ライフサイエンスコーパス: antipsychotics

1 sives, or central nervous system agents (eg, antipsychotics).

2 patients treated only with second-generation antipsychotics.

3 ing memory and also modulate the response to antipsychotics.

4 ereotypical behaviors, which are relieved by antipsychotics.

5 he same subjects and from monkeys exposed to antipsychotics.

6 leads to a novel approach to potent atypical antipsychotics.

7 e of the escalating prescription of atypical antipsychotics.

8 ent is an important moderator of response to antipsychotics.

9 regardless of whether they were also taking antipsychotics.

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

11 y of auditory thalamocortical projections to antipsychotics.

12 months) and treatment with second-generation antipsychotics.

13 ncertainty about the longer term benefits of antipsychotics.

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

15 n and death after adjustment for exposure to antipsychotics.

16 is patients was normalized by treatment with antipsychotics.

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

18 to structurally diverse typical and atypical antipsychotics.

19 group had less exposure to second-generation antipsychotics.

20 d known neurotransmitter receptor targets of antipsychotics.

21 onse, even when compared with other atypical antipsychotics.

22 ndividuals taking conventional than atypical antipsychotics.

23 patients who respond poorly to dopaminergic antipsychotics.

24 atic response to treatment with dopaminergic antipsychotics.

25 heory to phase III trials of novel mechanism antipsychotics.

26 erative pain, and, perhaps, judicious use of antipsychotics.

27 ious when given in combination with atypical antipsychotics.

28 (independently: n = 1), and 3/4 studies with antipsychotics.

29 Participants received usual care with antipsychotics.

30 with predictive validity for the effects of antipsychotics.

31 dementia were using atypical or conventional antipsychotics.

32 ations and these deficits can be reversed by antipsychotics.

33 ychosis show a better subsequent response to antipsychotics.

34 or antagonists, such as typical and atypical antipsychotics.

35 both first-generation and second-generation antipsychotics.

36 n Registry provided data on prescriptions of antipsychotics.

37 sorder, and 85.5% were receiving concomitant antipsychotics.

38 little difference between second-generation antipsychotics.

39 fects in schizophrenia patients treated with antipsychotics.

40 zapine compared with other second-generation antipsychotics.

41 er there are significant differences between antipsychotics.

42 atients unlikely to respond to non-clozapine antipsychotics.

43 ced by dopamine receptor blockers, including antipsychotics.

44 the motor-reducing and cataleptic effects of antipsychotics.

45 ide-effect profile compared with established antipsychotics.

46 + levels on antipsychotics compared with off antipsychotics.

47 led positive symptoms despite treatment with antipsychotics.

48 that is the current target of most effective antipsychotics.

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

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

51 lt outpatients with schizophrenia taking two antipsychotics (127 participants across 19 sites) were r

52 (95% confidence interval, 2.37-2.68) for any antipsychotics, 2.32 (95% confidence interval, 2.17-2.47

53 106 genes, p=0.00046, pcorrected =0.024) and antipsychotics (347 genes, p=0.00078, pcorrected=0.046).

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

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

56 speridone than among those who received oral antipsychotics (39% after 10.8 months vs. 45% after 11.3

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

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

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

60 Unlike reference antipsychotics, 72 displayed marked antipsychotic and an

61 %), the bulk of which was due to spending on antipsychotics (949% increase).

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

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

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

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

66 .06; 95% CI, 1.32-7.05) or second-generation antipsychotics (adjusted hazard ratio, 3.44; 95% CI, 1.7

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

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

69 Chronic use of atypical antipsychotics also was associated with decreased UBF.

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

71 ent therapeutic drugs such as beta-blockers, antipsychotics and analgesics.

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

73 BN rat may be useful for detecting atypical antipsychotics and antipsychotics with novel mechanisms

74 1DS thalamocortical projections sensitive to antipsychotics and causes a deficient acoustic startle r

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

76 Antipsychotics and lithium salts were implicated in 11.7

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

78 Antipsychotics and mood stabilisers are prescribed widel

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

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

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

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

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

84 tive association between the use of atypical antipsychotics and risk of clinically significant catara

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

86 Furthermore, antipsychotics and tobacco use may increase CB1R availab

87 s, anxiolytics, hypnotics, mood stabilizers, antipsychotics and treatments for opioid dependence are

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

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

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

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

92 ns induced at the mGlu2 promoter by atypical antipsychotics, and augmented their therapeutic-like eff

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

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

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

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

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

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

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

100 ents with schizophrenia who had responded to antipsychotics, and twelve healthy volunteers matched fo

101 We have previously shown that atypical antipsychotics antagonize DA D2 receptor (D2R)/beta-arre

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

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

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

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

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

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

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

109 treating an array of neurological disorders, antipsychotics are associated with deleterious metabolic

110 ral responses to hallucinogens and glutamate antipsychotics are both affected by maternal exposure to

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

112 Pharmacological treatment options, including antipsychotics are not satisfactory.

113 Because antipsychotics are prescribed for long periods for schiz

114 Antipsychotics are the most commonly prescribed group of

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

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

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

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

119 Second-generation antipsychotics are utilized extensively in the treatment

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

121 pproval Packages for eight second-generation antipsychotics-aripiprazole, iloperidone, olanzapine, pa

122 Use of atypical antipsychotics as a group increased during the no-warnin

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

124 ning, we previously identified phenothiazine antipsychotics as modulators of the human insulin promot

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

126 8.8% received prescriptions for recommended antipsychotics at higher than recommended dosages; 32.1%

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

128 es (benzodiazepines, ethanol, clomethiazole, antipsychotics, barbiturates, propofol, and dexmedetomid

129 Use of atypical antipsychotics began to decline significantly in 2003, a

130 Despite the expanding clinical utility of antipsychotics beyond psychotic disorders to include dep

131 reatment efficacy are strongest for atypical antipsychotics, but these agents must be used with great

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

133 Typical antipsychotics can cause disabling side effects.

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

135 Antipsychotics, cholinesterase inhibitors, and alpha-2 a

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

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

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

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

140 This work raises the possibility that antipsychotics could be designed that retain beneficial

141 Moreover, DRD2 is the target of most antipsychotics currently in use.

142 y-warning period, but rates of use for all 3 antipsychotics declined during the black box warning per

143 iously for antidepressants, possibly because antipsychotics demonstrate superiority to placebo more c

144 ation therapy to the standard treatment with antipsychotics, demonstrated encouraging results on meas

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

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

147 Antipsychotics differed substantially in side effects.

148 Here we found that chronic atypical antipsychotics downregulated the transcription of metabo

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

150 fit treatment decisions about using atypical antipsychotics during pregnancy.

151 Dose reduction/discontinuation of antipsychotics during the early stages of remitted FEP s

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

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

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

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

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

157 ative benefits and harms of first-generation antipsychotics (FGAs) and second-generation antipsychoti

158 antipsychotics (SGAs) with first-generation antipsychotics (FGAs) regarding relapse prevention in sc

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

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

161 ly supportive of short-term, low-dose use of antipsychotics for controlling the symptoms of delirium,

162 Use of atypical antipsychotics for neuropsychiatric symptoms of dementia

163 Psychotropic treatments included antipsychotics for schizophrenia and antipsychotics, ant

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

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

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

167 47.6% if hemoglobin A1c level>/=9%), use of antipsychotics (from 12.7% to 31.8%), alcohol-related di

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

169 cant symptoms should be offered EX/RP before antipsychotics given its superior efficacy and less nega

170 Users of antipsychotics had a 3-fold increased risk for type 2 di

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

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

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

174 from animal studies, our study suggests that antipsychotics have a subtle but measurable influence on

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 mphetamine prodrug, as adjunctive therapy to antipsychotics in adults with clinically stable schizoph

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

192 g Administration warned that use of atypical antipsychotics in dementia was associated with increased

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

194 The common use of antipsychotics in patients with 22q11.2DS to manage asso

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

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

197 ether the TR is associated with adherence to antipsychotics in patients with schizophrenia.

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

199 lar to that obtained in trials of parenteral antipsychotics in similar populations.

200 protein-dependent signaling, whereas typical antipsychotics inhibit both pathways with similar effica

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

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

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

204 Antidepressants, antipsychotics, lithium salts, sedatives and anxiolytics

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

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

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

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

209 he hypothesis that hERG1-mediated effects of antipsychotics may not be limited to their potential car

210 Conventional antipsychotics may pose an even greater safety risk.

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

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

213 Infants prenatally exposed to antipsychotics (mean=64.71) showed significantly lower I

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

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

216 months postpartum with pregnancy exposure to antipsychotics (n=22), antidepressants (n=202), or no ps

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

218 The impact of the atypical antipsychotics olanzapine, quetiapine, and risperidone o

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

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

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

222 The effects of receptor-binding profiles of antipsychotics on stroke risk were estimated, while the

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

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

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

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

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

228 There was no such association with antipsychotics or antidepressants.

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

230 006-09, 40,937 men in Sweden were prescribed antipsychotics or mood stabilisers, of whom 2657 (6.5%)

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

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

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

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

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

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

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

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

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

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) are increasingly used in the treat

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

246 antipsychotics (FGAs) and second-generation antipsychotics (SGAs) in treating schizophrenia.

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

248 controlled trials compared second-generation antipsychotics (SGAs) with first-generation antipsychoti

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

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

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

252 Atypical antipsychotics such as olanzapine often induce excessive

253 n cell lines, we found no TAAR activation by antipsychotics, suggesting that modulation of trace amin

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

255 To date all typical and atypical antipsychotics target the dopamine D(2) receptor.

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

257 function declined more in patients receiving antipsychotics than in those given placebo on multiple c

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

259 Of note, antipsychotics that do not cause metabolic side effects

260 n additional risk of treatment with atypical antipsychotics that should be considered when treating p

261 However, recent animal studies indicate that antipsychotics, the mainstay of treatment for schizophre

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

263 ms responsible for the beneficial effects of antipsychotics, the pathways underlying the most severe

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

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

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

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

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

269 The use of antipsychotics to manage challenging behaviour in adults

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

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

272 The use of antipsychotics to treat the behavioral symptoms of demen

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

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

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

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

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

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

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

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

281 Discontinuing one of two antipsychotics was followed by treatment discontinuation

282 The magnitude of publication bias found for antipsychotics was less than that found previously for a

283 death, but neither conventional nor atypical antipsychotics were associated with time to death.

284 In CATIE-AD, atypical antipsychotics were associated with worsening cognitive

285 n more often and more quickly than when both antipsychotics were continued.

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

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

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

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

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

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

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

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

294 vidence-based pharmacological treatments are antipsychotics which have limited benefits with increase

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

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

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

298 chanism that integrates a better response to antipsychotics with changes in chromatin structure remai

299 ul for detecting atypical antipsychotics and antipsychotics with novel mechanisms of action.

300 There was no widespread substitution of antipsychotics with other psychotropic drugs.