Psychothérapie interpersonnelle à l’intention des adolescents souffrant de dépression : théories, techniques et recherche

La psychothérapie interpersonnelle de l’adolescent souffrant de dépression (PTI-A) est une psychothérapie brève, basée sur des données probantes, reconnue efficace dans le traitement chez l’adolescent de la dépression unipolaire sans symptômes psychotiques. Cet article présente les principes théoriques de la PTI et ses adaptations reliées au développement de l’adolescent, la notion de cible du traitement (principaux domaines problématiques) et les techniques spécifiques à la PTI-A. Ce traitement se concentre sur les habiletés de communication et la gestion du réseau social actuel de l’individu. Le travail du focus thérapeutique vise à améliorer les relations sociales de l’adolescent en supposant que cela améliorera son humeur. Les bases empiriques relatives à l’efficacité et les résultats préliminaires d’essais cliniques de la PTI-A de même que les recherches futures sur la dépression unipolaire de l’adolescent sont exposées brièvement.Interpersonal psychotherapy for depressed adolescents (IPT-A) is a brief, evidence-based psychotherapy that has been found to be successful in treating unipolar depression in non-bipolar, non-psychotic adolescents. This article provides an overview of the theoretical principles, developmental adaptations, interpersonal focus and techniques of IPT-A. Treatment specifically targets communication skills and social support in current relationships from a skills perspective. Therefore, the therapeutic focus is on improving the adolescent’s relationships with the underlying assumption that this will improve the adolescent’s mood. The empirical support for the effectiveness of IPT-A, preliminary findings from clinical trials of adaptations of IPT-A and future directions for research in unipolar adolescent depression are presented briefly.La psicoterapia interpersonal del adolescente que sufre de depresión (PTI-A) es una psicoterapia breve de la depresión unipolar sin síntomas psicóticos, basada en datos probantes y reconocida como eficaz en el tratamiento del adolescente. Este artículo presenta los principios teóricos de la PTI y sus adaptaciones relacionadas al desarrollo del adolescente, la noción de blanco del tratamiento (principales áreas problemáticas) y las técnicas específicas de la PTI-A. Este tratamiento se concentra en las habilidades de comunicación y la gestión de la red social actual del individuo. El trabajo del foco terapéutico busca mejorar las relaciones sociales del adolescente al suponer que esto mejorará su humor. Se exponen brevemente las bases empíricas relacionadas a la eficacia y los resultados preliminares de las pruebas clínicas de la PTI-A, al igual que las investigaciones futuras sobre la depresión unipolar del adolescente.A psicoterapia interpessoal do adolescente que sofre de depressão (TIP-A) é uma psicoterapia breve, baseada em dados probantes, reconhecida como eficaz no tratamento do adolescente, da depressão unipolar sem sintomas psicóticos. Este artigo apresenta os princípios teóricos da TIP e suas adaptações ligadas ao desenvolvimento do adolescente, a noção de alvo do tratamento (principais áreas problemáticas) e as técnicas específicas da TIP-A. Este tratamento se concentra nas habilidades de comunicação e gestão da rede social atual do indivíduo. O trabalho do foco terapêutico visa melhorar as relações sociais do adolescente supondo que isto melhorará seu humor. As bases empíricas relativas à eficácia e os resultados preliminares de testes clínicos da TIP-A, além das pesquisas futuras sobre a depressão unipolar do adolescente são expostas brevemente

Innovations in Practice: The Relationship Between Sleep Disturbances, Depression, and Interpersonal Functioning in Treatment for Adolescent Depression

Sleep disturbance is frequently comorbid with depression and sleep complaints are the most common residual symptoms after treatment among adolescents with depression. The present analyses investigated the effect of sleep disturbance in depressed adolescents treated with interpersonal psychotherapy for adolescents (IPT-A) versus treatment as usual (TAU) in school-based mental health clinics

Offspring At High And Low Risk For Depression And Anxiety: Mechanisms Of Psychiatric Disorder

Objectives: To examine the effect of parental psychiatric diagnosis on the risk of psychiatric disorder in their offspring and to determine mediators and independent predictors of psychiatric disorder in offspring. Method: The sample consisted of 145 offspring (between the ages of 6 and 24 years, who were directly interviewed) of probands with earlyonset (before age 30 years) major depressive disorder (MDD) without panic, panic disorder with and without major depression, and a normal, never psychiatrically ill control group who were part of a large study conducted to determine the relationship between panic disorder and major depression. Results: The risk for offspring MDD was increased by proband recurrent early-onset MDD and coparent alcohol abuse. Chaotic family environment was the only independent predictor of dysthymia. The risk for offspring “any anxiety” disorder was increased by proband recurrent early-onset MDD and coparent impaired functioning. The association between MDD in proband and “panic spectrum” disorder in offspring was accounted for by chaotic family environment. Conclusion: Recurrent parental MDD has consistently been shown to be a strong risk factor for offspring MDD. Family environment plays an important role in low-level anxiety symptoms and dysthymia. Clinicians treating adults should be alert to risk factors for their offspring and to appropriate targets for early intervention. J. Am. Acad. Child Adolesc. Psychiatry, 1995, 34, 6:786-797. Key Words: depression, anxiety, environment, family

Mediators of Interpersonal Psychotherapy for Depressed Adolescents On Outcomes in Latinos: The Role of Peer and Family Interpersonal Functioning

Peer and family interpersonal functioning were examined as mediators of the impact of Interpersonal Psychotherapy for Depressed Adolescents (IPT-A; Mufson, Dorta, Moreau, & Weissman, 2004) on depression and suicidal ideation among Latino youth. Only youth self-identifying as Latino (n = 50) were included in the analyses. The majority were female (86%) with a mean age of 14.58 (SD = 1.91). The current sample was drawn from the intent to treat sample of a clinical trial examining the effectiveness of IPT-A as compared with treatment as usual (TAU; Mufson, Dorta, Wickramaratne et al., 2004). Youth were randomly assigned to receive IPT-A or TAU delivered by school-based mental health clinicians. Assessments, completed at baseline and at Weeks 4, 8, and 12 (or at early termination), included self-report measures of depression and interpersonal functioning as well as clinician-Administered measures of depression. Multilevel modeling indicated that IPT-A led to greater improvement in interpersonal functioning with family and peers. Improved family and peer interpersonal functioning emerged as significant partial mediators of the relationship between IPT-A and depression. Only improved family interpersonal functioning emerged as a significant partial mediator of the relationship between IPT-A and suicidal ideation. However, this indirect effect was small, suggesting that most of the benefit of IPT-A for suicidal ideation appears to proceed through a pathway other than family interpersonal functioning. These results suggest that the impact of IPT-A on depressive symptoms is partially mediated by family and peer interpersonal functioning and contributes to our understanding of the mechanisms of IPT-A

Nerve Growth Factor Pathobiology During The Progression Of Alzheimer\u27s Disease

The current review summarizes the pathobiology of nerve growth factor (NGF) and its cognate receptors during the progression of Alzheimer’s disease (AD). Both transcript and protein data indicate that cholinotrophic neuronal dysfunction is related to an imbalance between TrkA-mediated survival signaling and the NGF precursor (proNGF)/p75NTR-mediated pro-apoptotic signaling, which may be related to alteration in the metabolism of NGF. Data indicate a spatiotemporal pattern of degeneration related to the evolution of tau pathology within cholinotrophic neuronal subgroups located within the nucleus basalis of Meynert (nbM). Despite these degenerative events the cholinotrophic system is capable of cellular resilience and/or plasticity during the prodromal and later stages of the disease. In addition to neurotrophin dysfunction, studies indicate alterations in epigenetically regulated proteins occur within cholinotrophic nbM neurons during the progression of AD, suggesting a mechanism that may underlie changes in transcript expression. Findings that increased cerebrospinal fluid levels of proNGF mark the onset of MCI and the transition to AD suggests that this proneurotrophin is a potential disease biomarker. Novel therapeutics to treat NGF dysfunction include NGF gene therapy and the development of small molecule agonists for the cognate prosurvival NGF receptor TrkA and antagonists against the pan-neurotrophin p75NTR death receptor for the treatment of AD

The Long-Baseline Neutrino Experiment: Exploring Fundamental Symmetries of the Universe

The preponderance of matter over antimatter in the early Universe, the dynamics of the supernova bursts that produced the heavy elements necessary for life and whether protons eventually decay --- these mysteries at the forefront of particle physics and astrophysics are key to understanding the early evolution of our Universe, its current state and its eventual fate. The Long-Baseline Neutrino Experiment (LBNE) represents an extensively developed plan for a world-class experiment dedicated to addressing these questions. LBNE is conceived around three central components: (1) a new, high-intensity neutrino source generated from a megawatt-class proton accelerator at Fermi National Accelerator Laboratory, (2) a near neutrino detector just downstream of the source, and (3) a massive liquid argon time-projection chamber deployed as a far detector deep underground at the Sanford Underground Research Facility. This facility, located at the site of the former Homestake Mine in Lead, South Dakota, is approximately 1,300 km from the neutrino source at Fermilab -- a distance (baseline) that delivers optimal sensitivity to neutrino charge-parity symmetry violation and mass ordering effects. This ambitious yet cost-effective design incorporates scalability and flexibility and can accommodate a variety of upgrades and contributions. With its exceptional combination of experimental configuration, technical capabilities, and potential for transformative discoveries, LBNE promises to be a vital facility for the field of particle physics worldwide, providing physicists from around the globe with opportunities to collaborate in a twenty to thirty year program of exciting science. In this document we provide a comprehensive overview of LBNE's scientific objectives, its place in the landscape of neutrino physics worldwide, the technologies it will incorporate and the capabilities it will possess.Comment: Major update of previous version. This is the reference document for LBNE science program and current status. Chapters 1, 3, and 9 provide a comprehensive overview of LBNE's scientific objectives, its place in the landscape of neutrino physics worldwide, the technologies it will incorporate and the capabilities it will possess. 288 pages, 116 figure

Small Molecule, Non-Peptide p75NTR Ligands Inhibit Aβ-Induced Neurodegeneration and Synaptic Impairment

The p75 neurotrophin receptor (p75NTR) is expressed by neurons particularly vulnerable in Alzheimer's disease (AD). We tested the hypothesis that non-peptide, small molecule p75NTR ligands found to promote survival signaling might prevent Aβ-induced degeneration and synaptic dysfunction. These ligands inhibited Aβ-induced neuritic dystrophy, death of cultured neurons and Aβ-induced death of pyramidal neurons in hippocampal slice cultures. Moreover, ligands inhibited Aβ-induced activation of molecules involved in AD pathology including calpain/cdk5, GSK3β and c-Jun, and tau phosphorylation, and prevented Aβ-induced inactivation of AKT and CREB. Finally, a p75NTR ligand blocked Aβ-induced hippocampal LTP impairment. These studies support an extensive intersection between p75NTR signaling and Aβ pathogenic mechanisms, and introduce a class of specific small molecule ligands with the unique ability to block multiple fundamental AD-related signaling pathways, reverse synaptic impairment and inhibit Aβ-induced neuronal dystrophy and death

Interleukin-1 mediates ischaemic brain injury via distinct actions on endothelial cells and cholinergic neurons.

The cytokine interleukin-1 (IL-1) is a key contributor to neuroinflammation and brain injury, yet mechanisms by which IL-1 triggers neuronal injury remain unknown. Here we induced conditional deletion of IL-1R1 in brain endothelial cells, neurons and blood cells to assess site-specific IL-1 actions in a model of cerebral ischaemia in mice. Tamoxifen treatment of IL-1R1 floxed (fl/fl) mice crossed with mice expressing tamoxifen-inducible Cre-recombinase under the Slco1c1 promoter resulted in brain endothelium-specific deletion of IL-1R1 and a significant decrease in infarct size (29%), blood-brain barrier (BBB) breakdown (53%) and neurological deficit (40%) compared to vehicle-treated or control (IL-1R1fl/fl) mice. Absence of brain endothelial IL-1 signalling improved cerebral blood flow, followed by reduced neutrophil infiltration and vascular activation 24 h after brain injury. Conditional IL-1R1 deletion in neurons using tamoxifen inducible nestin-Cre mice resulted in reduced neuronal injury (25%) and altered microglia-neuron interactions, without affecting cerebral perfusion or vascular activation. Deletion of IL-1R1 specifically in cholinergic neurons reduced infarct size, brain oedema and improved functional outcome. Ubiquitous deletion of IL-1R1 had no effect on brain injury, suggesting beneficial compensatory mechanisms on other cells against the detrimental effects of IL-1 on endothelial cells and neurons. We also show that IL-1R1 signalling deletion in platelets or myeloid cells does not contribute to brain injury after experimental stroke. Thus, brain endothelial and neuronal (cholinergic) IL-1R1 mediate detrimental actions of IL-1 in the brain in ischaemic stroke. Cell-specific targeting of IL-1R1 in the brain could therefore have therapeutic benefits in stroke and other cerebrovascular diseases

Interpersonal psychotherapy for depressed adolescents, 2nd ed./ Laura Mufson (et al)

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