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Inicio Revista Colombiana de Psiquiatría Aplicación clínica de marcadores periféricos de respuesta a la terapia antide...
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Vol. 41. Issue 1.
Pages 165-184 (March 2012)
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Vol. 41. Issue 1.
Pages 165-184 (March 2012)
Artículos de revisión/actualización
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Aplicación clínica de marcadores periféricos de respuesta a la terapia antidepresiva: neurotrofinas y citocinas
Clinical Applications of Peripheral Markers of Response in Antidepressant Treatment: Neurotrophins and Cytokines
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Constanza Mendoza Bermúdez1,
Corresponding author
constanzamendozab@gmail.com

Correspondencia: Constanza Mendoza Bermúdez, Sargento Aldea No. 615 Chillán, Chile
1 Médica psiquiatra, estudiante del Doctorado en Salud Mental, Universidad de Concepción, Concepción, Chile
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Resumen
Introducción

Las teorías explicativas de la depresión han avanzado en las últimas décadas, desde la monoaminérgica hasta la alteración de la neurogénesis, pasando por la hipótesis neurohormonal, que incluye la disfunción de la respuesta inflamatoria. Actualmente existe un creciente interés por el desarrollo de biomarcadores que contribuyan diagnóstico y tratamiento adecuado.

Objetivos

Describir el rol de las neurotrofinas especialmente del factor neurotrópico derivado del cerebro (BDNF) y de las citocinas en la fisiopatología del trastorno depresivo; además, revisar y analizar la evidencia respecto de su aplicación clínica como biomarcadores de la terapia antidepresiva.

Método

Búsqueda de información relevante en diferentes bases de datos.

Resultados y conclusiones

En los últimos años ha crecido la evidencia de la alteración en la neurogénesis mediada por la expresión del BDNF en el hipocampo, en la fisiopatologia de la depresión y el respaldo en cuanto a su uso como biomarcador del diagnóstico y la efectividad del tratamiento antidepresivo. Existe menor información para otras neurotrofinas. También se observa un mayor interés respecto a la depresión como una “enfermedad inflamatoria”, relacionando también la “cascada” de citocinas con su patogénesis. Se ha reportado evidencia amplia acerca de la utilidad de algunas citosinas, especialmente de la IL-1 (interleucina 1), IL-6 (interleucina 6) y FNT (factor de necrosis tumoral) como biomarcadores de la respuesta farmacológica antidepresiva en humanos.

Palabras clave:
Factor neurotrófico derivado del cerebro
neurotrofinas
citocinas
biomarcadores
depresión
Abstract
Introduction

Explanatory theories of depression have advanced in recent decades from the monoaminergic hypothesis to neurogenesis alterations to the neurohormonal hypothesis that includes the dysfunction of the inflammatory response. Currently there is a growing interest in the development of biomarkers that can contribute to diagnosis and proper treatment.

Objectives

To describe the role of neurotrophins such as brain-derived neurotrophic factor (BDNF) and cytokines in the pathophysiology of depressive disorder in addition to reviewing and analyzing evidence about their clinical application as biomarkers of antidepressant therapy.

Method

Relevant data research in several databases.

Results and conclusions

In recent years evidence of alterations in neurogenesis mediated by the expression of BDNF in the hippocampus in the pathophysiology of depression has increased and there is ample evidence that BDNF is a marker of the diagnosis of depressive disorder and also of treatment effectiveness. There is little information about other neurotrophins. There has also been increased interest in relation to depression as an “inflammatory disease” and the link with cytokines in its pathogenesis. Evidence has been found for the usefulness of some cytokines especially IL-1 (interleukin 1), IL-6 (interleukin 6), and TNF (tumor necrosis factor) as biomarkers of antidepressant drug response in humans.

Key words:
Brain-derived neurotrophic factor
neurotrophins
cytokines
biomarkers
depression
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Referencias
[1]
JJ Schildkaut.
The catecholamine hypothesis of affective disorders: a review of supporting evidence.
Am J Psychiatry, 122 (1965), pp. 509-522
[2]
WE Bunney, J Davis.
Norepinephrine in depressive reactions: a review.
Arch Gen Psychiatry, 13 (1965), pp. 483-494
[3]
RS Duman, GR Heninger, EJ Nestler.
A molecular and cellular theory of depression.
Arch Gen Psychiatry, 54 (1997), pp. 597-606
[4]
RH Belmarker, G Agam.
Major depressive disorder mechanisms of disease.
N Engl J Med, 358 (2008), pp. 55-68
[5]
P Willner.
Chronic mild stress (CMS) revisited: consistency and behavioural-neurobiological concordance in the effects of CMS.
Neuropsychobiology, 52 (2005), pp. 90-110
[6]
A Beck.
The evolution of cognitive model of depression and its neurobiological correlates.
Am J Psychiatry, 165 (2008), pp. 969-977
[7]
M Rot, SJ Mathew, DS Charney.
Neurobiological mechanisms in major depressive disorder.
CMAJ, 180 (2009), pp. 309-313
[8]
H Manji.
Depression, III: Treatments.
Am J Psychiatry, 160 (2003), pp. 24
[9]
O Arias-Carrión, T Olivares-Buñuelos, R Drucker-Colín.
Neurogénesis en el cerebro adulto.
Rev Neurol, 44 (2007), pp. 541-550
[10]
JA Posener, L Wang, JL Price, et al.
Trazado dimensional del hipocampo en la depresión.
Am J Psychiatry, 160 (2003), pp. 83-89
[11]
M Ballmaier, KL Narr, AW Toga, et al.
Morfología del hipocampo y distinción entre la depresión de inicio tardío y la depresión de inicio precoz en ancianos.
Am J Psychiatry, 165 (2008), pp. 229-237
[12]
P Videbech, B Ravnkilde.
Hippocampal volume and depression: a meta-analysis of MRI studies.
Am J Psychiatry, 161 (2004), pp. 1957-1966
[13]
S Campbell, M Marriott, C Nahmias, et al.
Lower hippocampal volume in patients suffering from depression: a meta-analysis.
Am J Psychiatry, 161 (2004), pp. 598-607
[14]
K Martinowich, Bai Lu.
Interaction between BDNF and Serotonin: role in mood disorders.
Neuropsychopharmacology, 33 (2008), pp. 73-83
[15]
RM Thomas, G Hotsenpiller, DA Peterson.
Acute psychosocial stress reduces cell survival in adult hippocampal neurogenesis without altering proliferation.
J Neurosci, 27 (2007), pp. 2734-2743
[16]
E Nestler, M Barrot, RJ Dileone, et al.
Neurobiology of depression.
Neuron, 34 (2002), pp. 13-25
[17]
Z Kronfol, DG Remick.
Cytokines and the brain: implications for clinical psychiatry.
Am J Psychiatry, 157 (2000), pp. 683-694
[18]
K Hashimoto.
Brain-derived neurotrophic factor as a biomarker for mood disorders: An historical overview and future directions.
Psychiatry Clin Neurosci, 64 (2010), pp. 341-357
[19]
S Taleisnik.
Receptores celulares y la transmisión de señales. Temas de Biología Celular, Editorial Encuentro, (2006),
[20]
EJ Huang, LF Reichardt.
Neurotrophins: roles in neuronal development and function.
Annu Rev Neurosci, 24 (2001), pp. 677-736
[21]
UE Lang, MC Jockers-Scherûbl, R Hellweg.
State of the art of the neurotrophin hipótesis in psychiatric disorders: implications and limitations.
J Neural Transm, 111 (2004), pp. 387-411
[22]
Álamo C, López-Muñoz F, Cuenca E. Contribución de los antidepresivos y estabilizadores del humor al conocimiento de las bases neurobiológicas de los trastornos afectivos. Psiquiatría. Com (revista electronic). 1998;2. ISSN 1137-3148.
[23]
LM Monteggia, B Luikart, M Barrot, et al.
BDNF conditional knockouts show gender differences in depression related behaviors.
Biol Psychiatry, 61 (2007), pp. 187-197
[24]
T Frodl, C Shûle, G Schmitt, et al.
Association of the brain-derived neurotrophic factor val66met polymorphism with reduced hippocampal volumes in major depression.
Arch Gen Psychiatry, 64 (2007), pp. 410-416
[25]
YI Sheline, MH Gado, HC Kraemer.
Untreated Depression and hippocampal volume loss.
Am J Psychiatry, 160 (2003), pp. 1516-1518
[26]
C Pittenger, RS Duman.
Stress, depression, and neuroplasticity: a convergence of mechanisms.
Neuropsychopharmacology, 33 (2008), pp. 88-109
[27]
C Sandi, R Bisaz.
A model for the involvement of neural cell adhesion molecules in stress-related mood disorders.
Neuropsychopharmacology, 85 (2007), pp. 158-176
[28]
AA Russo-Neustadt, H Alejandre, C García, et al.
Hippocampal brain-derived neurotrophic factor expression following treatment with reboxetine, citalopram, and physical exercise.
Neuropsychopharmacology, 29 (2004), pp. 2189-2199
[29]
T Rantamâki, P Hendolin, A Kankaanpââ, et al.
Pharmacologically diverse antidepressants rapidly activate brain-derived neurotrophic factor receptor TrkB and nduce phospholipase-Cy signaling pathways in mouse brain.
Neuropsychopharmacology, 32 (2007), pp. 2152-2162
[30]
R Molteni, F Calabrese, A Cattaneo, et al.
Acute stress responsiveness of the neurotrophin bdnf in the rat hippocampus is modulated by chronic treatment with the antidepressant duloxetine.
Neuropsychopharmacology, 34 (2009), pp. 1523-1532
[31]
E Castrén, T Rantamâki.
The Role of BDNF and its receptors in depression and antidepressant drug action: reactivation and developmental plasticity.
Dev Neurobiol, 70 (2010), pp. 289-297
[32]
F Karege, G Perret, G Bondolfi, et al.
Decreased serum brain-derived neurotrophic factor levels in major depressed patients.
Psychiatry Res, 109 (2002), pp. 143-148
[33]
E Shimizu, K Hashimoto, N Okamura, et al.
Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants.
Biol Psychiatry, 54 (2003), pp. 70-75
[34]
A Deveci, O Aydemir, O Taskin, et al.
Serum BDNF levels in suicide attempters related to psychosocial stressors: a comparative study with depression.
Neuropsychobiology, 56 (2007), pp. 93-97
[35]
O Aydemir, A Deveci, F Taneli.
The effect of chronic antidepressant treatment on serum brain-derived neurotrophic factor levels in depressed patients: a preliminary study.
Prog Neuropsychopharmacol Biol Psychiatry, 29 (2005), pp. 261-265
[36]
AS Gonul, F Akdeniz, F Taneli, et al.
Effect of treatment on serum brain-derived neurotrophic factor levels in depressed patients.
Eur Arch Psychiatry Clin Neurosci, 255 (2005), pp. 381-386
[37]
S Sen, R Duman, G Sanacora.
Serum brain-derived neurotrophic factor, depression, and antidepressant medications: meta-analyses and implications.
Biol Psychiatry, 64 (2008), pp. 527-532
[38]
AR Brunoni, M Lopes, F Fregni.
A systematic review and meta-analysis of clinical studies on major depression and BDNF levels: Implications for the role of neuroplasticity in depression.
Int. J. Neuropsychopharmacol, 11 (2008), pp. 1169-1180
[39]
UE Lang, M Bajbouj, J Gallinat, et al.
Brain-derived neurotrophic factor serum concentrations in depressive patients during vagus nerve stimulation and repetitive transcranial magnetic stimulation.
Psychopharmacology, 187 (2006), pp. 56-59
[40]
JP Godbout, M Moreau, J Lestage, et al.
Aging exacerbates depresssion-like behavior in mice in response to activation of the peripheral innate inmune system.
Neuropsychopharmacology, 33 (2008), pp. 2341-2351
[41]
R Grassi-Oliveira, E Brietzke, JC Pezzi, et al.
Increased soluble tumor necrosis factor-alpha receptors in patients with major depressive disorder.
Psychiatry Clin Neurosci, 63 (2009), pp. 202-208
[42]
M Maes, HY Meltzer, E Bosmans, et al.
Increased plasma concentrations of interleukin-6, soluble interleukin-6, soluble interleukin-2 and transferrin receptor in major depression.
J Affect Disord, 34 (1995), pp. 301-309
[43]
M Maes.
Major depression and activation of the inflammatory response syndrome.
Adv Exp Med Biol, 461 (1999), pp. 25-46
[44]
E Domenici, DR Willé, F Tozzi, et al.
Plasma protein biomarkers for depression and schizophrenia by multi analyte profiling of case-control collections.
Plos One, 5 (2010), pp. 1-12
[45]
JK Kiecolt-Glaser, L McGuire, TR Robles, et al.
Emotions, morbidity, and mortality: new perspectives from psychoneuroimmunology.
Annu Rev Psychol, 53 (2002), pp. 83-107
[46]
M Rothermundt, V Arolt, M Peters, et al.
Inflammatory markers in major depression and melancholia.
J Affect Disord, 63 (2001), pp. 93-102
[47]
J Schlatter, F Ortuño, J Pla, et al.
Parámetros de inmunidad natural como marcadores biológicos de la depresión.
Psiquiatría Biológica, 13 (2006), pp. 158-166
[48]
YW-Y Yu, T-J Chen, C-J Hong, et al.
Association study of the interleukin-1beta (C-511T) genetic polymorphism with major depressive disorder, associated symptomatology, and antidepressant response.
Neuropsychopharmacology, 28 (2003), pp. 1182-1185
[49]
AJ Thomas, S Davis, C Morris, et al.
Increase in interleukin-1β in late-life depression.
Am J Psychiatry, 162 (2005), pp. 175-177
[50]
S Lanquillon, JC Krieg, U Bening-Abu-Shach, et al.
Cytokine production and treatment response in major depressive disorder.
Neuropsychopharmacology, 22 (2000), pp. 370-379
[51]
HD Schmidt, RS Duman.
Peripheral BDNF produces antidepressant-like effects in cellular and behavioral models.
Neuropsychopharmacology, 10 (2010), pp. 1-14

Conflictos de interés: La autora manifiesta que no tiene conflictos de interés en este artículo.

Copyright © 2012. Asociación Colombiana de Psiquiatría
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