2 REGLAMENTO RM 0912-2024 DE MODALIDADES DE GRADUACIÓN_.pptx
Depresion como enfermedad sistemica
1. DESORDENES AFECTIVOS ANDREA MARQUEZ LOPEZ MATO Instituto de Psiquiatría Biológica Integral www. ipbi. com. ar Asociación Argentina de Psiquiatría Biológica www. aapb. org. ar
19. CASO M E M ESCUELA DE MEDICINA NUCLEAR I nst . NEUROCIENCIAS y SALUD MENTAL DRA. ROXANA GALENO DR. MANUEL GUIRAO MENDOZA ARGENTINA Alteraciones Neurofisiológicas trastorno depresivo PET
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22. ESTRÉS DEPRESIÓN INSUFICIENCIA CEREBRO VASCULAR REPETICION DE EPISODIOS DEPRESIVOS FACTORES GENÉTICOS Y DE DESARROLLO FALLA DE LA SEÑAL NEUROPLASTICA Glutamato NMDA Ca 2+ PROGRESIÓN DE LAS ENFERMEDADES ROS Cortisol GR Capacidad Energética Litio Akt BAD Bcl-x ROS Ca 2+ Litio VPA Bcl-2 Citocromo C RSK-2 Ras GTP Raf MEK ERK CREB Bcl-2 Antidepresivos GSK-3 Litio 5HT NA trkB trkB BDNF P P trkB trkB BDNF P P
23. 5HT y DEPRESION Reducción en los niveles 5-HIAA en LCR Reducción de la unión de transportadores de serotonina plaquetarios Disminución de síntomas m CPP Lopez Mato A. PINE II, Polemos 04 NA y DEPRESION Reducción de los sitios de unión plaquetarios alpha-2 Respuesta hormonal Clonidina GH chata Disminución atenuado de MOPEG PEPTIDOS y DEPRESION Hiperactividad CRH Hipoactividad TRH Hipoactividad GH, GnRH D isminución del T ono A minérgico
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34. GTP GDP Trk B Trk A NGF BDNF Resiliencia celular ADs GCs NMDA Glu R. M. Zaratiegui. Tomado de Manji y col., Mol Psychiatry 2000, Nature Medicine 2001, Manji & Duman, Psychopharmacology Bull 2001 GRB2 SOS RasGTP Raf MEK ERK GSk-3 PI3-K Akt CREB Bcl-2 RSK-2 Elk-1 -catenina GR BDNF Isquemia Factores genéticos y ambientales Episodios afectivos Ca Trk B CASPASA 9 Apaf 1 Ruta de las CASPASAS m BAX Bcl-x BAD Citocromo C p53 Bcl-2
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52. CRH LCR en distintos Trastornos Psiquiátricos CSF CRH (pg/ml) 120 80 40 0 160 Control Alzheimer Manía Depresión Esquizofrenia Alzheimer y Depresión
53. Reducción en las concentraciones de CRH en LCR después de TEC * 0 20 40 60 80 100 CRF (pg/mL ± SEM) Pre-TEC Post-TEC
54. Tratamiento crónico con venlafaxina en monos reduce CRH en LCR *p 0.05 320 160 0 CSF CRH (pg/mL) Vehículo Venlafaxina (15 mg/kg/día) n=12 n=12 * Kalin et al. Observaciones no publicadas.
96. Fenotipo vulnerable Hiperactividad eje CL HHPA Hiperactividad NA Disminucion neurogénesis Aumento neurotoxicidad Predisposición genética Eventos adversos tempranos Vulnerabilidad al Stress ante Eventos Vitales Alteraciones Biológicas Cambios Conductuales y Emocionales - Depresión - Ansiedad Eventos Vitales o Traumas de Adultez Nemeroff
97. Fenotipo vulnerable Lesión Primaria Sistema CRH NA y 5HT Neuropéptidos Sistema Inmune DA ? ACh ? TRH / GH ? Lopez Mato, 04
98. Fenotipo vulnerable Hiperactividad eje CL HHPA Hiperactividad NA Disminucion neurogénesis Aumento neurotoxicidad Predisposición genética Eventos adversos tempranos Vulnerabilidad al Stress ante Eventos Vitales Alteraciones Biológicas Cambios Conductuales y Emocionales - Depresión - Ansiedad Eventos Vitales o Traumas de Adultez
99. INFLUENCE OF LIFE STRESS ON DEPRESSION: Moderation by a Polymorphism in the 5-HTT Gene Avshalom Caspi,1,2 Karen Sugden,1 Terrie E. Mofett,1,2* Alan Taylor,1 Ian W. Craig,1 Hona Lee Harrington,2 Joseph McClay,1 Jonathan Mill,1 Judy Martin,3 Antony Braithwaite,4 Richie Poulton,3 1 Medical Research Council Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King’s College London, UK. 2 Department of Psychology, University of Wisconsin, Madison, USA 3 Dunedin School of Medicine, University of Otago, Dunedin, NZ 4 Department of Pathology, University of Otago, Dunedin, NZ
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103. Fenotipo vulnerable Hiperactividad eje CL HHPA Hiperactividad NA Disminución neurogénesis Aumento neurotoxicidad Predisposición genética Eventos adversos tempranos Vulnerabilidad al Stress ante Eventos Vitales Alteraciones Biológicas Cambios Conductuales y Emocionales - Depresión - Ansiedad Eventos Vitales o Traumas de Adultez
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Notas del editor
To examine the role of NA in the pathophysiology of depression, much evidence was gathered over time. Among pharmacological models, the syndrome induced by reserpine has been the most widely used. The interest came from the observation that animals who were exposed to reserpine, which depletes both NA and 5-HT, were reported to induce depression. More evidence of the role of NA in depression was detected when the first antidepressant drugs were introduced, which were affecting the NA system. Furthermore, Bipolar I patients had low urinary MHPG levels, a metabolite of NA, and patients with lower MHPG levels responded to NA uptake blockers whereas high MHPG excretors did not. On the other hand, some unipolar depressed patients had significantly higher MHPG levels in comparison with the Bipolar I depressed patients and controls.
Later on, in the early '80s, a significant positive relationship between the urinary levels of MHPG and the plasma cortisol levels in depressed patients was detected. Several studies point to activation of peripheral NA systems in depressed patients with pronounced HPA axis activity. The MHPG-cortisol relationships suggest a relationship between increased activity of both the HPA axis and central NA systems. 2 -Receptors control release of growth hormone (GH). In depressed patients, blunted GH responses to clonidine have been observed. Of particular interest is the observation that the blunted GH response to clonidine may be a trait marker that persists in depressed patients after recovery. Considerable attention has been paid not only to 2 -receptors but also to the 2 -receptors in depression. These receptors have been studied extensively, also via the brains of suicide victims. It turned out that the availability of both receptors was increased in these patients, whereas in response to NA drugs, a down-regulation of these receptors could be detected.
ERK: Extracellular signal regulated MAP kinasa Rsk: Ribosomal 6 kinasa SH2: src homology – 2 domain; SHc: src homology containing protein SOS-GRB2: proteínas de ligazón; GRB2: growth factor binding pr 2 Raf: serina treosina kinasa Ras: una pequeña proteína C 3 tipos de MAP kinasa: ERKs, JNK y p38 PI3: fosfoinositol 3 kinasa, se liga con IRS (insuline responding sustrate) Elk 1: factor de transcripción Trk = tropomiosin-related receptor kinase