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1 der, bipolar spectrum disorder and any major affective disorder).
2 active neuromodulatory agents (used to treat affective disorders).
3 Lithium is a first-line therapy for bipolar affective disorder.
4 time of the offence (53% v 23%), most often affective disorder.
5 , 1.6-4.5) times more likely to have bipolar affective disorder.
6 2.7-20.6) times more likely to have bipolar affective disorder.
7 izophrenia that has also been diagnosed with affective disorder.
8 polar T3 syndrome, and subsyndromal seasonal affective disorder.
9 sorder (N=26 380), of which 1928 had bipolar affective disorder.
10 rotrophic factor in the aetiology of bipolar affective disorder.
11 overrepresented in the patients with bipolar affective disorder.
12 define more homogeneous subtypes of bipolar affective disorder.
13 and course, is a familial feature of bipolar affective disorder.
14 would be more prevalent than summer seasonal affective disorder.
15 uropsychiatric conditions, including bipolar affective disorder.
16 ficantly more prevalent than summer seasonal affective disorder.
17 affective disorder and subsyndromal seasonal affective disorder.
18 were not aware of the existence of seasonal affective disorder.
19 gene expression in schizophrenia and bipolar affective disorder.
20 licated in the pathogenesis and treatment of affective disorders.
21 ar how glucocorticoid signaling is linked to affective disorders.
22 genetic and nongenetic determinants of major affective disorders.
23 ight be better represented as a continuum of affective disorders.
24 for personalised and new treatments for all affective disorders.
25 nts an emerging approach to the treatment of affective disorders.
26 ceptor 1 gene (CRHR1) that increase risk for affective disorders.
27 arded as a potential genetic risk factor for affective disorders.
28 s a viable therapeutic strategy for treating affective disorders.
29 hippocampus is an integral brain region for affective disorders.
30 of this midbrain structure is implicated in affective disorders.
31 roach to major depressive disorder and other affective disorders.
32 span, and in patients with schizophrenia and affective disorders.
33 may include novel pharmacologic targets for affective disorders.
34 ifferentially expressed in schizophrenia and affective disorders.
35 , and for their increased vulnerabilities to affective disorders.
36 implications in terms of susceptibility for affective disorders.
37 tic implications for circadian disruption in affective disorders.
38 nism underlying treatment-resistant forms of affective disorders.
39 normal and pathological conditions including affective disorders.
40 l models that accurately reflect symptoms of affective disorders.
41 .007) was predictive of later onset of major affective disorders.
42 es in this pathway might contribute to human affective disorders.
43 ecome a first-line drug for the treatment of affective disorders.
44 tive stimuli appears to be involved in other affective disorders.
45 icated in the pathophysiology of anxiety and affective disorders.
46 s the amygdala, a key player in emotions and affective disorders.
47 elopment of schizophrenia-like and psychotic affective disorders.
48 nsmission, such as autism, schizophrenia and affective disorders.
49 ons among psychiatric inpatients with severe affective disorders.
50 ses to potential threat is a core feature of affective disorders.
51 ed disorders, and neonates whose mothers had affective disorders.
52 hophysiology and treatment of stress-related affective disorders.
53 ight for treatment of seasonal cognitive and affective disorders.
54 variation in CHRM2 predisposes to AD, DD and affective disorders.
55 enotyped in a sample of 137 EA subjects with affective disorders.
56 for several decades for chronic treatment of affective disorders.
57 rsely affect risk for AD and DD and risk for affective disorders.
58 ve as a treatment for anxiety-related and/or affective disorders.
59 rs of the stress response and play a role in affective disorders.
60 multistate sample of inpatients with severe affective disorders.
61 number of neurological conditions, including affective disorders.
62 ications for classification and treatment of affective disorders.
63 HT) neurons that has also been implicated in affective disorders.
64 eafood consumption suggests a specificity to affective disorders.
65 possible predictor of treatment response in affective disorders.
66 ot all individuals exposed to stress develop affective disorders.
67 ance to suppression of emotional memories in affective disorders.
68 obstructive pulmonary disease, migraine, and affective disorders.
69 ISC1) is a risk factor for schizophrenia and affective disorders.
70 Serotonin is implicated in mood and affective disorders.
71 europsychophysiologic model of MDD and other affective disorders.
72 ess-sensitive circuits in the development of affective disorders.
73 understanding vulnerability or resilience in affective disorders.
74 eventually facilitate better treatments for affective disorders.
75 plays a protective role in rodent models of affective disorders.
76 ne, and by behavioral alterations, including affective disorders.
77 nal responding, with potential relevance for affective disorders.
78 ight into the role of these brain regions in affective disorders.
79 tributing to vulnerability and resilience to affective disorders.
80 treatment strategies for depression or other affective disorders.
81 l intervention for preventing stress-related affective disorders.
82 ly compared with network activity in primary affective disorders.
83 ophysiological mechanism in risk for SCZ and affective disorders.
84 involved in the pathomechanisms of specific affective disorders.
85 l (HPA) axis dysregulation, a key feature of affective disorders.
86 likely as men to suffer from stress-related affective disorders.
87 r mechanisms implicated in schizophrenia and affective disorders.
88 in the treatment of circadian rhythm-related affective disorders.
89 in the pathophysiology of seasonal and other affective disorders.
90 (27 adults [28%] and ten children [27%]) and affective disorders (33 adults [34%] and ten children [2
91 0) for anxiety disorders, 8.1% (6.5-9.8) for affective disorders, 5.7% (4.4-7.1) for intermittent exp
92 d dissociative (42 versus 0%, P = 0.001) and affective disorders (85 versus 50%, P = 0.01) significan
93 that awareness of the existence of seasonal affective disorder, a condition with safe and effective
94 was to estimate the incidence of postpartum affective disorder (AD), duration of treatment, and rate
95 ign residence had increased IRRs for bipolar affective disorder, affective disorders, personality dis
96 and anxiety-central symptoms of anxiety and affective disorders afflicting large populations of peop
97 hizophrenia, anxiety disorder, OCD, and most affective disorders also showed mean dissociation scores
98 as characterized by high familial loading of affective disorders among patients (p = .001) and high C
100 as carried out in 1099 patients with bipolar affective disorder and 1152 healthy comparator individua
103 ted States, through a proband with bipolar I affective disorder and a sibling with bipolar I or schiz
104 lness onset is a familial feature of bipolar affective disorder and is associated with important clin
105 arities in cognitive impairments in seasonal affective disorder and major depressive disorder in coll
106 GF receptors are altered in individuals with affective disorder and modulate emotionality in animal m
108 mplicating dopamine dysregulation in bipolar affective disorder and schizophrenia, in line with the r
110 re and to estimate the frequency of seasonal affective disorder and subsyndromal seasonal affective d
111 r schizophrenia, was associated with bipolar affective disorder and tested this hypothesis using a ca
114 t ketamine exposure of pregnant rats induces affective disorders and cognitive impairments in offspri
116 Chronic stress increases the likelihood for affective disorders and has been shown to induce changes
117 iated with the development of stress-related affective disorders and individual variability in therap
118 andomized controlled trial (Stepped Care for Affective Disorders and Musculoskeletal Pain [SCAMP]) co
119 ubjects (~700), including patients with SCZ, affective disorders and nonpsychiatric controls (from 14
120 disorders, including Prader-Willi syndrome, affective disorders and obsessive-compulsive disorder, a
121 Investigations of medications approved for affective disorders and other forms of substance abuse,
122 n University in St Louis Kiddie Schedule for Affective Disorders and Schizophrenia (WASH-U-KSADS).
123 iagnosis assessed by the DSM-IV Schedule for Affective Disorders and Schizophrenia for School-Age Chi
124 view SED diagnoses with blinded Schedule for Affective Disorders and Schizophrenia for School-Age Chi
125 linical interviews based on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
126 tional Diagnostic Interview and Schedule for Affective Disorders and Schizophrenia for School-Age Chi
127 linical interviews based on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
128 d at 3-month intervals with the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
129 essive disorder symptoms on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
130 d study were assessed using the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
131 on of a modified version of the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
132 gnosis was established with the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
133 rrent mental disorder using the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
134 ve symptoms, and took part in a Schedule for Affective Disorders and Schizophrenia for School-Age Chi
136 Efficacy was assessed with the Schedule for Affective Disorders and Schizophrenia, Change Version (w
137 ypic assessment with either the Schedule for Affective Disorders and Schizophrenia-Lifetime Version o
138 Diagnosis was assessed with the Schedule for Affective Disorders and Schizophrenia-Lifetime Version.
142 rstand the underlying brain abnormalities in affective disorders and target more effective treatments
143 other functional GI disorders with co-morbid affective disorders and temporal association of symptom
144 eful tools for the differential diagnosis of affective disorders and the prediction of both treatment
145 jects had no schizophrenia spectrum or major affective disorders and were matched to patients by date
148 y helpless rat, a model of susceptibility to affective disorder, and we wished to test whether admini
149 as having a schizophrenia spectrum or major affective disorder, and were matched to cases on date of
150 h a schizophrenia spectrum disorder or major affective disorder, and were matched to subjects with sc
152 ular filtration rate (eFGR) in patients with affective disorders, and explore predictors for a decrea
153 with subthreshold mood symptoms, with DSM-IV affective disorders, and for those who have received tre
154 cally innervated, are involved in stress and affective disorders, and have high densities of the CRF
155 el mechanisms involved in the development of affective disorders, and highlight the noradrenergic sys
156 actor for the development and maintenance of affective disorders, and insights into the underlying br
157 Longer intake episodes, a family history of affective disorders, and poor previous social functionin
158 reat predicts the development of anxiety and affective disorders, and primate lesion studies suggest
159 ences in stress reactivity, vulnerability to affective disorders, and response to pharmacotherapy.
161 nosed with a schizophrenia spectrum or major affective disorder; and were matched to cases on date of
162 r schizoaffective disorder; 55.8%, for major affective disorders; and the remainder met criteria for
164 iated with schizophrenia spectrum disorders, affective disorders, anxiety disorders, and other neurot
165 intellectual disability, schizophrenia, mood affective disorders, anxiety disorders, autism spectrum
166 sociated with other substance use disorders, affective disorders, anxiety, and personality disorders.
167 ely to contain genes contributing to bipolar affective disorder are also relevant to schizophrenia, a
170 itive decline, osteoporosis, sarcopenia, and affective disorders, are the world's biggest killers.
171 tudying molecular processes of patients with affective disorders, as they share considerable similari
172 diagnoses in the larger Amish Study of Major Affective Disorder (ASMAD) cohort, and studied mutant po
173 he problem of pain, but are also relevant to affective disorders associated with disruption of reward
178 been implicated in susceptibility to bipolar affective disorder (BP) through genome-wide association
180 Decades of longitudinal research on bipolar affective disorder (BPAD) revealed cosegregation of high
182 lly treat depression, in particular seasonal affective disorder, but the neural pathways and molecula
183 rrelation exists between chronic disease and affective disorders, but the biological mechanisms under
184 epresent a classic susceptibility factor for affective disorders by biasing the functional reactivity
186 etic variation in CRHR1 affects the risk for affective disorders by influencing the function of the n
187 spite the growing literature suggesting that affective disorders can arise after a traumatic event is
188 atory condition that is highly comorbid with affective disorders characterized by problems with emoti
189 showed a 23.4% lifetime prevalence of major affective disorders compared with 4.4% in controls (P =
190 fective disorder and 74 without a history of affective disorder completed a mailed questionnaire that
191 ization with nonaffective psychosis, bipolar affective disorder, depressive disorder, eating disorder
193 ive HPA stress axis, an important feature of affective disorders, during a dynamic hormonal period, a
194 atment available for individuals with severe affective disorders, ECT's availability is limited and d
196 onist agents together with stress related to affective disorders emphasize the pathogenic role of sym
198 f a schizophrenia spectrum (ICD10 F20-29) or affective disorder (F30-39 with psychotic symptoms), and
201 isk among psychiatric inpatients with severe affective disorders from an estimated 12.3% among indivi
202 ntrolling for neuroticism and self efficacy, affective disorder history continued to predict current
203 urce of vulnerability for the development of affective disorders; however, genetic substrates for the
207 d pattern (winter versus summer) of seasonal affective disorder in African American college students.
209 d for major depressive disorder and seasonal affective disorder in late autumn and completed the Cogn
211 s is frequently accompanied by cognitive and affective disorders in association with neurostructural
213 antidepressant drug used in the treatment of affective disorders in humans, leads to a rapid lengthen
215 atment approach or augmentation strategy for affective disorders including anxiety disorders and majo
216 ctor for the exacerbation and development of affective disorders including major depression and postt
217 , has been associated with vulnerability for affective disorders, including anxiety and depression.
218 of emotional memory is a feature of several affective disorders, including depression, anxiety and p
221 y designed for relapse prevention in bipolar affective disorder is a useful tool in conjunction with
224 Rapid cycling among patients with bipolar affective disorders is important because of its implicat
225 e of testosterone levels on vulnerability to affective disorders is not straightforward, research sug
226 cadian nature of mood and its dysfunction in affective disorders is well recognized, but the underlyi
227 enia, schizoaffective disorders, and bipolar affective disorders) is well described, but little is kn
229 pports the hypothesis that symptoms of human affective disorders may reflect ancestral adaptations to
230 JNK as an avenue for novel therapies against affective disorders.Molecular Psychiatry advance online
231 eficit/hyperactivity disorder (N=18 726) and affective disorder (N=26 380), of which 1928 had bipolar
234 g 3 vulnerable populations: individuals with affective disorders (n = 56) or opioid dependence (n = 6
235 .3 [95% confidence interval (CI), 1.7-3.1]); affective disorders occurred equally in men and women (I
236 ct effects (via self efficacy) of history of affective disorder on the experience of fatigue in RA.
239 also remained associated with a diagnosis of affective disorder (OR, 2.3; 95% CI, 1.3 to 4.2), anxiet
240 or patients with winter depression (seasonal affective disorder, or SAD) uses low-dose melatonin admi
242 old increase in risk for midlife anxiety and affective disorder (P<.05), whereas psychological ill he
244 creased IRRs for bipolar affective disorder, affective disorders, personality disorders, and schizoph
245 er first-line drugs used in the treatment of affective disorders (quetiapine, olanzapine, and semisod
246 ith evidence that this region is involved in affective disorders raise the possibility that glucocort
247 (DMN) is common in individuals with primary affective disorders relative to healthy volunteers (HVs)
250 psychoses associated with schizophrenia and affective disorder represent manifestations of different
251 asure of cognitive deficits in patients with affective disorders, representing a mechanism to study a
254 e supports light therapy for winter seasonal affective disorder (SAD), data on cognitive-behavioral t
257 esults reveal that individuals with seasonal affective disorder showed cognitive impairments similar
258 lly designed to prevent relapses for bipolar affective disorder showed encouraging results when used
260 responding and via that route predispose for affective disorder.SIGNIFICANCE STATEMENT Previously pro
261 tion, light therapy is effective for certain affective disorders, sleep problems, and circadian rhyth
262 susceptibility to adult cardiometabolic and affective disorders spawning the notion of fetal "progra
263 psychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrop
264 state and motor activity, and implicated in affective disorders such as depression and schizophrenia
267 d sets off a general alarm system as seen in affective disorders, such as chronic anxiety and post-tr
268 sensory signaling may have implications for affective disorders that include sensory dysfunctions li
270 these two diplotypes also increased risk for affective disorders, the magnitude of the increased risk
271 en reported to display behaviors relevant to affective disorders, the seizure susceptibility of anima
272 d risk for posttraumatic stress disorder and affective disorders; the other group did not carry this
273 ntagonists have efficacy in the treatment of affective disorders through effects on the dorsal raphe
274 ge age = 34 +/- 16.5) diagnosed with Bipolar Affective Disorder to three patient groups all diagnosed
275 American patients with a diagnosis of major affective disorder treated over the period from November
276 on in CHRM2 and AD, drug dependence (DD) and affective disorders, using a novel extended case-control
281 us winter pattern of seasonality of seasonal affective disorder was compared by using multinomial pro
286 ects of gender and the awareness of seasonal affective disorder were evaluated with a two-way analysi
289 g the preschool period and family history of affective disorders were the most robust and significant
290 s known about the neural correlates of these affective disorders when they occur in mothers, but they
291 cingulate, a region strongly associated with affective disorder, whereas patients with FESZ evinced w
292 on learned helplessness, an animal model of affective disorder wherein a subset of mice exposed to i
293 play a role in the susceptibility to bipolar affective disorder, which underscores a potentially impo
294 is part of a spectrum of apparently familial affective disorders, which have been organized by severi
296 tential marker for personalized treatment of affective disorders with drugs targeting the metabotropi
297 lso evident among participants with seasonal affective disorder, with more women qualifying than men.
300 mental illnesses including schizophrenia and affective disorders, yet the neurodevelopmental processe
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