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1 der, bipolar spectrum disorder and any major affective disorder).
2 active neuromodulatory agents (used to treat affective disorders).
3 der and 49.7% (95% CI 48.1-51.3) 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 rotrophic factor in the aetiology of bipolar affective disorder.
10 overrepresented in the patients with bipolar affective disorder.
11 define more homogeneous subtypes of bipolar affective disorder.
12 and course, is a familial feature of bipolar affective disorder.
13 would be more prevalent than summer seasonal affective disorder.
14 Lithium is a first-line therapy for bipolar affective disorder.
15 sorder (N=26 380), of which 1928 had bipolar affective disorder.
16 operiod and are consistently associated with affective disorders.
17 ne, and by behavioral alterations, including affective disorders.
18 nal responding, with potential relevance for affective disorders.
19 tributing to vulnerability and resilience to affective disorders.
20 treatment strategies for depression or other affective disorders.
21 l intervention for preventing stress-related affective disorders.
22 ly compared with network activity in primary affective disorders.
23 ophysiological mechanism in risk for SCZ and affective disorders.
24 involved in the pathomechanisms of specific affective disorders.
25 likely as men to suffer from stress-related affective disorders.
26 tics with incident dementia in patients with affective disorders.
27 r mechanisms implicated in schizophrenia and affective disorders.
28 in the treatment of circadian rhythm-related affective disorders.
29 in the pathophysiology of seasonal and other affective disorders.
30 ar how glucocorticoid signaling is linked to affective disorders.
31 genetic and nongenetic determinants of major affective disorders.
32 ight be better represented as a continuum of affective disorders.
33 for personalised and new treatments for all affective disorders.
34 nts an emerging approach to the treatment of affective disorders.
35 ceptor 1 gene (CRHR1) that increase risk for affective disorders.
36 tion may contribute to memory distortions in affective disorders.
37 arded as a potential genetic risk factor for affective disorders.
38 s a viable therapeutic strategy for treating affective disorders.
39 hippocampus is an integral brain region for affective disorders.
40 avenues for pharmacological interventions in affective disorders.
41 of this midbrain structure is implicated in affective disorders.
42 roach to major depressive disorder and other affective disorders.
43 span, and in patients with schizophrenia and affective disorders.
44 may include novel pharmacologic targets for affective disorders.
45 ifferentially expressed in schizophrenia and affective disorders.
46 , and for their increased vulnerabilities to affective disorders.
47 implications in terms of susceptibility for affective disorders.
48 nism underlying treatment-resistant forms of affective disorders.
49 normal and pathological conditions including affective disorders.
50 l models that accurately reflect symptoms of affective disorders.
51 .007) was predictive of later onset of major affective disorders.
52 es in this pathway might contribute to human affective disorders.
53 ecome a first-line drug for the treatment of affective disorders.
54 tive stimuli appears to be involved in other affective disorders.
55 ence significant and disabling cognitive and affective disorders.
56 icated in the pathophysiology of anxiety and affective disorders.
57 s the amygdala, a key player in emotions and affective disorders.
58 elopment of schizophrenia-like and psychotic affective disorders.
59 nsmission, such as autism, schizophrenia and affective disorders.
60 ervention that could circumvent pain-induced affective disorders.
61 ed disorders, and neonates whose mothers had affective disorders.
62 hophysiology and treatment of stress-related affective disorders.
63 ight for treatment of seasonal cognitive and affective disorders.
64 variation in CHRM2 predisposes to AD, DD and affective disorders.
65 enotyped in a sample of 137 EA subjects with affective disorders.
66 for several decades for chronic treatment of affective disorders.
67 rsely affect risk for AD and DD and risk for affective disorders.
68 ve as a treatment for anxiety-related and/or affective disorders.
69 tial of the eCB system for treating negative affective disorders.
70 ocessing can underlie the pathophysiology of affective disorders.
71 licated in the pathogenesis and treatment of affective disorders.
72 ons among psychiatric inpatients with severe affective disorders.
73 possible predictor of treatment response in affective disorders.
74 Serotonin is implicated in mood and affective disorders.
75 ight into the role of these brain regions in affective disorders.
76 l (HPA) axis dysregulation, a key feature of affective disorders.
77 are often therapeutically targeted to treat affective disorders.
78 tic implications for circadian disruption in affective disorders.
79 ses to potential threat is a core feature of affective disorders.
80 underlying mechanisms in the development of affective disorders.
81 multistate sample of inpatients with severe affective disorders.
82 ot all individuals exposed to stress develop affective disorders.
83 ance to suppression of emotional memories in affective disorders.
84 e reward circuitry underlies many aspects of affective disorders.
85 obstructive pulmonary disease, migraine, and affective disorders.
86 ISC1) is a risk factor for schizophrenia and affective disorders.
87 europsychophysiologic model of MDD and other affective disorders.
88 ess-sensitive circuits in the development of affective disorders.
89 understanding vulnerability or resilience in affective disorders.
90 eventually facilitate better treatments for affective disorders.
91 plays a protective role in rodent models of affective disorders.
92 cidence rate ratio 1.44 [1.27-1.62]) and non-affective disorders (1.60 [1.44-1.77]) than women, but n
94 (2.8% [95% CI, 2.2% to 3.4%] vs. 0.7%), mood affective disorders (19.5% [CI, 18.0% to 21.0%] vs. 8.1%
95 (27 adults [28%] and ten children [27%]) and affective disorders (33 adults [34%] and ten children [2
96 0) for anxiety disorders, 8.1% (6.5-9.8) for affective disorders, 5.7% (4.4-7.1) for intermittent exp
97 d dissociative (42 versus 0%, P = 0.001) and affective disorders (85 versus 50%, P = 0.01) significan
98 ation registers reported higher rates of non-affective disorders (9.64 [2.72-31.82]), schizophrenia (
99 the serotonin (5-HT) system in fear-related affective disorders, a precise definition of this neurom
100 was to estimate the incidence of postpartum affective disorder (AD), duration of treatment, and rate
101 ign residence had increased IRRs for bipolar affective disorder, affective disorders, personality dis
102 and anxiety-central symptoms of anxiety and affective disorders afflicting large populations of peop
103 hizophrenia, anxiety disorder, OCD, and most affective disorders also showed mean dissociation scores
104 as characterized by high familial loading of affective disorders among patients (p = .001) and high C
105 as carried out in 1099 patients with bipolar affective disorder and 1152 healthy comparator individua
109 lness onset is a familial feature of bipolar affective disorder and is associated with important clin
110 arities in cognitive impairments in seasonal affective disorder and major depressive disorder in coll
111 GF receptors are altered in individuals with affective disorder and modulate emotionality in animal m
113 mplicating dopamine dysregulation in bipolar affective disorder and schizophrenia, in line with the r
115 r schizophrenia, was associated with bipolar affective disorder and tested this hypothesis using a ca
118 t ketamine exposure of pregnant rats induces affective disorders and cognitive impairments in offspri
120 iety is a risk factor for the development of affective disorders and has been associated with decreas
121 Chronic stress increases the likelihood for affective disorders and has been shown to induce changes
122 iated with the development of stress-related affective disorders and individual variability in therap
123 andomized controlled trial (Stepped Care for Affective Disorders and Musculoskeletal Pain [SCAMP]) co
124 ubjects (~700), including patients with SCZ, affective disorders and nonpsychiatric controls (from 14
125 disorders, including Prader-Willi syndrome, affective disorders and obsessive-compulsive disorder, a
126 Investigations of medications approved for affective disorders and other forms of substance abuse,
128 ve symptoms, and took part in a Schedule for Affective Disorders and Schizophrenia for School-Age Chi
129 iagnosis assessed by the DSM-IV Schedule for Affective Disorders and Schizophrenia for School-Age Chi
130 view SED diagnoses with blinded Schedule for Affective Disorders and Schizophrenia for School-Age Chi
131 linical interviews based on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
132 tional Diagnostic Interview and Schedule for Affective Disorders and Schizophrenia for School-Age Chi
133 linical interviews based on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
134 d at 3-month intervals with the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
135 essive disorder symptoms on the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
136 d study were assessed using the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
137 on of a modified version of the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
138 rrent mental disorder using the Schedule for Affective Disorders and Schizophrenia for School-Age Chi
140 ypic assessment with either the Schedule for Affective Disorders and Schizophrenia-Lifetime Version o
141 Diagnosis was assessed with the Schedule for Affective Disorders and Schizophrenia-Lifetime Version.
142 ent and Lifetime version or the Schedule for Affective Disorders and Schizophrenia-Lifetime version.
143 lly on average, with the Kiddie Schedule for Affective Disorders and Schizophrenia-Present and Lifeti
146 rstand the underlying brain abnormalities in affective disorders and target more effective treatments
147 other functional GI disorders with co-morbid affective disorders and temporal association of symptom
148 eful tools for the differential diagnosis of affective disorders and the prediction of both treatment
149 jects had no schizophrenia spectrum or major affective disorders and were matched to patients by date
151 y helpless rat, a model of susceptibility to affective disorder, and we wished to test whether admini
152 h a schizophrenia spectrum disorder or major affective disorder, and were matched to subjects with sc
154 ular filtration rate (eFGR) in patients with affective disorders, and explore predictors for a decrea
155 with subthreshold mood symptoms, with DSM-IV affective disorders, and for those who have received tre
156 cally innervated, are involved in stress and affective disorders, and have high densities of the CRF
157 el mechanisms involved in the development of affective disorders, and highlight the noradrenergic sys
158 actor for the development and maintenance of affective disorders, and insights into the underlying br
159 reat predicts the development of anxiety and affective disorders, and primate lesion studies suggest
160 ences in stress reactivity, vulnerability to affective disorders, and response to pharmacotherapy.
162 nosed with a schizophrenia spectrum or major affective disorder; and were matched to cases on date of
163 r schizoaffective disorder; 55.8%, for major affective disorders; and the remainder met criteria for
165 iated with schizophrenia spectrum disorders, affective disorders, anxiety disorders, and other neurot
166 intellectual disability, schizophrenia, mood affective disorders, anxiety disorders, autism spectrum
167 sociated with other substance use disorders, affective disorders, anxiety, and personality disorders.
168 ely to contain genes contributing to bipolar affective disorder are also relevant to schizophrenia, a
171 itive decline, osteoporosis, sarcopenia, and affective disorders, are the world's biggest killers.
173 tudying molecular processes of patients with affective disorders, as they share considerable similari
174 diagnoses in the larger Amish Study of Major Affective Disorder (ASMAD) cohort, and studied mutant po
175 he problem of pain, but are also relevant to affective disorders associated with disruption of reward
176 e impact of our study is broadly relevant to affective disorders associated with disruption of reward
177 thelium as a target to treat respiratory and affective disorders associated with vascular diseases.
182 been implicated in susceptibility to bipolar affective disorder (BP) through genome-wide association
184 Decades of longitudinal research on bipolar affective disorder (BPAD) revealed cosegregation of high
185 lly treat depression, in particular seasonal affective disorder, but the neural pathways and molecula
186 rrelation exists between chronic disease and affective disorders, but the biological mechanisms under
187 epresent a classic susceptibility factor for affective disorders by biasing the functional reactivity
189 etic variation in CRHR1 affects the risk for affective disorders by influencing the function of the n
190 spite the growing literature suggesting that affective disorders can arise after a traumatic event is
191 atory condition that is highly comorbid with affective disorders characterized by problems with emoti
192 showed a 23.4% lifetime prevalence of major affective disorders compared with 4.4% in controls (P =
193 fective disorder and 74 without a history of affective disorder completed a mailed questionnaire that
194 ization with nonaffective psychosis, bipolar affective disorder, depressive disorder, eating disorder
196 ive HPA stress axis, an important feature of affective disorders, during a dynamic hormonal period, a
197 atment available for individuals with severe affective disorders, ECT's availability is limited and d
199 onist agents together with stress related to affective disorders emphasize the pathogenic role of sym
200 f a schizophrenia spectrum (ICD10 F20-29) or affective disorder (F30-39 with psychotic symptoms), and
203 isk among psychiatric inpatients with severe affective disorders from an estimated 12.3% among indivi
204 urce of vulnerability for the development of affective disorders; however, genetic substrates for the
205 a significant role in alcohol use and other affective disorders; however, the genetically-defined ne
210 d for major depressive disorder and seasonal affective disorder in late autumn and completed the Cogn
212 s is frequently accompanied by cognitive and affective disorders in association with neurostructural
214 antidepressant drug used in the treatment of affective disorders in humans, leads to a rapid lengthen
216 model to study several cardinal symptoms of affective disorders in the female targets of female aggr
217 atment approach or augmentation strategy for affective disorders including anxiety disorders and majo
218 ctor for the exacerbation and development of affective disorders including major depression and postt
219 , has been associated with vulnerability for affective disorders, including anxiety and depression.
220 of emotional memory is a feature of several affective disorders, including depression, anxiety and p
226 e of testosterone levels on vulnerability to affective disorders is not straightforward, research sug
227 cadian nature of mood and its dysfunction in affective disorders is well recognized, but the underlyi
228 enia, schizoaffective disorders, and bipolar affective disorders) is well described, but little is kn
230 pports the hypothesis that symptoms of human affective disorders may reflect ancestral adaptations to
231 JNK as an avenue for novel therapies against affective disorders.Molecular Psychiatry advance online
232 eficit/hyperactivity disorder (N=18 726) and affective disorder (N=26 380), of which 1928 had bipolar
235 g 3 vulnerable populations: individuals with affective disorders (n = 56) or opioid dependence (n = 6
237 .3 [95% confidence interval (CI), 1.7-3.1]); affective disorders occurred equally in men and women (I
238 ct effects (via self efficacy) of history of affective disorder on the experience of fatigue in RA.
241 also remained associated with a diagnosis of affective disorder (OR, 2.3; 95% CI, 1.3 to 4.2), anxiet
242 or patients with winter depression (seasonal affective disorder, or SAD) uses low-dose melatonin admi
243 to treatment of many patients, debilitating affective disorders (other disorders including anxiety a
245 old increase in risk for midlife anxiety and affective disorder (P<.05), whereas psychological ill he
246 creased IRRs for bipolar affective disorder, affective disorders, personality disorders, and schizoph
247 er first-line drugs used in the treatment of affective disorders (quetiapine, olanzapine, and semisod
248 ith evidence that this region is involved in affective disorders raise the possibility that glucocort
249 (DMN) is common in individuals with primary affective disorders relative to healthy volunteers (HVs)
252 asure of cognitive deficits in patients with affective disorders, representing a mechanism to study a
256 age of the general population, with seasonal affective disorder (SAD) representing the most common pr
257 e supports light therapy for winter seasonal affective disorder (SAD), data on cognitive-behavioral t
260 esults reveal that individuals with seasonal affective disorder showed cognitive impairments similar
262 responding and via that route predispose for affective disorder.SIGNIFICANCE STATEMENT Previously pro
263 tion, light therapy is effective for certain affective disorders, sleep problems, and circadian rhyth
264 susceptibility to adult cardiometabolic and affective disorders spawning the notion of fetal "progra
265 psychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrop
268 d sets off a general alarm system as seen in affective disorders, such as chronic anxiety and post-tr
269 sensory signaling may have implications for affective disorders that include sensory dysfunctions li
271 these two diplotypes also increased risk for affective disorders, the magnitude of the increased risk
272 en reported to display behaviors relevant to affective disorders, the seizure susceptibility of anima
273 d risk for posttraumatic stress disorder and affective disorders; the other group did not carry this
274 ge age = 34 +/- 16.5) diagnosed with Bipolar Affective Disorder to three patient groups all diagnosed
275 nform inquiries ranging from the etiology of affective disorders to the neurological basis of emotion
276 American patients with a diagnosis of major affective disorder treated over the period from November
277 on in CHRM2 and AD, drug dependence (DD) and affective disorders, using a novel extended case-control
285 people may be more vulnerable to developing affective disorders, we investigated whether serotonin-r
286 ects of gender and the awareness of seasonal affective disorder were evaluated with a two-way analysi
288 g the preschool period and family history of affective disorders were the most robust and significant
289 s known about the neural correlates of these affective disorders when they occur in mothers, but they
290 cingulate, a region strongly associated with affective disorder, whereas patients with FESZ evinced w
291 on learned helplessness, an animal model of affective disorder wherein a subset of mice exposed to i
292 play a role in the susceptibility to bipolar affective disorder, which underscores a potentially impo
295 tential marker for personalized treatment of affective disorders with drugs targeting the metabotropi
296 lso evident among participants with seasonal affective disorder, with more women qualifying than men.
297 ive disorder), 192 presenting with a primary affective disorder without psychosis (unipolar depressio
300 mental illnesses including schizophrenia and affective disorders, yet the neurodevelopmental processe