046).

50 rare disruptive variants in gene targets of antipsychotics (347 genes, p=0.0067) and in genes with e

51 tected between 2010 and 2014, especially for antipsychotics (35-fold), benzodiazepines (19-fold), and

52 visits for adverse drug events, followed by antipsychotics (4.5%; 95% CI, 3.3%-5.6%).

53 prevalent in patients currently treated with antipsychotics (45.3% [95% CI=39.6-50.9] than in patient

54 nificant enrichment both in known targets of antipsychotics (70 genes, p=0.0078) and novel predicted

55 Unlike reference antipsychotics, 72 displayed marked antipsychotic and an

56 hizophrenia spectrum disorders with atypical antipsychotics (AAPs), there is still need for compounds

57 The efficacy of antipsychotics across the initial severity range in pati

58 hotics on the insulin promoter, finding that antipsychotics activated SMAD3, a downstream effector of

59 -line treatment with either first-generation antipsychotics (adjusted hazard ratio, 3.06; 95% CI, 1.3

60 .06; 95% CI, 1.32-7.05) or second-generation antipsychotics (adjusted hazard ratio, 3.44; 95% CI, 1.7

61 calculated for users of atypical and typical antipsychotics adjusting for known cataractogenic factor

62 fracture, 1.48; 95% CI, 1.18-1.85; P < .05), antipsychotics (aHR for MOF, 1.43; 95% CI, 1.15-1.77; P

63 ere enrolled: 353 who used second-generation antipsychotics and 134 comparison women.

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

65 1DS thalamocortical projections sensitive to antipsychotics and causes a deficient acoustic startle r

66 s on patients treated with second-generation antipsychotics and first-generation antipsychotics revea

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

68 Antipsychotics and lithium salts were implicated in 11.7

69 tenance therapy, and women who required both antipsychotics and lithium to achieve remission were mai

70 Antipsychotics and mood stabilisers are prescribed widel

71 psychiatric symptom relief, the benefits of antipsychotics and mood stabilisers might also include r

72 We aimed to establish the effect of antipsychotics and mood stabilisers on the rate of viole

73 on of behavior by psychoactive drugs such as antipsychotics and mood stabilizers.

74 including benzodiazepines, antidepressants, antipsychotics and mood-stabilising agents, and various

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

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

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

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

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

80 onships between receptor-binding profiles of antipsychotics and the risk of cerebrovascular events ar

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

82 Furthermore, antipsychotics and tobacco use may increase CB1R availab

83 f the relationship between second-generation antipsychotics and type 2 diabetes (outcome) in Medicaid

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

85 scular disease screening in adults receiving antipsychotics and/or those with serious mental illness.

86 ce interval, 2.17-2.47) for first-generation antipsychotics, and 2.74 (95% confidence interval, 2.49-

87 ensitivity of thalamocortical projections to antipsychotics, and an abnormal acoustic-startle respons

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

89 r use of mood stabilizers, by 60% for use of antipsychotics, and by 13% for use of benzodiazepines.

90 use of mood stabilizers, by 171% for use of antipsychotics, and by 31% for use of benzodiazepines.

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

92 (1.63%) to 862 (2.02%) of 42 600 patients on antipsychotics, and in 343 (1.37%) to 419 (1.67%) of 25

93 the sequential addition of benzodiazepines, antipsychotics, and lithium may result in high rates of

94 S: Central neuromodulators (antidepressants, antipsychotics, and other central nervous system-targete

95 e (n=12) who had not responded to first-line antipsychotics, and patients who had responded to first-

96 nosis, prescriptions for antidepressants and antipsychotics, and reports of heavy alcohol use.

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

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

99 ncluded antipsychotics for schizophrenia and antipsychotics, anticonvulsants, and lithium for bipolar

100 ions included were antidepressants, atypical antipsychotics, anticonvulsants, lithium, and other medi

101 mulative low, moderate, and high exposure to antipsychotics, antidepressants, and benzodiazepines fro

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

103 ed prescription of psychotropic medications (antipsychotics, antidepressants, psychostimulants, drugs

104 chosis, 80% develop dementia, and the use of antipsychotics (APs) in the population with PD is common

105 Although the mechanisms of action of antipsychotics (APs) on neuronal function are well under

106 Antipsychotics are commonly used; however, the associate

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

108 Although antipsychotics are effective in treating mania, few anti

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

110 Pharmacological treatment options, including antipsychotics are not satisfactory.

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

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

113 zophrenia, or some other condition for which antipsychotics are the only generally recognized therapy

114 cuits and mechanisms of their sensitivity to antipsychotics are unknown.

115 Antipsychotics are used to prevent delirium, but their b

116 Long-acting injectable antipsychotics are used to reduce medication nonadherenc

117 Second-generation antipsychotics are used to treat a spectrum of psychiatr

118 Second-generation antipsychotics are utilized extensively in the treatment

119 (AMP), and those that alleviate it, such as antipsychotics, are suggested to exert behavioral effect

120 Further analysis pointed to antipsychotics as having independent enrichment after re

121 imately twice as many patients improved with antipsychotics as with placebo, but only a minority expe

122 8.8% received prescriptions for recommended antipsychotics at higher than recommended dosages; 32.1%

123 total of 241 patients (25%) were exposed to antipsychotics at some time during follow-up (convention

124 Antipsychotics blocked synaptic vesicle release during e

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

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

127 viewed the available evidence and found that antipsychotics can be reduced or discontinued in a subst

128 Typical antipsychotics can cause disabling side effects.

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

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

131 deacetylase (HDAC) inhibitors, but not other antipsychotics, chemical chaperones, or VPA structural a

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

133 s indicated no difference in GABA+ levels on antipsychotics compared with off antipsychotics.

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

135 ng memory processing, and poorer response to antipsychotics compared with the C allele.

136 um-plus-OPT group received second-generation antipsychotics compared with the OPT-only group (48.3% a

137 The package inserts of all approved antipsychotics contain precautions regarding their admin

138 in the identification of safe and effective antipsychotics devoid of extrapyramidal symptoms liabili

139 Treatment with antipsychotics did not exceed 6 months at study entry.

140 Antipsychotics differed substantially in side effects.

141 s among infants exposed to second-generation antipsychotics during pregnancy relative to a comparison

142 fit treatment decisions about using atypical antipsychotics during pregnancy.

143 Some second-generation antipsychotics (eg, clozapine, olanzapine, quetiapine, a

144 , lamotrigine, carbamazepine, oxcarbazepine, antipsychotics, electroconvulsive therapy and various li

145 aluable lead for the development of atypical antipsychotics endowed with a unique pharmacological pro

146 , males were more likely than females to use antipsychotics, especially during childhood and adolesce

147 The adjusted odds ratio of stroke risk with antipsychotics exposure was 1.60 (95% confidence interva

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

149 f adverse event profiles when choosing among antipsychotics for children and adolescents who often re

150 The increased prescribing of antipsychotics for children and youth has heightened con

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

152 Psychotropic treatments included antipsychotics for schizophrenia and antipsychotics, ant

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

154 attention-deficit/hyperactivity disorder, or antipsychotics for schizophrenia.

155 of pharmacological agents in some patients: antipsychotics for severe psychosis or agitation; benzod

156 ials.gov for randomised controlled trials of antipsychotics for the acute treatment of first-episode

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

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

159 All current antipsychotics function primarily by blocking D2-type do

160 Children and youth prescribed antipsychotics had an increased risk of type 2 diabetes

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

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

163 able versions of second-generation and older antipsychotics has not been assessed.

164 What is less clear is why antipsychotics have a therapeutic latency of weeks.

165 f randomized clinical trials (RCTs) of other antipsychotics have been published.

166 Typical and atypical antipsychotics have been shown to alleviate N-methyl-D-a

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

168 s metabolite paliperidone and other atypical antipsychotics have similar potencies for the two isofor

169 Pharmacogenomic studies of antipsychotics have typically examined effects of indivi

170 lent crime fell by 45% in patients receiving antipsychotics (hazard ratio [HR] 0.55, 95% CI 0.47-0.64

171 higher mortality during treatment with other antipsychotics (hazard ratio: 1.45, 95% CI: 0.86-2.45).

172 was increased for use restricted to atypical antipsychotics (HR = 2.89 [95% CI = 1.64-5.10]) or to ri

173 Stable dosages of antidepressants, antipsychotics, hypnotics, and antidementia medications

174 schizophrenia show an inadequate response to antipsychotics-ie, treatment resistance.

175 y modest benefit to suboptimal responders to antipsychotics, if any.

176 sociated with haloperidol, second-generation antipsychotics, iliac fascia block, gabapentin, melatoni

177 The percentages of young people using antipsychotics in 2006 and 2010, respectively, were 0.14

178 ately 29.3% of younger children treated with antipsychotics in 2010 received 1 or more antipsychotic

179 Among young people treated with antipsychotics in 2010, receiving a prescription from a

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

181 lled or usual care (UC) controlled trials of antipsychotics in adult patients with delirium.

182 en used to treat delirium, the evidence that antipsychotics in cardiac surgery patients reduce durati

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

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

185 pical (haloperidol) and atypical (clozapine) antipsychotics in MET mice mimicked effects in human sch

186 pecific recommendations regarding the use of antipsychotics in patients with breast cancer.

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

188 response to treatment with second-generation antipsychotics in patients with schizophrenia.

189 al physiology and response to treatment with antipsychotics in schizophrenia.

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

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

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

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

194 Recent data suggest that treatment with antipsychotics is associated with reductions in cortical

195 The cataleptic effect of antipsychotics is triggered by blockade of D2R on cholin

196 lterations occur in treatment with different antipsychotics is unclear.

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

198 Sedatives and anxiolytics, antidepressants, antipsychotics, lithium salts, and stimulants were impli

199 Antidepressants, antipsychotics, lithium salts, sedatives and anxiolytics

200 equential administration of benzodiazepines, antipsychotics, lithium, and ECT.

201 The use of antipsychotics may be associated with a subtle loss of w

202 We review evidence suggesting that antipsychotics may counter both the increased propensity

203 g and rule updating, and that treatment with antipsychotics may have the potential to counteract this

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

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

206 e care needs, and raise the possibility that antipsychotics may restore white matter integrity as par

207 ons between NF-L and treatment with atypical antipsychotics, MBP and lamotrigine, and H-FABP and lith

208 -episode schizophrenia who received atypical antipsychotics (medicated patient group) (n = 23) and th

209 and patients who had responded to first-line antipsychotics (n=12) were recruited.

210 as by the M1R/M4R agonist xanomeline, or the antipsychotics olanzapine (M1R antagonist) and haloperid

211 As a group, the atypical antipsychotics (olanzapine, quetiapine, and risperidone)

212 The absolute effect of antipsychotics on mortality in elderly patients with dem

213 ss of intervention strategies, the effect of antipsychotics on patient-centered outcomes, and the inf

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

215 to the growing literature on the effects of antipsychotics on the brain and suggests caution in inte

216 ) pathway as being involved in the effect of antipsychotics on the insulin promoter, finding that ant

217 nvestigated the effects of second-generation antipsychotics on white matter integrity using tract-bas

218 rotonin reuptake inhibitors, with or without antipsychotics, on the outcomes of interest.

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

220 ntial target for the development of putative antipsychotics or adjunct treatments that oppose metabol

221 There was no such association with antipsychotics or antidepressants.

222 cases, practice guidelines recommend adding antipsychotics or cognitive-behavioral therapy consistin

223 006-09, 40,937 men in Sweden were prescribed antipsychotics or mood stabilisers, of whom 2657 (6.5%)

224 to study 82,647 patients who were prescribed antipsychotics or mood stabilisers, their psychiatric di

225 ample sizes, and psychotic patients being on antipsychotics or not being in the first episode of thei

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

227 end < .001), whereas use of anticonvulsants, antipsychotics, or antidepressants was not.

228 is (schizophrenia only studies), concomitant antipsychotics, or pathway of drugs to enhance the gluta

229 tion, relatively few RCTs were available for antipsychotics other than clozapine, haloperidol, olanza

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

231 use they had been exposed to higher doses of antipsychotics (P<0.001).

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

233 depressants (PR = 1.13; 95% CI = 1.07-1.19), antipsychotics (PR = 1.39; 95% CI = 1.21-1.60), and pote

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

235 Many antipsychotics promote weight gain, which can lead to no

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

237 ng periods when individiduals were dispensed antipsychotics, psychostimulants, and drugs for addictiv

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

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

240 he results suggest a harmful effect of other antipsychotics regarding self-harm compared with clozapi

241 The rate of violence reduction for antipsychotics remained between 22% and 29% in sensitivi

242 omere length and mitochondrial function with antipsychotics response in schizophrenia (SCZ).

243 neration antipsychotics and first-generation antipsychotics revealed a different and contrasting mode

244 Second-generation antipsychotics (SGAs) have increasingly been prescribed

245 Pooled second-generation antipsychotics (SGAs) were associated with shorter TTR (

246 s with improved therapeutic profile.Atypical antipsychotics show reduced extrapyramidal side effects

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

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

249 ion has been described in schizophrenia, and antipsychotics such as clozapine and olanzapine have bee

250 Atypical antipsychotics such as olanzapine often induce excessive

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

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

253 tients with psychiatric disorders and use of antipsychotics suggests that imbalance of dopamine signa

254 ate of self-harm was higher for nonclozapine antipsychotics than for clozapine (hazard ratio: 1.36, 9

255 stimulants that exacerbate the disorder, and antipsychotics that ameliorate the disorder.

256 ntal disorders in 2009 who were treated with antipsychotics, the most common diagnoses were attention

257 tum is the primary target of all efficacious antipsychotics, the relationship between its functional

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

259 irst-trimester exposure to second-generation antipsychotics, three major malformations were confirmed

260 A study of the selected binding of antipsychotics to 14 neurotransmitter receptors revealed

261 diagnosed with Schizophrenia taking Atypical Antipsychotics to Depressive patients medicated with Sel

262 erived from putative and clinically relevant antipsychotics to develop designed multiple ligands.

263 The use of antipsychotics to manage challenging behaviour in adults

264 t it would be unlikely for second-generation antipsychotics to raise the risk of major malformations

265 The effectiveness of prophylactic antipsychotics to reduce the risk of delirium is controv

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

267 The clinical implication is to start antipsychotics treatment at low dosages and to closely m

268 e generalisability of these results to other antipsychotics, trial designs, and medical conditions re

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

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

271 nt group) (n = 23) and those who received no antipsychotics (unmedicated patient group) (n = 22) and

272 There is a perception that antipsychotics used in this context can be reduced or di

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

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

275 hazard ratio (HR) associated with dispensed antipsychotics was 0.58 (95% CI, 0.39-0.88), based on 10

276 ted rate ratio for current users of atypical antipsychotics was 0.84 (95% confidence interval, 0.80 t

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

278 Although short-term treatment with antipsychotics was associated with prefrontal cortical t

279 The National Pregnancy Registry for Atypical Antipsychotics was established to determine the risk of

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

281 Antipsychotics were increasingly more commonly prescribe

282 than 0.6 mEq/l, and use of first-generation antipsychotics were independently associated with risk.

283 However, antipsychotics were nearly as efficacious as antiparkins

284 Compared with risperidone, newer antipsychotics were not associated with decreased risk.

285 onditions, or receiving mood stabilizers and antipsychotics were not included.

286 ith schizophrenia on chronic stable atypical antipsychotics were randomized to encenicline 0.27 or 0.

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

288 Several second-generation antipsychotics were superior to haloperidol in terms of

289 When pooled as a group, antipsychotics were superior to placebo/UC in terms of r

290 Information is limited about the effects of antipsychotics when used as mood stabilizer treatment.

291 ternatives, with judicious short-term use of antipsychotics, when appropriate.

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

293 pression data from human brains treated with antipsychotics, which showed altered expression of SMAD3

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

295 The use of antipsychotics with a high binding affinity of M1 muscar

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

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

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

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

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

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