ライフサイエンスコーパス: antipsychotic drug

1 cted probability that they would be users of antipsychotic drugs).

2 D4 receptor (one of the principal targets of antipsychotic drugs).

3 ive to treatment with clozapine, an atypical antipsychotic drug.

4 ntrolled trial in comparison with a standard antipsychotic drug.

5 ession influences the therapeutic effects of antipsychotic drugs.

6 ed as models for the characterization of new antipsychotic drugs.

7 ent in patients undergoing first exposure to antipsychotic drugs.

8 verbal hallucinations that are refractory to antipsychotic drugs.

9 ia, as well as in the mechanism of action of antipsychotic drugs.

10 potential target for the development of new antipsychotic drugs.

11 preclinical animal models used to screen new antipsychotic drugs.

12 mesolimbic selectivity of second-generation antipsychotic drugs.

13 of possible anti-inflammatory roles of some antipsychotic drugs.

14 coupled receptor that is a common target for antipsychotic drugs.

15 in general, will be useful as broad-spectrum antipsychotic drugs.

16 espectively, and 186,600 matched nonusers of antipsychotic drugs.

17 cs and the atypical and glutamate classes of antipsychotic drugs.

18 hibitors, a phospholipase C inhibitor, and 2 antipsychotic drugs.

19 tor 2 (DRD2), the best-established target of antipsychotic drugs.

20 istant to treatment with dopamine antagonist antipsychotic drugs.

21 than did patients assigned to either of the antipsychotic drugs.

22 tual disability and it is often treated with antipsychotic drugs.

23 r country's regulations regarding the use of antipsychotic drugs.

24 prospective treatment with second-generation antipsychotic drugs.

25 and is a potential target of action of some antipsychotic drugs.

26 peutic drugs, including typical and atypical antipsychotic drugs.

27 not smoke and were concurrently treated with antipsychotic drugs.

28 These effects were ameliorated by antipsychotic drugs.

29 ubtype (D2) are important sites of action of antipsychotic drugs.

30 receptors are the best-established target of antipsychotic drugs.

31 tion might reveal chemical targets for novel antipsychotic drugs.

32 evelopment of NT1 receptor agonists as novel antipsychotic drugs.

33 receptor blockade to that of other atypical antipsychotic drugs.

34 isorders, making those receptors targets for antipsychotic drugs.

35 e, is a common consequence of treatment with antipsychotic drugs.

36 gets for LSD-like hallucinogens and atypical antipsychotic drugs.

37 of EEG abnormalities associated with various antipsychotic drugs.

38 of PFC neuronal activity and the actions of antipsychotic drugs.

39 the PFC, is one of the principal targets of antipsychotic drugs.

40 tegy for the development of a novel class of antipsychotic drugs.

41 rapeutic efficacy in comparison with current antipsychotic drugs.

42 ch is likely to affect the mode of action of antipsychotic drugs.

43 potential biomarker of treatment response to antipsychotic drugs.

44 en suggested as a promising target for novel antipsychotic drugs.

45 d in animal models and preclinical trials of antipsychotic drugs.

46 de the discovery of safer and more efficient antipsychotic drugs.

47 , low physical activity, and side-effects of antipsychotic drugs.

48 yle risks and direct and indirect effects of antipsychotic drugs.

49 rtant target for antidepressant and atypical antipsychotic drugs.

50 within 90 days of prescription for atypical antipsychotic drugs.

51 mplicate NRXN1 in the therapeutic actions of antipsychotic drugs.

52 pectrum disorders who had chosen not to take antipsychotic drugs.

53 ectrum disorders who have chosen not to take antipsychotic drugs.

54 phrenia that are often resistant to existing antipsychotic drugs.

55 We followed those who initiated use of antipsychotic drugs (9,777 FGA users and 21,164 SGA user

56 enia patients receiving typical and atypical antipsychotic drugs; a two-alternative, forced-choice ps

57 The atypical antipsychotic drugs (AAPDs) have markedly enhanced the t

58 ophrenia is based on evidence that the major antipsychotic drugs act by blocking dopamine D2 receptor

59 ody of research on dopamine as a mediator of antipsychotic drug action and putative roles for this tr

60 of schizophrenia (SCZ) both as a target for antipsychotic drug action as well as a SCZ-associated ri

61 e-related epigenetic changes that may impact antipsychotic drug action.

62 rats depolarization block requires weeks of antipsychotic drug administration, whereas schizophrenia

63 Atypical and typical antipsychotic drugs alter GSK-3 activity, as do drugs th

64 reductions, 32 strategies that augmented any antipsychotic drug and 5 strategies that augmented cloza

65 es often involves treatment with the typical antipsychotic drug and dopamine D2 receptor antagonist h

66 ompared separately for combinations with any antipsychotic drug and for combinations with clozapine.

67 The first randomized trials of antipsychotic drug and psychological interventions aimed

68 aid program with 28 858 recent initiators of antipsychotic drugs and 14 429 matched controls.

69 he relative effects of the second-generation antipsychotic drugs and an older representative agent on

70 for understanding the mechanism of action of antipsychotic drugs and drugs of abuse and may have pote

71 ently used to study both the pharmacology of antipsychotic drugs and drugs of abuse.

72 er medications, they do suggest that typical antipsychotic drugs and lithium have contrasting effects

73 e effect of the second-generation (atypical) antipsychotic drugs and older agents on neurocognition h

74 urotensin in both the mechanism of action of antipsychotic drugs and the pathophysiology of schizophr

75 the pharmacology of a new class of glutamate antipsychotic drugs and their crosstalk mechanism throug

76 ments may show cognitive benefits from newer antipsychotic drugs, and there may be differences betwee

77 ons in patients who fail to respond to other antipsychotic drugs, and to reduce the risk of suicide.

78 in the neocortex, but only in cases without antipsychotic drug (APD) treatment; Kv3.1 levels are nor

79 Defining the mechanisms of action of the antipsychotic drug (APD), clozapine, is of great importa

80 d., Tokyo, Japan), a newly approved atypical antipsychotic drug (APD), on NMDAR synaptic function in

81 Increasing evidence suggests that antipsychotic drugs (APD) might affect brain structure d

82 Antipsychotic drugs (APD)s and anticonvulsant mood-stabi

83 Antipsychotic drugs (APDs) are best classified as typica

84 Mood stabilizers (e.g., valproic acid) and antipsychotic drugs (APDs) are commonly co-administered

85 Atypical antipsychotic drugs (APDs) have been hypothesized to sho

86 The main class of atypical antipsychotic drugs (APDs) in current use includes the p

87 Current antipsychotic drugs (APDs) show efficacy with positive s

88 Atypical antipsychotic drugs (APDs) such as clozapine, but not th

89 All FDA-approved antipsychotic drugs (APDs) target primarily dopamine D2

90 red imaging in cultured hippocampal neurons, antipsychotic drugs (APDs) were proposed to accumulate i

91 ted to contribute to the ability of atypical antipsychotic drugs (APDs), e.g. clozapine, risperidone,

92 alproic acid and carbamazepine, and atypical antipsychotic drugs (APDs), e.g., clozapine, quetiapine,

93 Acute treatment with atypical antipsychotic drugs (APDs), which are serotonin (5-HT)(2

94 igm shift due to development of new atypical antipsychotic drugs (APDs), with better tolerability due

95 Weight gain is one side effect of many antipsychotic drugs (APDs).

96 ) NC and SZ treated with typical or atypical antipsychotic drugs (APDs).

97 All antipsychotic drugs are D2 antagonists, but D2 antagonis

98 First-generation antipsychotic drugs are effective and cost effective for

99 Antipsychotic drugs are effective in the acute treatment

100 Although there are indications that antipsychotic drugs are increasingly used to treat child

101 However, antipsychotic drugs are not clinically effective at reve

102 ins a challenge, and the currently available antipsychotic drugs are slow acting and produce a number

103 te transporters moderate CNS availability of antipsychotic drugs are summarised.

104 Because antipsychotic drugs are used as mood stabilizers our stu

105 Antipsychotic drugs are used to treat dementia-related s

106 Antipsychotic drugs are usually the first line of treatm

107 Antipsychotic drugs are widely prescribed to elderly pat

108 Typical antipsychotic drugs are widely thought to alleviate the

109 Second-generation (atypical) antipsychotic drugs are widely used to treat psychosis,

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

111 ffectiveness of second-generation (atypical) antipsychotic drugs as compared with that of older agent

112 e incidence-rate ratio for users of atypical antipsychotic drugs as compared with users of typical an

113 the data support the notion that many of the antipsychotic drugs associated with the development of m

114 ng the actions of hallucinogens and atypical antipsychotic drugs at 5-HT(2A) and 5-HT(2C) serotonergi

115 s with schizophrenia who were medicated with antipsychotic drugs at their time of death display incre

116 ated with 5-HT2A receptors to which atypical antipsychotic drugs bind with high affinity, little is k

117 ain changes are not explained by exposure to antipsychotic drugs but likely play a role in psychosis

118 Atypical antipsychotic drugs, by definition, differ from typical

119 This demonstrates that antipsychotic drugs can attenuate AMP disruption of lear

120 We demonstrate that, like in mammals, antipsychotic drugs can suppress disruptions in zebrafis

121 ipling of the odds of subsequent need of the antipsychotic drug (chi-square = 108, df = 1, p =.0001,

122 , risperidone and not the prototype atypical antipsychotic drug clozapine increased the frequency of

123 Treatment with the antipsychotic drug clozapine reverses the behavioral and

124 As demonstrated with the antipsychotic drug clozapine, the DTome tool was effecti

125 tagonist ketanserin, and inverse agonist and antipsychotic drug clozapine.

126 tices, resembling the action of the atypical antipsychotic drug clozapine.

127 ed clinical trials comparing the efficacy of antipsychotic drugs combined with other antipsychotic or

128 At present, treatment mainly consists of antipsychotic drugs combined with psychological therapie

129 ty disorder drugs, antidepressant drugs, and antipsychotic drugs) comparing the 10- to 36-month perio

130 further highlight p110delta as a target for antipsychotic drug development.

131 erable attention regarding schizophrenia and antipsychotic drug development.

132 Typical antipsychotic drugs do not improve this deficit while so

133 Because current antipsychotic drugs do not provide optimal therapy, we h

134 Subjects continued their current antipsychotic drug during the trial and were nonsmokers.

135 all McLean Hospital inpatients treated with antipsychotic drugs during 3 months in 1998 (N=349) and

136 Antipsychotic drug effects were explored in mice treated

137 opamine, long implicated in psychosis and in antipsychotic drug effects, is crucial in optimizing sig

138 Several lines of evidence suggest that antipsychotic drug efficacy is mediated by dopamine type

139 Antipsychotic drug efficacy may have decreased over rece

140 cs has been most commonly used in studies of antipsychotic drug efficacy, antidepressant drug respons

141 sual contrast detection, those given typical antipsychotic drugs exhibited higher visual contrast det

142 Here we demonstrate that chronic antipsychotic drug exposure increases nuclear translocat

143 Antipsychotic drug exposure was defined as the receipt o

144 ry management of schizophrenia regardless of antipsychotic drug exposure.

145 associated with the use of first-generation antipsychotic drugs (FGAs) compared with second-generati

146 ture model of tau aggregation and that other antipsychotic drugs (flupenthixol, perphenazine, and zot

147 Repeated administration of either antipsychotic drug for 1, 3, 7, 15, and 21 d continued t

148 There is support for the use of antipsychotic drugs for all types of psychosis in the el

149 l consideration is required when prescribing antipsychotic drugs for patients with an existing diagno

150 ectrum disorders, who had chosen not to take antipsychotic drugs for psychosis, were randomly assigne

151 asingly important role in the development of antipsychotic drugs for schizophrenia and related condit

152 A side-effect of treatment with antipsychotic drugs for schizophrenia is increased body

153 ffset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggr

154 get with comparable efficacy as conventional antipsychotic drugs for treating positive and negative s

155 cytosis does not exceed that of conventional antipsychotic drugs, for which no such requirement exist

156 antimetastatic potential of penfluridol, an antipsychotic drug frequently prescribed for schizophren

157 %), antidepressants (from 1.5% to 2.6%), and antipsychotic drugs (from 0.2% to 1.2%).

158 Current users of typical and of atypical antipsychotic drugs had a similar, dose-related increase

159 Current users of typical and of atypical antipsychotic drugs had higher rates of sudden cardiac d

160 Former users of antipsychotic drugs had no significantly increased risk

161 We report that in vivo treatment with the antipsychotic drug haloperidol acts with a delay of days

162 The antipsychotic drug haloperidol is an antagonist of Sigma

163 icantly potentiated the ability of a typical antipsychotic drug haloperidol, a D2 receptor antagonist

164 We previously reported that the antipsychotic drug haloperidol, a multifunctional D2-lik

165 strongly reduced cataleptic response to the antipsychotic drug haloperidol.

166 Furthermore, pretreatment with the antipsychotic drugs haloperidol and clozapine prevented

167 Antipsychotic drugs haloperidol and clozapine, which tar

168 D2LR signaling mediated effects of a typical antipsychotic drug, haloperidol, in inducing catalepsy b

169 ta(9)-tetrahydrocannabinol, and opiates; the antipsychotic drug, haloperidol; juvenile enrichment; su

170 Users of typical antipsychotic drugs have an increased risk of serious ve

171 related to Alzheimer's disease indicate that antipsychotic drugs have equivocal efficacy in improving

172 Newer antipsychotic drugs have shown promise in ameliorating n

173 ting the effects of both psychostimulant and antipsychotic drugs; however, these drugs are known to h

174 These patients had decreased use of antipsychotic drugs immediately after the transition; th

175 psychostimulants or have potential use as an antipsychotic drug in humans.

176 of neurotensin(8-13), acts like an atypical antipsychotic drug in several dopamine-based animal mode

177 sudden cardiac death among current users of antipsychotic drugs in a retrospective cohort study of M

178 y of pharmacologic combination strategies of antipsychotic drugs in adults with schizophrenia.

179 thought to be the primary mode of action of antipsychotic drugs in alleviating psychotic symptoms.

180 tor antagonism is a unifying property of all antipsychotic drugs in clinical use.

181 with canonical first- and second-generation antipsychotic drugs in mice.

182 We assessed the effectiveness of atypical antipsychotic drugs in outpatients with Alzheimer's dise

183 xicity of both the conventional and atypical antipsychotic drugs in relation to their effects on gluc

184 tive against extrapyramidal motor effects of antipsychotic drugs in the adult life.

185 ety and efficacy of antidepressants added to antipsychotic drugs in the treatment of schizophrenia.

186 nd there may be differences between atypical antipsychotic drugs in their patterns of cognitive effec

187 es were noted for several phenothiazine-like antipsychotic drugs, including trifluoperazine.

188 Because atypical antipsychotic drugs increase dopamine (DA) and acetylcho

189 Acute injection of either antipsychotic drug induced an immediate reduction in the

190 independent cohorts of subjects assessed for antipsychotic drug-induced weight gain.

191 ied a genetic factor that is associated with antipsychotic drug-induced weight gain.

192 Most antipsychotic drugs influence dopaminergic transmission

193 n this issue of Neuron reveal that weak base antipsychotic drugs inhibit presynaptic function in an a

194 The use of classic antipsychotic drugs is limited by the occurrence of extr

195 hophysiology of schizophrenia or exposure to antipsychotic drugs is unknown.

196 an inadequate response to treatment with an antipsychotic drug, it is unclear what other antipsychot

197 operties and showed that it was inhibited by antipsychotic drugs, leading to a large body of research

198 and UNC9994 (36), which have robust in vivo antipsychotic drug-like activities.

199 The present data are consistent with an antipsychotic drug-like profile of activity for VU015210

200 ty model, compound (+)-19 showed significant antipsychotic-drug-like activity.

201 phase schizophrenia and minimal exposure to antipsychotic drugs (<2 years), who underwent resting st

202 Recent evidence suggests that some atypical antipsychotic drugs may protect against oxidative stress

203 The differential response to first-line antipsychotic drugs may reflect a different underlying n

204 s underlying the response to psychedelic and antipsychotic drugs might lead to unification of the ser

205 pisode of psychosis (including N=17 who were antipsychotic drug-naive at the time of scanning) and 41

206 SIGN, SETTING, AND PARTICIPANTS: Twenty-five antipsychotic drug-naive, acutely ill patients with firs

207 ral chronic stimuli, such as drugs of abuse, antipsychotic drugs, natural rewards, and stress.

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

209 is a putative therapeutic target of atypical antipsychotic drugs, notably clozapine, as well as some

210 addressed by antidepressant, anxiolytic, and antipsychotic drugs, often administered off-label.

211 conducted to examine the potential effect of antipsychotic drugs on expression of the three proteins.

212 nvestigated the effects of dopamine-blocking antipsychotic drugs on visual contrast detection in schi

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

214 zers our studies focused on a newly-marketed antipsychotic drug, paliperidone.

215 els play a role in the therapeutic action of antipsychotic drugs, particularly risperidone, and furth

216 We identified the antipsychotic drug perphenazine in both screens due to i

217 There was a large reduction in antipsychotic drug prescription in dementia from 22.1% (

218 Current antipsychotic drugs produce fairly robust clinical benef

219 One-quarter of patients with stable antipsychotic drug regimens had their medication changed

220 Antipsychotic drugs remain the standard for schizophreni

221 Similar to 1 and other second-generation antipsychotic drugs, repeated treatment with 2 significa

222 Antipsychotic drugs require days of treatment to begin t

223 morphisms in NRXN1 have been associated with antipsychotic drug response in patients with schizophren

224 ier was significantly associated with poorer antipsychotic drug response relative to the Ins/Ins geno

225 relationship between DRD2 polymorphisms and antipsychotic drug response.

226 ntly potentiated the effects of the atypical antipsychotic drug risperidone (0.1 mg/kg) on DA, but no

227 ment) and after 1 week of treatment with the antipsychotic drug risperidone (1-week post-treatment).

228 The atypical antipsychotic drug risperidone, a multireceptor antagoni

229 of haloperidol (a typical, first-generation antipsychotic drug), risperidone (an atypical, second-ge

230 a long-term comparison of a newer, atypical antipsychotic drug, risperidone, and an older, conventio

231 electrochemical ligand-binding approach for antipsychotic drug screening where competitive binding o

232 results show increasing enrichment for known antipsychotic drugs, selective calcium channel blockers,

233 drugs (FGAs) compared with second-generation antipsychotic drugs (SGAs).

234 Antipsychotic drugs should no longer be regarded as an a

235 Patients receiving atypical antipsychotic drugs showed unimpaired visual contrast de

236 eral adverse outcomes attributed to atypical antipsychotic drugs, specifically quetiapine, risperidon

237 visits, patients' vital status, and current antipsychotic drug status was collected and reported by

238 Other antipsychotic drugs stimulated phosphorylation of a subs

239 Data from antipsychotic drug studies indicate that polymorphisms w

240 peated exposure to several stimuli including antipsychotic drugs such as haloperidol.

241 Atypical antipsychotic drugs, such as clozapine and risperidone,

242 (5-HT2AR) is a prominent target for atypical antipsychotic drugs, such as clozapine.

243 The closely related non-antipsychotic drugs, such as ritanserin and methysergide

244 Several antipsychotic drugs, such as sertraline, trifluoperazine

245 Furthermore, newer antipsychotic drugs target 5-HT2AR.

246 Antipsychotic drugs target dopamine and serotonin recept

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

248 Whereas haloperidol, a typical antipsychotic drug that is primarily a dopamine receptor

249 lled by glucose starvation and by classes of antipsychotic drugs that inhibit glucose uptake.

250 relevant randomised controlled trials of 12 antipsychotic drugs that involved 2669 participants.

251 Among users of typical antipsychotic drugs, the incidence-rate ratios increased

252 e in the actions of the second generation of antipsychotic drugs, the so-called atypical antipsychoti

253 hotic episode who had no previous history of antipsychotic drug therapy began a regimen of olanzapine

254 We identified the FDA-approved antipsychotic drug thioridazine as an EAG2 channel block

255 nd- (sertindole; 2.5 mg/kg, i.p.) generation antipsychotic drug to rapidly induce depolarization bloc

256 Repeated administration of antipsychotic drugs to normal rats has been shown to ind

257 t essential either for AMP to disrupt or for antipsychotic drugs to reverse AMP disruption of learnin

258 uthors recently demonstrated that successful antipsychotic drug treatment alters resting-state functi

259 functional connectivity predict response to antipsychotic drug treatment in acutely psychotic patien

260 Atypical antipsychotic drug treatment is clinically effective wit

261 Clinical response to antipsychotic drug treatment is highly variable, yet pro

262 Thus, antipsychotic drug treatment may account for the inconsi

263 olled trials are needed to determine whether antipsychotic drug treatment of prodromal patients can d

264 y in the course of illness and the impact of antipsychotic drug treatment on these deficits are not w

265 phrenia prompted the testing of combining an antipsychotic drug treatment with a second psychotropic

266 Antipsychotic drug treatment, including the atypical clo

267 elated with the clinical efficacy of chronic antipsychotic drug treatment.

268 xhibit initial effects soon after initiating antipsychotic drug treatment.

269 gene is associated with clinical response to antipsychotic drug treatment.

270 tion is associated with clinical response to antipsychotic drug treatment.

271 ponse in negative and depressive symptoms to antipsychotic drug treatment.

272 polymorphism influences symptom response to antipsychotic drug treatment.

273 nitial years after diagnosis despite ongoing antipsychotic drug treatment.

274 function but not with duration of illness or antipsychotic drug treatment.

275 This alteration was absent after antipsychotic drug treatment.

276 Although the currently approved antipsychotic drug treatments, which primarily modulate

277 nited States and Germany and from a European antipsychotic drug trial.

278 ectrometry/mass spectrometry showed that the antipsychotic drug trifluoperazine penetrates well into

279 we repurposed an existing phenothiazine-like antipsychotic drug, trifluoperazine, as a potential anti

280 rect effect was equal to the total effect of antipsychotic drug type (FGA vs. SGA) on mortality risk

281 Atypical antipsychotic drug use is associated with an increased r

282 Atypical antipsychotic drug use versus nonuse was associated with

283 uding two process measures (catheter use and antipsychotic drug use) and three outcome measures (pres

284 the interaction of chlorpromazine (CPZ), an antipsychotic drug used in the treatment of schizophreni

285 otic drugs as compared with users of typical antipsychotic drugs was 1.14 (95% CI, 0.93 to 1.39).

286 Chronic exposure to antipsychotic drugs was not associated with changes in b

287 elated to factors associated with the use of antipsychotic drugs, we performed a secondary analysis o

288 Some atypical antipsychotic drugs were identified by their high affini

289 Some antipsychotic drugs were identified by their high affini

290 Until recently, all known antipsychotic drugs were thought to block the dopamine D

291 enazine, and periciazine, used clinically as antipsychotic drugs, were identified as weak AR antagoni

292 regarding the cardiac safety of the atypical antipsychotic drugs, which have largely replaced the old

293 e performed a secondary analysis of users of antipsychotic drugs who had no baseline diagnosis of sch

294 of UNC9975 and transformed it into a typical antipsychotic drug with a high propensity to induce cata

295 Amisulpride is an atypical antipsychotic drug with selective affinity for D(2)/D(3)

296 phrenia, but few studies have compared newer antipsychotic drugs with both clozapine and conventional

297 Thus, proven or putative antipsychotic drugs with different mechanisms of action

298 r designing anti-parkinsonian, anti-ADHD and antipsychotic drugs with greater therapeutic efficacy an

299 of sudden cardiac death than did nonusers of antipsychotic drugs, with adjusted incidence-rate ratios

300 w extrapyramidal symptom profile of atypical antipsychotic drugs, without the need for 5-HT(2A) recep