Views
8 years ago

Psicofarmacología 73

  • Text
  • Verde
  • Alfa
  • Serotonina
  • Dopamina
  • Memoria
  • Concentracion
  • Estres
  • Teanina
  • Delirio
  • Dopaminergicos
  • Neuropsiquiatricos
  • Parkinson
  • Neuronal
  • Genes
  • Adictivo
  • Epigenetica
  • Adiccion
Revista Latinoamericana de Psicofarmacología y Neurociencia.

Referencias

Referencias bibliográficas 1. Büttner A. 2011. Review: The neuropathology of drug abuse. Neuropathol Appl Neurobiol. 37(2):118-34. 2. Nestler, E. J. 2001. Molecular basis of longterm plasticity underlying addiction. Nature Rev. Neurosci. 2, 119–128. 3. Andersen, S. L. & Teicher, M. H. 2009.Desperately driven and no brakes: developmental stress exposure and subsequent risk for substance abuse. Neurosci.Biobehav. Rev. 33, 516–524. 4. Malanga, C. J. & Kosofsky, B. E. 2003Does drug abuse beget drug abuse? Behavioral analysis of addiction liability in animal models of prenatal drug exposure. Brain Res. Dev. Brain Res. 147, 47–57. 5. Nestler, E. J. 2008. Review. Transcriptional mechanisms of addiction: role of DeltaFosB. Phil. Trans. R. Soc. Lond. B 363, 3245–3255. 6. Jorissen, H. J. et al. 2007. Dimerization and DNA-binding properties of the transcription factor DeltaFosB. Biochemistry 46, 8360–8372. 7. Hiroi, N. et al. 1997. FosB mutant mice: loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine’s psychomotor and rewarding effects. Proc. Natl Acad. Sci. USA 94,10397–10402. 8. Perrotti, L. I. et al. 2008. Distinct patterns of DeltaFosB induction in brain by drugs of abuse. Synapse 62, 358–369. 9. Carle, T. L. et al. 2007. Proteasome-dependent and -independent mechanisms for FosB destabilization: identification of FosB degron domains and implications for DeltaFosB stability. Eur. J. Neurosci. 25, 3009–3019. 10. Ulery, P. G., Rudenko, G. & Nestler, E. J. 2006. Regulation of DeltaFosB stability by phosphorylation. J. Neurosci. 26, 5131–5142. 11. Kelz, M. B. et al. 1999. Expression of the transcription factor deltaFosB in the brain controls sensitivity to cocaine.Nature 401, 272–276. 12. Zachariou, V. et al. 2006. An essential role for DeltaFosB in the nucleus accumbens in morphine action. Nature Neurosci. 9, 205–211. 13. Colby, C. R., Whisler, K., Steffen, C., Nestler, E. J. & Self, D. W. 2003. Striatal cell type-specific overexpression of DeltaFosB enhances incentive for cocaine. J. Neurosci. 23, 2488–2493. 14. Wallace, D. L. et al. 2008. The influence of DeltaFosB in the nucleus accumbens on natural reward-related behavior. J. Neurosci. 28, 10272–10277. 15. Teegarden, S. L., Nestler, E. J. & Bale, T. L. 2008. Delta FosBmediated alterations in dopamine signaling are normalized by a palatable high-fat diet. Biol.Psychiatry 64, 941–950. 16. Cao, J. L. et al. 2010. Essential role of the cAMP-cAMP response-element binding protein pathway in opiateinduced homeostatic adaptations of locus coeruleus neurons. Proc. Natl Acad. Sci. USA 107, 17011–17016. 17. Robison AJ, Nestler EJ. 2011. Transcriptional and epigenetic mechanisms of addiction. Nat Rev Neurosci. 12;12(11):623-37. 18. McClung, C. A. & Nestler, E. J. Regulation of gene expression and cocaine reward by CREB and DeltaFosB. Nature Neurosci.6, 1208–1215 (2003). 19. Renthal, W. et al. Genome-wide analysis of chromatin regulation by cocaine reveals a role for sirtuins. Neuron 62, 335–348 (2009). 20. Bibb, J. A. et al. Effects of chronic exposure to cocaine are regulated by the neuronal protein Cdk5. Nature 410, 376–380 (2001). 21. Russo, S. J. et al. 2010. The addicted synapse: mechanisms of synaptic and structural plasticity in nucleus accumbens. Trends Neurosci. 33, 267–276. 22. Robinson, T. E. & Kolb, B. 2004. Structural plasticity associated with exposure to drugs of abuse.Neuropharmacology 47, 33–46. 23. Kalivas, P. W. 2009. The glutamate homeostasis hypothesis of addiction. Nature Rev. Neurosci.10, 561–572. 24. Russo, S. J., Mazei-Robison, M. S., Ables, J. L. & Nestler, E. J. 2009. Neurotrophic factors and structural plasticity in addiction. Neuropharmacology 56, 73–82. 25. Huang, Y. H. et al. 2008. CREB modulates the functional output of nucleus accumbens neurons: a critical role of N‐methyl‐D-aspartate glutamate receptor (NMDAR) receptors. J. Biol. Chem. 283, 2751–2760. 26. Carlezon, W. A. Jr, Duman, R. S. & Nestler, E. J. 2005. The many faces of CREB. Trends Neurosci. 28, 436–445. 27. Edwards, S., Graham, D. L., Bachtell, R. K. & Self, D. W. 2007. Region-specific tolerance to cocaine-regulated cAMP-dependent protein phosphorylation following chronic self-administration. Eur. J. Neurosci. 25, 2201–2213. 28. Carlezon, W. A. Jr. et al. 1998. Regulation of cocaine reward by CREB. Science 282, 2272–2275. 29. Meffert, M. K., Chang, J. M., Wiltgen, B. J., Fanselow, M. S. & Baltimore, D. 2003. NF‐κB functions in synaptic signaling and behavior. Nature Neurosci. 6, 1072–1078. 30. Russo, S. J. et al. 2009. Nuclear factor κB signaling regulates neuronal morphology and cocaine reward. J. Neurosci. 29, 3529–3537. 31. Pulipparacharuvil, S. et al. 2008. Cocaine regulates MEF2 to control synaptic and behavioral plasticity. Neuron 59, 621–633. 32. Jenuwein, T. & Allis, C. D. 2001. Translating the histone code. Science 293, 1074–1080. 33. McQuown, S. C. & Wood, M. A. 2010. Epigenetic regulation in substance use disorders. Curr. Psychiatry Rep. 12, 145–153. 34. Kumar, A. et al. 2005. Chromatin remodeling is a key mechanism underlying cocaineinduced plasticity in striatum. Neuron 48, 303–314. 35. Pandey, S. C., Ugale, R., Zhang, H., Tang, L. & Prakash, A. 2008. Brain chromatin remodeling: a novel mechanism of alcoholism. J. Neurosci. 28, 3729–3737. 36. Khare, M., Taylor, A. H., Konje, J. C. & Bell, S. C. 2006. Delta 9‐tetrahydroannabinol inhibits cytotrophoblast cell proliferation and modulates gene transcription. Mol. Hum. Reprod. 12, 321–333 (). 37. Renthal, W. et al. 2007. Histone deacetylase 5 epigenetically controls behavioral adaptations to chronic emotional stimuli. Neuron 56, 517–529. 38. Levine, A. A. et al. 2005. CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum. Proc. Natl Acad. Sci. USA 102, 19186–19191. 39. Levine, A. A. et al. 2005. CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum. Proc. Natl Acad. Sci. USA 102, 19186–19191. 40. Maze, I. et al. Cocaine dynamically regulates heterochromatin and repetitive element unsilencing in nucleus accumbens. 2011Proc. Natl Acad. Sci. USA 108, 3035–3040. 20 // EDITORIAL SCIENS

Psicofarmacología 12:73, Abril 2012 Dr. Guillermo Delmonte Médico psiquiatra universitario, Universidad de Buenos Aires (UBA), Miembro adherente de la Asociación Psicoanalítica Argentina (APA), Magister en Psiconeurofarmacología, Universidad Favaloro, Miembro de la Asociación Psiquiátrica Americana (APA), Profesor titular de Neurociencias III de la Facultad de Psicología, Universidad del Salvador (USAL). Fecha de recepción: 27 de enero de 2012 Fecha de aceptación: 21 de marzo de 2012 Aspectos sintomáticos neuropsiquiátricos asociados a la enfermedad de Parkinson con demencia Symptomatic and Neuropsychiatric Aspects Associated with Parkinson’s Disease with Dementia Resumen Como es sabido, la enfermedad de Parkinson suele presentar una evolución crónica, prolongada, e insidiosa. Para la cual aún no se disponen de terapéuticas efectivas que curen a dicha enfermedad, si no se posee un arsenal de fármacos (agonistas dopaminérgicos) capaces de mitigar los síntomas, mejorar y prolongar la calidad de vida y enlentecer el propio desarrollo de la enfermedad, que lleva hacia un deterioro profundo de la motricidad, funcionalidad y de las funciones neurocognitivas. También es sabida la asociación de la enfermedad de Parkinson con la demencia por la misma enfermedad. Pero a lo largo de ella, con o sin demencia, se suelen presentar en una proporción importante, una serie de síntomas asociados neuropsiquiátricos (NP), y neuroconductuales (NC) que hay que diferenciar si son producto de la propia enfermedad de Parkinson, o son desencadenados por el tratamiento. Algunos de estos síntomas asociados, los más importantes en cuanto a su frecuencia y gravedad sobre todo asociados a demencia son, depresión, excitación psicomotriz, ideación patológica, delirios, alucinaciones visuales, síndrome confusional (delirium), trastornos del sueño, ansiedad, apatía. Estos síntomas agravan la evolución de la propia enfermedad de Parkinson y la demencia asociada haciendo que su pronóstico se torne más desfavorable, y más deteriorante, afectando también a los cuidadores y alterando la calidad de vida del paciente y su entorno. En este trabajo me propongo dar una noción básica de dichos trastornos para su rápido reconocimiento y tratamiento, teniendo en cuenta la posible polifarmacia en estos pacientes, con las implicancias de las interacciones farmacológicas. La rápida resolución de estos síntomas asociados a la EP, con o sin demencia redundará en un menor deterioro funcional del paciente, mejorando su pronóstico y la calidad de vida del propio paciente y sus cuidadores. Palabras clave Enfermedad de Parkinson (EP) – Trastornos neuropsiquiátricos y neuroconductuales (NP) y (NC) – Agonistas dopaminérgicos – Delirium. Abstract As it is known, Parkinson’s Disease may have a chronic, prolonged and insidious progression, for which there are still no effective treatments available to cure it, but a series of drugs (dopamine agonists) which are capable of relieving symptoms and prolonging the patient’s quality of life, and slowing the development of the disease that leads to a deep worsening of the individual’s motility, functionality and neurocognitive functions. The association between Parkinson’s Disease and dementia caused by the first disease is also known. But throughout the disease, whether it is accompanied with dementia or not, a series of associated neuropsychiatric (NP) and neurobehavioral (NB) symptoms may appear in large proportion. These symptoms need to be identified as resulting from Parkinson ’s Disease itself or the treatment. Among some of the associated symptoms, the most relevant ones in terms of frequency and severity, which are mainly associated to dementia, are depression, psychomotor agitation, suicidal ideation, delirium, visual hallucinations, confusional syndrome (delirium), sleep disorders, anxiety and apathy. These symptoms aggravate the progression of Parkinson’s Disease and associated dementia, making its prognosis more unfavorable and deteriorating, and also affecting the caregivers and the quality of life of patients and the people around them. In this article I shall set out to provide the basic concept of such disorders, taking into account the possible polypharmacy among these patients, as well as the implications of pharmacological interactions. The prompt resolution of the symptoms associated with PD with or without dementia shall result in a less functional deterioration of patients and the improvement of their and their caregivers’ condition and quality of life. Key words Parkinson’s Disease (PD) – Neuropsychiatric (NP) and neurobehavioral (NB) disorders – Dopamine agonists – Delirium. Delmonte, Guillermo. “Aspectos sintomáticos neuropsiquiátricos asociados a la enfermedad de Parkinson con demencia” Psicofarmacología 2012;73:23-34. Puede consultar otros artículos publicados por los autores en la revista Psicofarmacología en www.sciens.com.ar EDITORIAL SCIENS // 23

Biblioteca

Av. García del Río 2585 Piso 12 A - C.A.B.A
+54 11 2092 1646 | info@sciens.com.ar

Editorial Sciens, Todos los Derechos Reservados 2015