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 act to affect the likelihood of developing a mood disorder.

3 f those neural interactions may characterize mood disorder.

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

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

6 r adjusting for the familial transmission of mood disorder.

7 e stages of disease; and antidepressants for mood disorder.

8 schizophrenia, schizoaffective disorder, or mood disorder.

9 presents in older adults as a heterogeneous mood disorder.

10 sychosocial functioning; and parental age at mood disorder.

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

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

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

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

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

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

17 the neural systems subserving addiction and mood disorders.

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

19 onclusively the role of genetic variation in mood disorders.

20 lying neuronal circuitry and neurobiology of mood disorders.

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

22 ed receptor in brain regions associated with mood disorders.

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

24 are two novel pathways to pathophysiology in mood disorders.

25 familial trait markers for vulnerability to mood disorders.

26 may represent an intermediate phenotype for mood disorders.

27 relationship to relapse and vulnerability to mood disorders.

28 vioural abnormalities, including anxiety and mood disorders.

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

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

31 of individual differences to stress-induced mood disorders.

32 nalyses across ethnicities, particularly for mood disorders.

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

34 otonergic and cholinergic systems related to mood disorders.

35 triking differences in the rates of recorded mood disorders.

36 hickness abnormalities have been observed in mood disorders.

37 to understand neurobiological disruptions in mood disorders.

38 ately contributing to their vulnerability to mood disorders.

39 m to the pathophysiology and therapeutics of mood disorders.

40 ic strategies for major depression and other mood disorders.

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

42 and role for NG2 glia in CNS homeostasis and mood disorders.

43 s can lead to the development of anxiety and mood disorders.

44 Stress is an important risk factor for mood disorders.

45 strate an increased incidence of anxiety and mood disorders.

46 N) has been identified within the context of mood disorders.

47 lient whereas others are prone to developing mood disorders.

48 ) remains the most widely used treatment for mood disorders.

49 ical-subcortical abnormalities that underlie mood disorders.

50 ands with a broad range of manifestations of mood disorders.

51 ns, 5-HT(1A)R-expressing cells implicated in mood disorders.

52 ve been implicated in the pathophysiology of mood disorders.

53 SNPs with weak effects, and may overlap with mood disorders.

54 lycemia, nausea, fatigue, transaminitis, and mood disorders.

55 get for alternative treatment strategies for mood disorders.

56 -based therapeutics for treatment-refractory mood disorders.

57 ery of novel targets to treat stress-related mood disorders.

58 ere stress increases the risk for developing mood disorders.

59 tifying traits linked to the genetic risk of mood disorders.

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

61 ences susceptibility to bipolar and unipolar mood disorders.

62 ian disruption to major depression and other mood disorders.

63 abilizer lithium in various animal models of mood disorders.

64 st 20 years, affecting the long-term risk of mood disorders.

65 thought to play a role in the development of mood disorders.

66 iction, schizophrenia, depression, and other mood disorders.

67 d we conclude that HC may protect women from mood disorders.

68 reducing suicidal behaviors in patients with mood disorders.

69 e a genetically increased risk of developing mood disorders.

70 in the susceptibility and drug treatment of mood disorders.

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

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

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

74 of the hippocampus have been associated with mood disorders.

75 ed with impairment of cognitive function and mood disorders.

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

77 adian function have strong associations with mood disorders.

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

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

80 ln460Arg has repeatedly been associated with mood disorders.

81 pharmacological targets for the treatment of mood disorders.

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

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

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

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

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

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

88 masome-dependent signaling may contribute to mood disorders.

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

90 uence susceptibility for substance abuse and mood disorders.

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

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

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

94 disorder (11.1%; 95% CI, 9.7% to 12.4%), any mood disorder (6.5%; 95% CI, 5.5% to 7.5%), any somatofo

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

96 ations for the neuronal circuitry underlying mood disorders across the lifespan.

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

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

99 o psychotic features, agitated features, and mood disorder and describe their natural history, showin

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

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

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

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

104 Mood disorders and alcohol dependence frequently co-occu

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

106 Mood disorders and antidepressant therapy involve altera

107 rain area important for behaviors related to mood disorders and anxiety.

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

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

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

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

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

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

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

115 2 processes implicated as excessive in both mood disorders and dementia.

116 ghts to the molecular mechanisms controlling mood disorders and drug addiction.

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

118 te to glutamate alterations in patients with mood disorders and increased inflammation.

119 o metabolic syndrome, and the development of mood disorders and neurodegenerative diseases.

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

121 e the onset, prevalence, and early course of mood disorders and other psychopathology.

122 ding on our previous blood biomarker work in mood disorders and psychosis, we decided to identify blo

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

124 for assessing novel interventions to prevent mood disorders and reduce longer-term risk of neurodegen

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

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

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

128 een increasing attention to the subgroups of mood disorders and their boundaries with other mental di

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

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

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

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

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

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

135 nterneurons (p=0.005) in HD cases with major mood disorder, and no interneuron loss was observed in c

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

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

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

139 icated the amygdala in emotion processing in mood disorders, and adult depression studies have sugges

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

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

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

143 ficit/hyperactivity disorder, schizophrenia, mood disorders, and autism.

144 ent models of epilepsy, Parkinson's disease, mood disorders, and chronic pain.

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

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

147 Perimenopause is a period of high risk for mood disorders, and it has been proposed that perimenopa

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

149 r of psychiatric illnesses including autism, mood disorders, and schizophrenia.

150 to psychiatric illnesses such as addiction, mood disorders, and schizophrenia.

151 omia, prolonged postoperative ileus, anxiety/mood disorders, and sleep disturbance) met all inclusion

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

153 ng attention deficit hyperactivity disorder, mood disorders, and substance use disorders.

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

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

156 s, substance abuse disorders, schizophrenia, mood disorders, anxiety, eating disorders, personality d

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

158 , 3.01; 95% CI, 2.23-4.06), and epilepsy and mood disorders (aOR, 1.41; 95% CI, 1.16-1.72).

159 Although episodes of postpartum mood disorder are more common in bipolar I disorder and

160 Both mood disorders are characterized by emotion regulation d

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

162 he growing assertion that the major types of mood disorders are manifestations of a common underlying

163 Mood disorders are serious diseases that affect a large

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

165 l peptide oxytocin (OT) in the modulation of mood disorders as well as drug addiction.

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

167 The risk of a first lifetime diagnosis of mood disorder assigned by a psychiatrist in a hospital,

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

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

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

171 Anxiety disorders were more prevalent than mood disorders at all ages, but especially in children a

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

173 1 is an important gene for schizophrenia and mood disorders based on both human and animal studies.

174 genes in the blood of subjects with a major mood disorder (bipolar disorder), a high-risk population

175 on of subthreshold (NOS) DSM-IV diagnoses of mood disorder, bipolar disorder, and anxiety disorder in

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

177 ect the brain and might increase the risk of mood disorders, but longitudinal studies of comorbidity

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

179 0.48), may be accounted for by ADHD and, for mood disorders, by OCD.

180 Mood disorders can be debilitating, and are often correl

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

184 In total, 24% of offspring with a unipolar mood disorder developed a bipolar spectrum disorder over

185 e disease increased the risk of a subsequent mood disorder diagnosis by 45% (IRR, 1.45; 95% CI, 1.39-

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

187 ilding deficient neural circuitry underlying mood disorders, epilepsy, and pain modulation among othe

188 of suicide attempt in offspring at risk for mood disorder, even after adjusting for the familial tra

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 previously identified, well-known psychosis/mood disorder genes.

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 for brain diseases such as schizophrenia and mood disorders has stagnated.

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

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

201 Nearly all people suffering from mood disorders have significant disruptions in circadian

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

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

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

205 ivation predict the onset of mania and other mood disorders in high-risk children.

206 The subjective measures used to study mood disorders in humans cannot be replicated in animals

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

208 mmunologic hypothesis for the development of mood disorders in subgroups of patients.

209 t for the understanding of increased risk of mood disorders in transplanted patients treated with imm

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

211 rmore, the ACC appears as a critical hub for mood disorders, including for the anxiodepressive conseq

212 milial specificity of the major subgroups of mood disorders, including psychotic, manic and major dep

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

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

215 es that recovery from depression and related mood disorders is a gradual process that develops slowly

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 ing and neuroplasticity in relationship with mood disorders is scarce.

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

222 Co-occurring schizophrenia and mood disorder may be better coded as separate diagnoses,

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

224 ction in a VP orexin hotspot in addiction or mood disorders might also contribute to some types of af

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

226 n unaffected individuals at familial risk of mood disorder (n = 70) and comparison subjects (n = 62).

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

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

229 ce use; schizophrenia and related disorders; mood disorders; neurotic, stress-related, and somatoform

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

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

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

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

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

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

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

237 logical changes implicated in the genesis of mood disorders or dementia have not been identified.

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

239 bition may represent a viable means to treat mood disorders or enhance the efficacy of serotonergic a

240 anding of stress-related conditions, such as mood disorders or post-traumatic stress disorder (PTSD).

241 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

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

243 tment in 56 910 patients with schizophrenia, mood disorders, or dementia first hospitalized or visiti

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

245 blood from the antenatal period of pregnant mood disorder patients who would and would not develop d

246 ore pathophysiological defect in a subset of mood disorder patients.

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

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

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

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

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

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

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

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

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

256 luence on the serotonergic signals mediating mood disorders remain unclear.

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

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

259 oblematic, but those who develop anxiety and mood disorders respond more poorly to both pharmacologic

260 The specific mood disorders reviewed are bipolar and major depressive

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

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

263 tal episodes are highly prevalent across the mood disorder spectrum.

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 was no significant cross-aggregation between mood disorder subtypes suggesting that the familial tran

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

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

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

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

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

272 iated with GM changes in regions involved in mood disorders, suggest altered structural connectivity

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

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

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

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

277 aggregation patterns of the full spectrum of mood disorders (that is, bipolar, schizoaffective (SAF),

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

279 ough these symptoms are not exclusive to the mood disorder, they could alert pediatricians to the nee

280 al diseases to Na(+) pump mutations and some mood disorders to altered Na(+) pump function has renewe

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

282 Beginning at puberty, women develop mood disorders twice as often as men.

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

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

285 e been identified in patients diagnosed with mood disorders using magnetic resonance imaging-related

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

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

288 Anxiety and unipolar mood disorders were overrepresented in females.

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

290 Major mood disorders, which primarily include bipolar disorder

291 n the symptomatic onset of schizophrenia and mood disorders, which typically occurs during adolescenc

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

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

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

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

296 developing therapeutics for the treatment of mood disorders with a concomitant dysfunction in circadi

297 ive Disorder (SAD) is one of the most common mood disorders with depressive symptoms recurring in win

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

299 s argue for a single boundary distinguishing mood disorders with psychosis from schizophrenia (kraepe

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