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Indice de autores Major depression represents mqnual public health problem due to its high prevalence. The etiology of major depression is complex because involves psychosocial, genetic, and biological factors. Among psychosocial factors, different studies report that the first depressive episode appear after some stressful event and produces long-term changes in brain physiology.
These long-lasting changes produce variations at the structural level and in the functioning of different brain areas. Among the genetic factors involved in depressive illness, it has been reported that about genes are related to major depressive disorder.
Despite years of study, the biological basis of major lkscher and precise mechanisms of antidepressant efficacy remain unclear. The objective of the present review is to summarize the main conclusions of the clinical and experimental literature regarding to the etiology of major depressive disorder. Molecular mechanisms of depression: The relationship of presenting physical complaints to depressive symptoms in primary care patients. J Gen Intern Med.
Behavioral Neurology and Neuropsychiatry. The epidemiology of major depressive disorder: JAMA, ;— New approaches to antidepressant drug discovery: El suicidio, conceptos actuales. Salud Mental, ; 29 5: Norepinephrine in depressive reactions. The catecholamine hypothesis of affective disorders: Poor replication of candidate genes for major depressive disorder using genome-wide association data.
Meta-analyses of genetic studies on major depressive disorder. Child maltreatment and HPA axis dysregulation: Psychological interventions for major depression in primary care: Are psychological and pharmacologic interventions equally effective in the treatment of adult depressive disorders? A meta-analysis of descaryar studies. How Immune-inflammatory processes link CNS and psychiatric disorders: Classification and Treatment Implications. Current understanding of the neurobiology of major depressive disorder.
Rom J Morphol Embryol. The cellular neurobiology of depression. Anterior cingulate cortex pathology in schizophrenia and bipolar disorder.
Reduced volume of limbic system-affiliated basal ganglia in mood disorders: J Neuropsychiatry Clin Neurosci. Morphometric evidence for neuronal and glial prefrontal cell pathology in fe depression.
Hippocampal atrophy in major depression: Quantitative MRI of the hippocampus and amygdala in severe depression.
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Hippocampal changes and white matter lesions in early-onset depression. Hippocampal volume change in depression: A longitudinal study of hippocampal volume, cortisol levels, and cognition manaul older depressed subjects. Reduced hippocampal volumes and memory loss in patients with early- and late-onset depression. Reduced hippocampal volume in unmedicated, remitted patients with major depression versus control subjects.
What causes the hippocampal volume decrease in depression? Are neurogenesis, glial changes and apoptosis implicated?
Eur Arch Psychiatry Clin Neurosci. Amygdala and hippocampal volumes in familial early onset major descargarr disorder. Hippocampal volume and subcortical white matter lesions in late-life depression: J Neurol Neurosurg Psychiatry.
Hippocampal morphology and distinguishing late-onset from early-onset elderly depression. Hippocampal and amygdala changes in patients lusvher major depressive disorder and healthy controls during a 1-year follow-up.
J Manusl Psychiatry ; Depression-related variation in brain morphology over 3 years: Arch Gen Psychiatry ; Enlarged amygdala volume and reduced hippocampal volume in young women with major depression. Psychol Med ; Childhood trauma associated with smaller hippocampal volume in women with major depression.
Am J Psychiatry ; Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells. The density and spatial distribution of GABAergic neurons, labelled using calcium binding proteins, in the anterior cingulate cortex in major depressive disorder, bipolar disorder, and schizophrenia.
Reduced glial cell density and neuronal size in the anterior cingulate cortex in major depressive disorder. GluR5,6,7 subunit immunoreactivity on apical pyramidal cell dendrites in hippocampus of schizophrenics and manic depressives.
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Morphological brain changes in depression: Glial reduction in the subgenual prefrontal cortex in mood disorders. Reduced neuronal size and glial cell density in area 9 of the dorsolateral prefrontal cortex in subjects with major depressive disorder. ,anual glial numbers in the amygdala in major depressive disorder. Die Catecholamin- und Serotonin hypothese der Depression. The neuropharmacology of serotonin and noradrenaline in depression.
Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders. The clinical relevance of majual interaction with neurotransmitter transporters and receptors. Depression, cytokines, and glial function.
Elevated serotonin transporter binding in major depressive disorder assessed using positron emission tomography and [11C]DASB; comparison with bipolar disorder. Serotonin receptor binding in a colony model of chronic social stress. Biol Psychiatry ; Regulation of hippocampal 5-HT1A receptor mRNA and binding in transgenic mice with a targeted disruption of the glucocorticoid receptor. Brain Res Mol Descarggar Res ; Eur J Neurosci ; ddescargar Regulation of serotonin1A glucocorticoid, and mineralocorticoid receptor in rat and human hippocampus: Circumscribed changes of the cerebral cortex in neuropsychiatric disorders of later life.
Attenuated 5-HT1A receptor signaling in brains of suicide victims: Luscger modulation of limbic forebrain noradrenergic circuitry. Understanding the impact of 5-HTTLPR, antidepressants, and acute tryptophan depletion on brain activation during facial emotion processing: A review of the imaging literature.
Serotonin pathway polymorphisms and the treatment of major depressive disorder and anxiety disorders. History and evolution of the monoamine hypothesis of depression.
The revised monoamine theory of depression: Animal models of neuropsychiatric disorders. Cellular and molecular mechanisms in the long-term action of antidepressants. Causal relationship between stressful life events and the onset of major depression. Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Organization of the stress system and its dysregulation in melancholic and atypical depression: The corticosteroid receptor hypothesis of depression.
Neuropeptides and the hypothalamic-pituitary-adrenocortical HPA system: World J Biol Psychiatry. The CRF system, stress, depression and anxiety-insights from human genetic studies.
A neurotrophic model for stress-related mood disorders. Stress, lusdher, and neuroplasticity: Impaired Functional Connectivity in the Prefrontal Cortex: The monocyte-T-lymphocyte hypothesis of major depression. Mice with mutations in the HPA-system as models for symptoms of depression.
Cytokines and glucocorticoid receptor signaling.