ライフサイエンスコーパス: mood

1 play an important role in the regulation of mood.

2 erstood to be largely a disorder of elevated mood.

3 lusions could arise directly from a euphoric mood.

4 airments in attention, cognition, memory and mood.

5 effects of OC on hormones that are linked to mood.

6 luence physiology, behavior, perception, and mood.

7 al a novel mechanism by which bacteria alter mood.

8 perience, social connectedness, and positive mood.

9 pleiotropic functions affecting appetite and mood.

10 6-9) and negative self-cognitions during low mood(10-12)) in adolescents at risk due to early life st

11 the optimal schedules reported more positive moods after their trips.

12 ppocampal neurons to influence cognitive and mood alterations with stress.

13 e was significantly associated with positive mood-an effect sequentially mediated by self-reported tr

14 basic action features reflecting the agent's mood and affective states.

15 s found to be negatively correlated with low mood and anhedonia in females while photoperiod was foun

16 Q-9 (which assess the frequency of depressed mood and anhedonia) and can be used as a first step to i

17 neural systems model through which negative mood and anxiety are modulated by stimulation of the ven

18 were about six times as likely to have had a mood and anxiety disorder health care visit, more than t

19 his study was to ascertain the prevalence of mood and anxiety disorder health care visits and antidep

20 Outcome measures were mood and anxiety disorder health care visits, antidepres

21 Mood and anxiety disorders are complex heterogeneous syn

22 thovagal balance, which are dysfunctional in mood and anxiety disorders, are insensitive to alteratio

23 mPFC) is a key brain structure implicated in mood and anxiety disorders, based primarily on evidence

24 ilocybin, and ayahuasca for the treatment of mood and anxiety disorders, trauma and stress-related di

25 also demonstrated associations with risk for mood and anxiety disorders.

26 ing of interventions for sleep impairment in mood and anxiety disorders.

27 ell-known risk factor for the development of mood and anxiety disorders.

28 uals and individuals suffering from a mix of mood and anxiety disorders.

29 in mood regulation is successful in treating mood and anxiety disorders.

30 rcuits implicated in sleep impairment and in mood and anxiety disorders: the default mode network and

31 the common marmoset, similar to that seen in mood and anxiety disorders?

32 Improvement in mood and anxiety following deep brain stimulation was as

33 Mood and anxiety symptoms were evaluated.

34 Current diagnostic criteria for mood and anxiety tend to lump different forms of sleep d

35 imb of the internal capsule rapidly improves mood and anxiety with optimal stimulation parameters.

36 action was mirrored by decreases of negative mood and anxiety.

37 y of life, self-efficacy, coping strategies, mood and asthma symptoms.

38 h clinically-significant, harmful changes in mood and behaviour attributable to DBS, based upon an an

39 atic beta-cell function, energy homeostasis, mood and behaviour in several species, including zebrafi

40 s behavior, which while adaptive, can affect mood and cognition.

41 The findings indicate that mood and cognitive deficits in T2DM patients has brain s

42 ect the human brain, increasing the risk for mood and cognitive disorders.

43 observed for any outcome measure, including mood and cognitive measures.

44 A battery of computer-based mood and cognitive tests to assess s-energy was conducte

45 Seasonal differences in mood and depressive symptoms affect a large percentage o

46 cal cortisol level, which include individual mood and dietary intake.

47 he basolateral amygdala (BLA) is integral in mood and emotion, and is sensitive to stress.

48 Chronic stress causes dysregulations of mood and energy homeostasis, but the neurocircuitry unde

49 D or psilocybin may have positive effects on mood and feelings of social connectedness.

50 population dynamics, which are important to mood and memory.

51 to be driven by positive effects on anxious mood and night-time sleep problems.

52 technologies hold great promise for treating mood and other brain disorders in next-generation therap

53 serotonin, that damage not only affects our mood and patterns of decision making, but how we move.

54 morbidity including sexual dysfunction, poor mood and physical capacity, changes in body composition

55 nistered with hourly assessment of depressed mood and proinflammatory cytokines (interleukin-6 (IL-6)

56 lyses, including interactions with depressed mood and sex across disorders.

57 study establishes the prevalence of gaming, mood and sleep disorders, in a large African sample.

58 e networks may underlie distinct features of mood and sleep impairment.

59 rs, preclinical MAPT carriers endorsed worse mood and sleep symptoms, and C9orf72 carriers endorsed m

60 Seasonal rhythms influence mood and sociability.

61 m might underlie seasonal variation in human mood and social behavior.

62 m might underlie seasonal variation in human mood and social behavior.SIGNIFICANCE STATEMENT Seasonal

63 resilience therapeutics for the treatment of mood and substance use disorders.

64 that may have efficacy for the treatment of mood and substance use disorders.

65 zing and externalizing behaviors relevant to mood and substance use disorders.

66 we describe how the immune system regulates mood and the potential causes of the dysregulated inflam

67 dversely impacted emotional state, such that mood and well-being levels were significantly decreased

68 Similarly, in shift workers, mood and well-being levels were significantly reduced th

69 a survivors are more likely to develop PTSD, mood, and anxiety disorders and demonstrate endocrine an

70 state that is related to changes in affect, mood, and behavior.

71 association was prevalent between nutrition, mood, and cortisol release.

72 is a critical region influencing addiction, mood, and food consumption through its effects on reinfo

73 de reduced negative mood, increased positive mood, and reduced amygdala response to negative affectiv

74 en by nutritional state, environmental cues, mood, and reward pathways.

75 Here, we tested the hypothesis that mood- and sex-dependent alterations in brain circuitry i

76 Our results revealed mood- and sex-dependent interactions in the central regu

77 Core depressive symptoms (low mood, anhedonia) were measured by the Short Form Survey

78 psychosocial factors including self-reported mood, anxiety, and health related quality of life (HRQoL

79 ed secondary outcomes of alcohol craving and mood, anxiety, and sleep disturbances, which are predict

80 condary outcomes were average drinks/day and mood, anxiety, craving, and sleep quality ratings.

81 heir correlations with cognitive impairment, mood, anxiety, disease severity and plasma lyso-Gb3 leve

82 is associated with an increased incidence of mood, anxiety, substance use, and personality disorders

83 Incident mental disorders (mood, anxiety, substance use, personality, posttraumatic

84 from medical records, and extracted data on mood/anxiety disorders until childbirth from the Care Re

85 obesity, diabetes/hypertensive disorders, or mood/anxiety disorders, increases the risk for adverse n

86 the remaining years of the 19th century, the mood-based model of mania competed for dominance with th

87 tive (e.g., spatial learning and memory) and mood behaviors.

88 al scores of motor disability, cognition and mood/behaviour were calculated.

89 gnal-to-noise ratio and motor, cognitive and mood/behavioural clinical scores were localized in disti

90 in non-human primates (motor, cognitive and mood/behavioural domains).

91 The observed differences in postpartum mood between patients of different SES in the context of

92 urrent knowledge regarding the modulation of mood by the central cholinergic system, drawing upon stu

93 Mood changes after syncope (n = 323; sensitivity, 3% [95

94 vel, ketamine affects the brain's reward and mood circuitry located in the corticomesolimbic structur

95 ed to symptoms including fatigue and altered mood/cognition, indicating that chronic liver inflammati

96 ncluded paired pre- vs. post-ATI measures of mood, cognitive performance, and neurologic examination,

97 differences were detected across a range of mood/cognitive/behavioral/s-energy-level tests after con

98 effects of mood state, medication, and other mood comorbidities, these findings serve as evidence of

99 nesis occurs with functional implications in mood control and cognition.

100 tionships between GM status of cognitive and mood control sites and these scores in T2DM.

101 PAM-AMPA treatment reverted memory, but not mood, deficits.

102 disorder is associated, in many cases, with mood destabilisation, especially during maintenance trea

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

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

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

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

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

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

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

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

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

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

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

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

115 Mood disorders (including major depressive disorder and

116 The mood disorders also differ in their genetic correlation

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

118 Mood disorders and constipation are often comorbid, yet

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

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

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

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

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

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

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

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

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

128 The mood disorders share several genetic associations, and g

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

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

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

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

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

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

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

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

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

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

139 Mood disorders, particularly depression, are often comor

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

141 In mood disorders, psychomotor and sensory abnormalities ar

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

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

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

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

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

147 al ideation and attempts in individuals with mood disorders.

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

149 atment of conditions ranging from obesity to mood disorders.

150 target for future drug discovery efforts in mood disorders.

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

152 ces in vulnerability to opioid addiction and mood disorders.

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

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

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

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

157 treatment of major depression and postpartum mood disorders.

158 ohol use disorders and bipolar and affective mood disorders.

159 and neuropsychiatric disorders, particularly mood disorders.

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

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

162 n evaluation tool for functional outcomes in mood disorders.

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

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

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

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

167 rders characterized by cognitive impairment, mood disturbances, or psychosis, such as Alzheimer's dis

168 alcohol-induced stimulation or sedation, or mood during alcohol administration.

169 otential mechanisms underlying cognitive and mood dysfunction in patients with IBD.

170 ed SRS and alleviated cognitive, memory, and mood dysfunction in the chronic phase of TLE.

171 outh with anxiety disorders, with disruptive mood dysregulation disorder, with ADHD, or without psych

172 hift work are susceptible to its deleterious mood effects.

173 erature (110-160 degrees C) on the potential mood-enhancing compounds corresponding to the distinct m

174 Outcomes were recurrence/relapse rate of any mood episode (RR-any, primary), depressive episode (RR-d

175 is associated with increased risk for first mood episode, episode recurrence, greater comorbidities,

176 er is a chronic relapsing condition in which mood episodes are interspersed with periods of wellbeing

177 at the inclusion of anxiety, as one relevant mood factor, could enhance the implementation of the int

178 sisting of four domain (functioning, fatigue/mood, fears/shame, nutrition) and total scores.

179 sadness, specifically, rather than negative mood, generally, would 1) increase craving, impatience,

180 diabetes mellitus (T2DM) show cognitive and mood impairment, indicating potential for brain injury i

181 amics may explain the evolution of a gradual mood improvement seen with these agents and provides a n

182 t identify a connectivity marker for overall mood improvement, suggesting that functional connectivit

183 nce, humour, relatability, shareability, and mood improving potential of 32 depressive and control (d

184 on of humour, relatability, shareability and mood improving potential of depressive, but not control,

185 erotonin reuptake inhibitors (SSRIs) improve mood in adults but have paradoxical long-term effects wh

186 light exposure for their positive effects on mood in depression.

187 novel neurocircuitry regulating feeding and mood in response to stress.

188 enforced isolation on physical activity and mood, in a naturalistic study of at-risk individuals.

189 psilocybin effects include reduced negative mood, increased positive mood, and reduced amygdala resp

190 rug) and can be augmented by stress/negative mood induction and withdrawal-effects amplified in those

191 ing, following a positive, but not negative, mood induction.

192 sely correlated with genetic effects on SBP, mood instability and neuroticism.

193 Here, we report the results of a GWAS of mood instability as a trait in a large population cohort

194 Forty six unique loci associated with mood instability were identified with a SNP heritability

195 c neuropsychiatric condition associated with mood instability, where patients present significant sle

196 loci, tissues and gene sets contributing to mood instability.

197 Altered mood is a common reason for OC cessation.

198 we examined whether post-endotoxin depressed mood is predicted by baseline activity of TFs related to

199 disturbances and subsequent disturbances in mood, it is difficult to determine from self-reported da

200 Across groups, mood lability correlated negatively with rsFC between IF

201 m of plasticity in brain functions including mood, learning and memory.

202 f light experience as a central modulator of mood, learning, and health [2].

203 In conclusion, death wishes, depressed mood, loss of interest, and pessimism constitute the "ba

204 Death wishes, depressed mood, loss of interest, and pessimism had the highest va

205 s revealed that in women with high depressed mood, lower cardiovagal activity in response to negative

206 overning certain evolutionary behaviours and mood modulation.

207 Circuit mechanisms driving the negative mood of prolonged abstinence likely involve the 5 main r

208 elated social restrictions on the postpartum mood of those living among different socioeconomic statu

209 en authentic posting and positive affect and mood on a within-person level.

210 Sustained changes in mood or action require persistent changes in neural acti

211 mized trial in patients with anhedonia and a mood or anxiety disorder (selective KOR antagonist (JNJ-

212 served in women with low levels of depressed mood or men.

213 No changes in mood or self-reports of suicidal ideation/behavior were

214 odds ratio (OR) 1.27; 95% CI 0.97-1.65), low mood (OR 1.42; 95% CI 1.15-1.77) and reduced energy or a

215 f "circadian alignment condition" vs. "day", mood: p < 0.001; well-being: p < 0.001; adjusted p-value

216 f "circadian alignment condition" vs. "day", mood: p = 0.002; well-being: p = 0.002; adjusted p-value

217 r relationships to individual differences in mood, personality, and physical and emotional well-being

218 ychological and socioeconomic factors (e.g., moods, personality, education, and income levels).

219 Seizure semiology, cognitive and mood phenotypes, alongside inflammatory investigation fi

220 Despite improved mood postpartum and independent of breastfeeding status,

221 e multiregional communication in the primate mood processing network and determine how neuromodulatio

222 d modulate interactions between areas of the mood processing network.

223 cing compounds corresponding to the distinct mood pyramid levels.

224 The mood pyramid of cocoa, which was previously proposed as

225 s, ictal piloerection, lowered self-reported mood, reduced attention, MRI limbic system changes and t

226 monstrate that both parenting experience and mood-regulating effects of oxytocin-MCH are associated w

227 T(3AB)) receptors in brain areas involved in mood regulation is successful in treating mood and anxie

228 ey role in memory formation, yet its role in mood regulation remains controversial.

229 We hypothesized that normal mood regulation requires proper circadian timing in the

230 , whereas women tend to smoke for stress and mood regulation, and have a harder time maintaining long

231 arious functions, for e.g. learning, memory, mood regulation, platelet aggregation and vasoconstricti

232 DR serotonergic neuron subtypes involved in mood regulation.

233 ts the homeostasis of adult neurogenesis and mood regulation.

234 le for the oxytocin-MCH signaling pathway in mood regulation.

235 te cortex (ACC), a brain region important in mood regulation.

236 al regions important for pain processing and mood regulation; and it is unclear which receptors regul

237 us accumbens, a brain region associated with mood regulation; however, the mechanisms involved are un

238 rain circuitries integrating homeostatic and mood regulatory responses.

239 nital anomaly) or efficacy (primary outcome, mood relapse prevention) of lithium treatment during pre

240 atal window is sufficient to program altered mood-related behavior, as well as functional changes in

241 s during postnatal life can evoke persistent mood-related behavioral changes.

242 ing to the nucleus accumbens (NAc) regulates mood-related behavioral responses to stress.

243 ction in the hippocampus, where it regulates mood-related behaviors, is poorly understood.

244 et for treating negative emotional states in mood-related disorders.

245 mechanisms whereby the microbiota modulates mood remain poorly understood.

246 on between the two, giving rise to a delayed mood response.

247 recurrent cases) and the mean difference in mood scores (8-item Patient Health Questionnaire depress

248 ost-ATI, there were no differences in median mood scores or neurologic findings and cognitive perform

249 elevant depressive symptoms or for change in mood scores over a median follow-up of 5.3 years.

250 erved between treatment groups for change in mood scores over time; mean change in PHQ-8 score was no

251 ent from zero (mean difference for change in mood scores, 0.01 points [95% CI, -0.04 to 0.05 points])

252 ze, audio-visual integration, intention, and mood) show that the third visual pathway is specialized

253 ) and nonmotor (eg, constipation, cognition, mood, sleep) signs and symptoms.

254 Lithium is the gold standard mood-stabilising agent for the treatment of people with

255 urocognitive function, motor performance and mood stability was applied on admission and at discharge

256 n a subset of patients (n = 88) who achieved mood stabilization with lithium monotherapy, we explored

257 mplementation of a personalized approach for mood stabilization.

258 Lithium is a widely used mood stabilizer also proposed to act via synaptic scalin

259 ark pharmacotherapy, functioning as a potent mood stabilizer in most, but not all patients.

260 Prescription of an antidepressant without a mood stabilizer increased substantially, from 17.9% in t

261 The widely used mood stabilizer valproate (VPA) causes perturbation of e

262 Lithium, a well-known mood stabilizer, has both neuroprotective, pro-neurogeni

263 0 to investigate which antipsychotics and/or mood stabilizers are better for patients with bipolar di

264 Use of mood stabilizers decreased from 62.3% of visits for bipo

265 d in obstacles to discovering more effective mood stabilizers with fewer adverse side effects.

266 s, the authors examined trends in the use of mood stabilizers, first- and second-generation antipsych

267 ics in large measure supplanting traditional mood stabilizers.

268 wer antipsychotics with those of traditional mood stabilizers.

269 's effect on the clock is fundamental to its mood-stabilizing effects.

270 Lithium is one of the most effective mood-stabilizing medications in bipolar disorder.

271 temperature, hormone levels, motivation and mood state but also by a versatile circadian system with

272 h limited by possible confounding effects of mood state, medication, and other mood comorbidities, th

273 eneral Status Check Scale and the Profile of Mood States 2nd edition brief form, and 2) cognitive mea

274 acterized by episodes of manic and depressed mood states and associated with cortical brain abnormali

275 s Questionnaire (TQ), severity of depressive mood states examined using the Beck Depression Inventory

276 elong mood disorder characterized by extreme mood swings between mania and depression.

277 is a chronic affective disorder with extreme mood swings that include mania or hypomania and depressi

278 , although more adverse events, particularly mood swings, were noted with the 300 mg dose.

279 posed social restrictions, were screened for mood symptomatology using the Edinburgh Postnatal Depres

280 = - 1.05, p = .293), a significant change in mood symptomatology was observed following COVID-19 rest

281 First, mood symptoms are associated with blunted striatal rewar

282 ing chronotype was associated with increased mood symptoms at baseline, including depression, mania,

283 Preclinical GRN carriers endorsed less mood symptoms compared with non-carriers, and worse ever

284 generally reported similar or lower rates of mood symptoms in hormonal contraceptive users compared w

285 c drug treatment each improved psychotic and mood symptoms in placebo-controlled trials.

286 associations between network dysfunction and mood symptoms.

287 ed symptoms of alcohol craving, anxiety, and mood symptoms.

288 ased or decreased related to the severity of mood symptoms.

289 into altered brain function and pathological mood, though the cellular and molecular mechanisms of th

290 brain function and cognition, attention, and mood; thus, minimizing nicotine exposure from any tobacc

291 wo previously associated with metabolism and mood: Trhr and Ucp2.

292 , with onset in childhood, and a "depression/mood" type, with onset in adolescence.

293 ontribute to the pathophysiology of seasonal mood variations.

294 whether lithium administration may stabilize mood via effects on reward processing.

295 exposure to circadian misalignment underpins mood vulnerability in simulated shift work.

296 ent is an important biological component for mood vulnerability, and that individuals who engage in s

297 ormone levels with self-reported measures of mood, well-being and depression.

298 bo, endotoxin-induced increases of depressed mood were moderated by baseline levels of perceived stre

299 The main outcome measures were 1) mood, which was assessed by using a General Status Check

300 tween photoperiod and both anhedonia and low mood, while midbrain volume mediated the relationship be