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antidepressants/atrophie
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Tricyclic antidepressant treatment evokes regional changes in neurotrophic factors over time within the intact and degenerating nigrostriatal system.
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In addition to alleviating depression, trophic responses produced by antidepressants may regulate neural plasticity in the diseased brain, which not only provides symptomatic benefit but also potentially slows the rate of disease progression in Parkinson's disease (PD). Recent in vitro and in vivo
[Progressive cerebellar atrophy following acute antidepressant intoxication].
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A 37-year-old woman presented with acute cerebellar atrophy after ingesting toxic doses of tricyclic antidepressants in an attempt of suicide. Two hours after ingestion, she was comatose and showed myoclonus of the limbs, and eventually developed status epileptics. The patient underwent general
The Antidepressant Agomelatine Improves Memory Deterioration and Upregulates CREB and BDNF Gene Expression Levels in Unpredictable Chronic Mild Stress (UCMS)-Exposed Mice.
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Agomelatine, a novel antidepressant with established clinical efficacy, acts as an agonist of melatonergic MT1 and MT2 receptors and as an antagonist of 5-HT2C receptors. The present study was undertaken to investigate whether chronic treatment with agomelatine would block unpredictable chronic mild
Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine.
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Major depressive illness is among the most prevalent neuropsychiatric disorders and is associated with neuroplasticity deficits in limbic structures such as the amygdala. Since exposure to stressful life events is proposed to contribute to depressive illness, our recent studies examined the effects
Whose depression deteriorates during acute phase antidepressant treatment?
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Deterioration/relapse of depression during pregnancy in Japanese women associated with interruption of antidepressant medications.
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This study examined the risk of deterioration/relapse in pregnant women who discontinued their antidepressant medications based on the discretion of the psychiatric specialists compared with those who performed self-interruption. We reviewed the obstetric records of all singleton deliveries beyond
Antidepressant medication and ocular factors in association with the need for anti-VEGF retreatment in neovascular age-related macular degeneration.
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OBJECTIVE
Vascular endothelial growth factor (VEGF) is a key player in the pathogenesis of neovascular age-related macular degeneration (nAMD) and is also involved in the final common pathway of antidepressant medication. This study investigated the relationship between the need for anti-VEGF
Antidepressant-like effect of the mGluR5 antagonist MTEP in an astroglial degeneration model of depression.
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The glutamatergic predominance in the excitatory-inhibitory balance is postulated to be involved in the pathogenesis of depression. Such imbalance may be induced by astrocyte ablation which reduces glutamate uptake and increases glutamate level in the synaptic cleft. In the present study, we tried
Cell atrophy and loss in depression: reversal by antidepressant treatment.
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Depression is associated with structural alterations in limbic brain regions that control emotion and mood. Studies of chronic stress in animal models and postmortem tissue from depressed subjects demonstrate that these structural alterations result from atrophy and loss of neurons and glial cells.
Exofocal dopaminergic degeneration as antidepressant target in mouse model of poststroke depression.
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BACKGROUND
Although poststroke depression (PSD) is a frequent chronic complication of stroke with high relevance for outcome and survival, underlying pathomechanisms remain inadequately understood. This may be because suitable animal models are largely lacking and existing models are poorly
Antidepressants reduce neuroinflammatory responses and astroglial alpha-synuclein accumulation in a transgenic mouse model of multiple system atrophy.
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Multiple system atrophy (MSA) is a neurodegenerative disease characterized by the pathological accumulation of alpha-synuclein (α-syn) within oligodendroglial cells. This accumulation is accompanied by neuroinflammation with astrogliosis and microgliosis, that leads to neuronal death and subsequent
Antidepressant effects of ginsenoside Rf on behavioral change in the glial degeneration model of depression by reversing glial loss
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Background: Depression is a common neuropsychiatric disease that shows astrocyte pathology. Ginsenoside Rf (G-Rf) is a saponin found in Panax ginseng which has been used to treat neuropsychiatric diseases. We aimed to investigate
No deterioration of cognitive performance in an aggressive unilateral and bilateral antidepressant rTMS add-on trial.
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BACKGROUND
Cognitive functions were assessed before and following a course of repetitive transcranial magnetic stimulation (rTMS) in patients with depression participating in a sham-controlled, randomized trial of rTMS as adjunct to antidepressant treatment.
METHODS
Forty-one medicated inpatients
Agomelatine: an antidepressant without deterioration of sexual response.
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Sexual dysfunctions caused by the use of antidepressants are relatively common. Agomelatine has demonstrated antidepressant properties in comparative studies with sertraline, fluoxetine, and venlafaxine as active controls. The aim of this study was to evaluate the effects of agomelatine on sexual
Glial degeneration as a model of depression.
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Major depression (MD) is a common and disabling disorder but knowledge of its pathophysiology is still incomplete. In the last years, degenerations or dysfunctions of glial cells, especially astrocytes, have been postulated to play a critical role in the pathogenesis of depression. Glial loss in
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