ライフサイエンスコーパス: mood disorder

1 and GRM7 (which potentially affects risk for mood disorders).

2 rders (eg, other substance use disorders and mood disorders).

3 schizophrenia, schizoaffective disorder, or mood disorder.

4 sychosocial functioning; and parental age at mood disorder.

5 est (TSST), in 208 offspring of parents with mood disorder.

6 mg/d, for 24 weeks or until development of a mood disorder.

7 act to affect the likelihood of developing a mood disorder.

8 f those neural interactions may characterize mood disorder.

9 ) and 12-month (F = 0.42; 95% CI, 0.26-0.66) mood disorder.

10 , and impulsive aggression as a precursor of mood disorder.

11 ach to the development of new treatments for mood disorder.

12 t response has been a clinical challenge for mood disorder.

13 r the development of opioid addiction and/or mood disorder.

14 uring the postpartum period to alleviate the mood disorder.

15 n evaluation tool for functional outcomes in mood disorders.

16 ed with impairment of cognitive function and mood disorders.

17 pharmacological targets for the treatment of mood disorders.

18 p and might increase the risk for developing mood disorders.

19 uence susceptibility for substance abuse and mood disorders.

20 eficit/hyperactivity, substance-related, and mood disorders.

21 he role of gut microbiota in obesity-related mood disorders.

22 and create new avenues for the treatment of mood disorders.

23 are two novel pathways to pathophysiology in mood disorders.

24 m to the pathophysiology and therapeutics of mood disorders.

25 sing a major unmet need for the treatment of mood disorders.

26 (PUFAs) is a hallmark of poor nutrition and mood disorders.

27 in the susceptibility and drug treatment of mood disorders.

28 (P2X7R) has repeatedly been associated with mood disorders.

29 lated isoforms in the brain of patients with mood disorders.

30 s stress sensitivity, a major risk factor in mood disorders.

31 of the hippocampus have been associated with mood disorders.

32 andidate for the treatment of stress-related mood disorders.

33 t-translational modifications play a role in mood disorders.

34 adian function have strong associations with mood disorders.

35 oral functions, or on addictive diseases and mood disorders.

36 (PCDH17) as a susceptibility gene for major mood disorders.

37 ln460Arg has repeatedly been associated with mood disorders.

38 roof of concept studies for the treatment of mood disorders.

39 cal response (SVR) on cognitive function and mood disorders.

40 ion and bipolar disorder are the most common mood disorders.

41 spines in the brains of patients with major mood disorders.

42 t role in the pathology of anxiety and other mood disorders.

43 masome-dependent signaling may contribute to mood disorders.

44 cadian timekeeping (amplitude and timing) in mood disorders.

45 utflow; all of these have been implicated in mood disorders.

46 ta-analysis, including 15 that are novel for mood disorders.

47 cteric, reproductive period, depression, and mood disorders.

48 lead to metabolic, reproductive, sleep, and mood disorders.

49 s disease, Down syndrome, schizophrenia, and mood disorders.

50 the neural systems subserving addiction and mood disorders.

51 s for the development of novel therapies for mood disorders.

52 onclusively the role of genetic variation in mood disorders.

53 lying neuronal circuitry and neurobiology of mood disorders.

54 ed receptor in brain regions associated with mood disorders.

55 account for core features of stress-related mood disorders.

56 al ideation and attempts in individuals with mood disorders.

57 familial trait markers for vulnerability to mood disorders.

58 may represent an intermediate phenotype for mood disorders.

59 relationship to relapse and vulnerability to mood disorders.

60 gativity (MMN) activity in participants with mood disorders.

61 vioural abnormalities, including anxiety and mood disorders.

62 ns but are not firmly established in primary mood disorders.

63 cause or increase risk for this and related mood disorders.

64 of individual differences to stress-induced mood disorders.

65 atment of conditions ranging from obesity to mood disorders.

66 nalyses across ethnicities, particularly for mood disorders.

67 ols in the development of new treatments for mood disorders.

68 otonergic and cholinergic systems related to mood disorders.

69 triking differences in the rates of recorded mood disorders.

70 hickness abnormalities have been observed in mood disorders.

71 to understand neurobiological disruptions in mood disorders.

72 ately contributing to their vulnerability to mood disorders.

73 target for future drug discovery efforts in mood disorders.

74 ic strategies for major depression and other mood disorders.

75 ce for the treatment of depression and other mood disorders.

76 Is) are the most widely prescribed drugs for mood disorders.

77 ces in vulnerability to opioid addiction and mood disorders.

78 ia and anxiety that are so often comorbid in mood disorders.

79 cated as a risk factor in the development of mood disorders.

80 ediated by NMDARs has been shown to regulate mood disorders.

81 treatment of major depression and postpartum mood disorders.

82 ohol use disorders and bipolar and affective mood disorders.

83 and neuropsychiatric disorders, particularly mood disorders.

84 e to stress increases the risk of developing mood disorders.

85 en implicated in drug addiction, reward, and mood disorders.

86 stem to develop a new wave of treatments for mood disorders.

87 the immune system and their relationship to mood disorders.

88 d, and its abnormal development is linked to mood disorders.

89 mesoaccumbal function such as addictions and mood disorders.

90 butyric acidergic neurosteroid implicated in mood disorders.

91 bute to stress susceptibility and associated mood disorders.

92 in the last several decades in the field of mood disorders.

93 t notably schizophrenia but also anxiety and mood disorders.

94 T Stress is a major variable contributing to mood disorders.

95 e in the meta-analysis of suicide attempt in mood disorders.

96 efficacy for treatment-resistant symptoms of mood disorders.

97 mily have been targeted for the treatment of mood disorders.

98 toms or rates of occurrence for a variety of mood disorders.

99 for acetylcholine in the pathophysiology of mood disorders.

100 ortionate use of opioids among patients with mood disorders.

101 across many psychiatric diseases, especially mood disorders.

102 tly higher rates of 12-month MDD (10.3%) and mood disorder (10.3%) than their urban counterparts (3.7

103 rs) of 334 clinically referred probands with mood disorders, 191 (57.2%) of whom had also made a suic

104 50.4]), and lowest in those diagnosed with a mood disorder (24.4% [23.6-25.2]).

105 th fatal and nonfatal suicidal behaviour was mood disorder (25% and 21%, respectively).

106 kers reliably distinguish schizophrenia from mood disorders across the life span and generalize to ne

107 Pre-donation history of mood disorder (adjusted ratio of means [95% confidence i

108 ystem to provide biomarkers for diagnosis of mood disorders, along with new targets for developing tr

109 The mood disorders also differ in their genetic correlation

110 ime and 12-month diagnoses of DSM-IV MDD and mood disorder among female respondents, who included non

111 omorbid OCD and ADHD; however, high rates of mood disorders among participants with TS (29.8%) may be

112 of lithium for prophylaxis of the recurrent mood disorder and encouraged its greater use.

113 Interventions that target mood disorder and impulsive aggression in high-risk offs

114 to be related to familial transmission (eg, mood disorder and impulsive aggression).

115 nd provide therapeutic targets to treat this mood disorder and promote resilience.

116 fected young adults at high familial risk of mood disorders and 93 healthy control subjects (HC).

117 s aids to psychotherapy for the treatment of mood disorders and alcohol dependence, drugs such as LSD

118 ches to understanding risk and expression of mood disorders and are a promising area of inquiry, in l

119 normalities in NRG3 transcriptomics occur in mood disorders and are genetically determined.

120 a variety of behaviors, including models of mood disorders and behavioral responses to nicotine.

121 ereas obesity was behaviourally similar with mood disorders and certain personality disorders.

122 investigate the causal relationship between mood disorders and circadian clock disruption, previous

123 ng factors in the phenotypic presentation of mood disorders and co-morbid medical conditions in this

124 cancer survivors are more likely to develop mood disorders and cognitive deficits than women in the

125 Mood disorders and constipation are often comorbid, yet

126 eas 24a and 24b) appears to be important for mood disorders and constitutes a neuroanatomical substra

127 on the use of ketamine for the treatment of mood disorders and highlights the limitations of the exi

128 been implicated in nociception, fear memory, mood disorders and ischemia.

129 for the understanding of sex differences in mood disorders and of the side effects of cytochrome P45

130 ations-with a focus on cognitive impairment, mood disorders and psychosis.

131 red a key research component in the study of mood disorders and relevant treatment mechanisms.

132 h to prioritize these genes for relevance to mood disorders and stress.

133 are targets of existing drugs used to treat mood disorders and suicidality (lithium, clozapine and o

134 ition, a differential pattern exists between mood disorders and SZ, with a preferential metabolism of

135 tive effects of research in individuals with mood disorders and to provide data to address ethical co

136 al studies report strong association between mood disorders and tobacco addiction.

137 n reward center may further promote comorbid mood disorders and vulnerability to addiction.

138 Parental mood disorders (and bipolar disorder in particular) conf

139 hologies including mental (schizophrenia and mood disorders) and neurological (Alzheimer's, prion enc

140 lifetime psychopathology and 25 had a non-BD mood disorder), and 80 unrelated healthy individuals.

141 jor depressive disorder (MDD) is a disabling mood disorder, and despite a known heritable component,

142 associated with transition from well to non-mood disorder, and psychotic symptoms in mood episodes w

143 Circadian clock abnormalities are related to mood disorder, and sleep abnormalities have been implica

144 dian clock can result in metabolic diseases, mood disorders, and accelerated aging.

145 dysfunction is not uniform across women with mood disorders, and activation is linked to performance

146 such as Parkinson's disease, schizophrenia, mood disorders, and addiction.

147 rs10748842 was genotyped in individuals with mood disorders, and association with NRG3 isoform expres

148 hizophrenia spectrum disorders and psychotic mood disorders, and associations of the empirically deri

149 chiatric syndromes, including schizophrenia, mood disorders, and autism spectrum disorders, are chara

150 treatment of insomnia, circadian rhythm and mood disorders, and cancer(3), and MT(2) has also been i

151 her covariates included age, sex, anxiety or mood disorders, and family history of drug, alcohol, and

152 agus nerve dysfunction resulting in obesity, mood disorders, and inflammation.

153 s in the hippocampus have been implicated in mood disorders, and mutations in several genes have now

154 e disorder with past-year anxiety disorders, mood disorders, and posttraumatic stress disorder by sex

155 Alzheimer's disease (AD), type II diabetes, mood disorders, and some cancers, but the approach poses

156 risk for developing psychological distress, mood disorders, and trauma and stressor-related disorder

157 s (substance abuse disorders, schizophrenia, mood disorder, anxiety, and personality disorder), separ

158 and 14 (88%) of the 16 patients had comorbid mood disorders, anxiety disorders, or both.

159 All athletes reported no premorbid mood disorders, anxiety disorders, substance abuse, or a

160 se disorders (aOR, 1.34; 95% CI, 1.05-1.72), mood disorders (aOR, 1.15; 95% CI, 1.01-1.30), anxiety (

161 proper circadian timing in the NAc, and that mood disorders are associated with dysfunctions of the N

162 Both mood disorders are characterized by emotion regulation d

163 Treatment options for these mood disorders are currently suboptimal for many patient

164 Mood disorders are highly prevalent and are the leading

165 Stress-related mood disorders are more prevalent in females than males,

166 el mechanism underlying learning deficits in mood disorders as well as a potential target - altering

167 Lifetime and 12-month MDD and mood disorder assessed via the World Mental Health Compo

168 Bipolar disorder (BD) is a serious mood disorder associated with circadian rhythm abnormali

169 terozygosity for the wild-type P2X7R and its mood disorder-associated variant P2X7R-Gln460Arg represe

170 uicide attempt, a strong effect of offspring mood disorder at each time point, and impulsive aggressi

171 attempt (OR, 5.69; 95% CI, 1.94-16.74), and mood disorder at the time point before the attempt (OR,

172 epressive phenotype and raise the issue that mood disorders at early developmental ages may reflect i

173 ead of the neuroprotective kynurenic acid in mood disorders but not in SZ.

174 dely used and highly effective treatment for mood disorders, but causes poorly characterised adverse

175 rontal cortices is implicated in anxiety and mood disorders, but the specific contributions of each r

176 Mood disorders can be debilitating, and are often correl

177 Bipolar disorder is a lifelong mood disorder characterized by extreme mood swings betwe

178 Bipolar disorder (BD) is a common mood disorder characterized by recurrent episodes of man

179 strual dysphoric disorder (PMDD) is a common mood disorder, characterized by distressing affective, b

180 data analysis (k = 9, N = 367 patients with mood disorders), clinical outcomes were compared across

181 icant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment.

182 diabetes, metabolic syndrome, heart disease, mood disorders, cognitive impairment, and accidents.

183 ociations were not replicated in independent mood disorder cohorts from the UK Biobank and iPSYCH.

184 cide among patients with unipolar or bipolar mood disorders compared with placebo.

185 The probability of suffering the mood disorder depression is up to 30% in women and 15% i

186 considerable sharing of risk factors across mood disorders despite their diagnostic distinction.

187 gnoses before schizophrenia were anxiety and mood disorders, direct transitions to schizophrenia usua

188 stic tools distinguishing schizophrenia from mood disorders early in the course of psychosis.

189 eline dyspnea index), quality of life (QoL), mood disorders, exacerbations, comorbidities, lung funct

190 ncluded age, sex, race/ethnicity, anxiety or mood disorders, family history of drug, alcohol, and beh

191 isorder share symptoms that may reflect core mood disorder features.

192 s10748842 risk genotype and are increased in mood disorders further implicates a molecular mechanism

193 eployment are posttraumatic stress disorder, mood disorders, GI problems and chronic fatigue.

194 ew areas of shared activation differences in mood disorder greater than healthy controls.

195 trols (P < 0.001), with more of those in the mood disorder group falling into the 'impaired' range wh

196 ers had impaired trajectories, and more with mood disorders had better functioning trajectories.

197 The difficulty in treating mood disorders has brought about clinical interest in al

198 Recent evidence suggests that some mood disorders have a circadian component, and disruptio

199 Trauma and mood disorders have been linked to alterations in brain

200 ts into the neurobiology of stress and human mood disorders have shed light on mechanisms underlying

201 diseases, such as neurological diseases and mood disorders, have deleterious effects on adult hippoc

202 flammation increase the risk and severity of mood disorders; however, only recently have the importan

203 id to quinolinic acid ratio are decreased in mood disorders (i.e., MDD and BD), whereas kynurenic aci

204 iod, 68% experienced nonpsychotic disorders: mood disorder in 49%, anxiety disorder in 35%, and subst

205 Major depressive disorder is a common mood disorder in the elderly.

206 Post-partum depression is a serious mood disorder in women that might be triggered by peripa

207 ural and functional brain changes, and thus, mood disorders in patients with heart disease should not

208 ty of the prefrontal cortex (PFC) is seen in mood disorders including depression and anxiety.

209 the treatment of migraine and stress-related mood disorders including depression, anxiety, and drug a

210 ions are dispensed to patients with comorbid mood disorders including major depressive disorder (MDD)

211 Diagnostic criteria for mood disorders including major depressive disorder (MDD)

212 Mood disorders (including major depressive disorder and

213 unity has been implicated in the etiology of mood disorders, including major depressive disorder (MDD

214 reference in arousal and activity) and sleep/mood disorders, including seasonal affective disorder (S

215 cal mechanism of a novel risk gene for major mood disorders involved in synaptic function and related

216 Finding robust brain substrates of mood disorders is an important target for research.

217 Increased risk for mood disorders is associated with progressive cortical t

218 are reduced in striatum and comorbidity with mood disorders is common.

219 epressive disorder (MDD), along with related mood disorders, is among the world's greatest public hea

220 mine may be beneficial to some patients with mood disorders, it is important to consider the limitati

221 Chronic stress is a key risk factor for mood disorders like depression, but the stress-induced c

222 isorder (MDD) is a complex and heterogeneous mood disorder, making it difficult to develop a generali

223 lar and molecular mechanisms associated with mood disorders may be localized to specific hippocampal

224 concurrently probed both components, or how mood disorders might modulate these processes.

225 T2DM patients without mood disorders (n = 20, aged 65.05 +/- 11.95 years) and

226 including schizophrenia-spectrum disorders, mood disorders, neurotic stress-related and somatoform d

227 Among all visits for mood disorders, NOS visits grew proportionally 1.5-fold

228 between obesity, stress, gut microbiota and mood disorders, obesity was induced in mice using a high

229 d adulthood, and included autistic features, mood disorders, obsessive-compulsive behaviors and heter

230 ptoms arise first and only later do incident mood disorders occur.

231 rebellar ataxia, (3) psychosis and/or severe mood disorder (only in the TS patients), and (4) a compl

232 ty, general psychosocial functioning, age at mood disorder onset in the bipolar parent, and age at ea

233 prior to conversion; earlier parental age at mood disorder onset was also significantly associated wi

234 d mania (and with a parent with older age at mood disorder onset) had a 2% predicted chance of conver

235 d environmental risk factors predisposing to mood disorders or emerge at illness onset.

236 ence: OR, 1.7; 95% CI, 1.2-2.4), but not any mood disorder (OR, 1.1; 95% CI, 0.8-1.4) or anxiety diso

237 ent offspring variables: baseline history of mood disorder (OR, 4.20; 95% CI, 1.37-12.86), baseline h

238 short attention spans, aggressive behaviors, mood disorders, or schizophrenia.

239 Many of the symptoms of mood disorders overlap with autoimmune disorders, which

240 osology now recognise the high prevalence in mood disorders, overlap with delirium, and comorbidity w

241 Mood disorders, particularly depression, are often comor

242 oth similarities and differences between the mood disorders, particularly in the mouse brain cell typ

243 meta-analyses was stratified for population (mood disorder patients/healthy volunteers), emotional va

244 stemic HCM stress can lead to development of mood disorders, possibly through inducing structural and

245 residence differentially influences MDD and mood disorder prevalence among African American women an

246 odents, they experience a 2-fold increase in mood disorder prevalence vs. males.

247 y, race/ethnicity, and sex on depression and mood disorder prevalence.

248 In mood disorders, psychomotor and sensory abnormalities ar

249 HCM females vs. controls and correlated with mood disorder-related symptoms.

250 the cognitive control task in patients with mood disorders relative to healthy controls (P < 0.001),

251 unction with the core behavioral features of mood disorder remain poorly understood.

252 Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, an

253 Lithium use for the treatment of mood disorders remains quite low, particularly in the Un

254 d 1.6-fold and 1.8-fold increases in risk of mood disorder, respectively, and depressive and manic sy

255 mainly abnormal in schizophrenia and the two mood disorders, respectively.

256 unctioning across domains and to anxiety and mood disorders, schizophrenia, and autism spectrum disor

257 The mood disorders share several genetic associations, and g

258 potentially able to convey susceptibility to mood disorders.SIGNIFICANCE STATEMENT Depression and bip

259 of psychosis, with the exception of bipolar mood disorders (similar risk) and brief psychotic episod

260 onfounders, including age, sex, comorbidity, mood disorder, smoking, alcohol consumption, physical ac

261 od maltreatment on disease vulnerability for mood disorders, specifically summarizing cross-sectional

262 lar disorder provides evidence for a genetic mood disorders spectrum.

263 Separate meta-analyses of mood disorder studies, MDD and BD, revealed moderate eff

264 gion are significantly associated with major mood disorders; subjects carrying the risk allele showed

265 r system is implicated (ie, persistent pain, mood disorders, substance use disorders, etc).

266 sity is associated with a high prevalence of mood disorders such as anxiety and depression.

267 (CRFR1) and is implicated in stress-related mood disorders such as anxiety and depression.

268 hanced learning and memory and resistance to mood disorders such as anxiety.

269 s in the analysis of mental disorders, using mood disorders such as depression and anxiety as example

270 vascular dysfunction is highly comorbid with mood disorders, such as anxiety and depression.

271 vo hippocampal subfield volumes and specific mood disorders, such as bipolar disorder (BD) and major

272 tuitary-adrenal axis and affects anxiety and mood disorders, such as depression and fear.

273 Controversy exists whether mood disorders, such as depression, are associated with

274 between glutamate-related genes and risk for mood disorders, suicide, and treatment response, particu

275 and 12-month (OR, 5.99; 95% CI, 3.01-11.94) mood disorder than rural African American women.

276 h further investigation to better understand mood disorders that are more prevalent in female populat

277 brain, giving rise to various cognitive and mood disorders that impair everyday functioning and over

278 ment target in neurodegenerative illness and mood disorders that increases oxidative stress and predi

279 These results indicated that among the mood disorders the hippocampal subfields were more affec

280 preserving the blind in ketamine studies for mood disorders through patient-level analyses of efficac

281 RRs ranging from 1.92 (95% CI 1.91-1.94) for mood disorders to 3.91 (3.87-3.94) for substance use dis

282 thmia, and higher rates of developmental and mood disorders/traits, possibly related to the smaller v

283 ement of glutamate-related genes in risk for mood disorders, treatment response, and phenotypic chara

284 are important targets for treating sleep and mood disorders, type-2 diabetes and cancer.

285 etamine are effective in treatment-resistant mood disorders, underscoring the potential importance of

286 ve, randomized, cross-over study in a French mood disorder unit for inpatients.

287 nergic (DA) neurons, known to be affected in mood disorders, using a novel, translational strategy th

288 A family history of mood disorders was associated with poorer overall cognit

289 and clinical research in other reproductive mood disorders was synthesized to describe a heuristic m

290 Patient premorbid mood disorders were associated with increased apathy (OR

291 rates of lifetime (6.7%) and 12-month (3.3%) mood disorder when compared to urban African American wo

292 Thus, membrane tubulin may play a role in mood disorders, which could be exploited for diagnosis a

293 Major mood disorders, which primarily include bipolar disorder

294 arkinson's disease, ADHD, schizophrenia, and mood disorders, which show stark differences in prevalen

295 chizophrenia, schizoaffective disorder, or a mood disorder who had moderate or severe tardive dyskine

296 ovide a therapeutic option for patients with mood disorders who have impaired neuroplasticity and cog

297 cts of inflammation on glia and glutamate in mood disorders will be discussed along with their transl

298 the concept of depression as an independent mood disorder with characteristic symptoms/signs and a g

299 ave merged patients with rigorously assessed mood disorders with major depressive features with patie

300 The same pattern was found for mood disorder, with rural African American women experie