medigraphic.com
Instituto Nacional de Neurología y Neurocirugía

2016, Número 4

<< Anterior Siguiente >>

Arch Neurocien 2016; 21 (4)


Mecanismos de neuroprotección de la deshidroepiandrosterona y su impacto cognitivo-conductual en la enfermedad de Parkinson

Pérez-Neri I

Idioma: Español
Referencias bibliográficas: 36
Paginas: 73-76
Archivo PDF: 101.91 Kb.


FRAGMENTO

La deshidroepiandrosterona (DHEA) es un esteroide que puede modular diferentes sistemas de neurotransmisión asociados con trastornos neurológicos y psiquiátricos. En los humanos, su concentración plasmática aumenta gradualmente hasta alcanzar sus máximos niveles durante la juventud y posteriormente se reduce hasta alcanzar valores mínimos en la edad avanzada. Por esta razón, se ha asociado la deficiencia en la secreción de este esteroide con el aumento en la prevalencia de trastornos neurodegenerativos conforme avanza la edad en los humanos.
El sistema dopaminérgico puede ser modulado por la DHEA posiblemente a través de la inhibición de monoamino oxidasa, lo cual podría tener implicaciones para la neuroprotección en los modelos experimentales de la enfermedad de Parkinson.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. 1.Pérez-Neri I, Montes S, Ojeda-López C, Ramírez-Bermúdez J, Ríos C. Modulation of neurotransmitter systems by dehydroepiandrosterone and dehydroepiandrosterone sulfate: Mechanism of action and relevance to psychiatric disorders. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2008 32(5):1118–30.

  2. 2.Hinson JP, Raven PW. DHEA deficiency syndrome: a new term for old age? J endocrinology 1999;163(1):1–5.

  3. 3.Pérez-Neri I, Méndez-Sánchez I, Montes S, Ríos C. Acute dehydroepiandrosterone treatment exerts different effects on dopamine and serotonin turnover ratios in the rat corpus striatum and nucleus accumbens. Progress in Neuro-Psychopharmacology and Biological Psychiatry 2008 32(6):1584–9.

  4. 4.Matsubara K, Senda T, Uezono T, Awaya T, Ogawa S, Chiba K, et al. L-Deprenyl prevents the cell hypoxia induced by dopaminergic neurotoxins, MPP+ and β-carbolinium: a microdialysis study in rats. Neuroscience letters 2001;302(2):65–8.

  5. 5.Tomas-Camardiel M, Sanchez-Hidalgo MC, Del Pino MS, Navarro A, Machado A, Cano J. Comparative study of the neuroprotective effect of dehydroepiandrosterone and 17β-estradiol against 1-methyl-4-phenylpyridium toxicity on rat striatum. Neuroscience 2002;109(3):569–84.

  6. 6.Aragno M, Parola S, Brignardello E, Mauro A, Tamagno E, Manti R, et al. Dehydroepiandrosterone prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats. Diabetes 2000;49(11):1924–31.

  7. 7.Aragno M, Tamagno E, Gatto V, Brignardello E, Parola S, Danni O, et al. Dehydroepiandrosterone protects tissues of streptozotocin-treated rats against oxidative stress. Free Radical Biology and Medicine 1999;26(11):1467–74.

  8. 8.Bastianetto S, Ramassamy C, Poirier J, Quirion R. Dehydroepiandrosterone (DHEA) protects hippocampal cells from oxidative stress-induced damage. Molecular Brain Research 1999 ;66(1-2):35–41.

  9. 9.Brignardello E, Gallo M, Aragno M, Manti R, Tamagno E, Danni O, et al. Dehydroepiandrosterone prevents lipid peroxidation and cell growth inhibition induced by high glucose concentration in cultured rat mesangial cells. J Endocrinol 2000 ;166(2):401–6.

  10. 10.Tamagno E, Guglielmotto M, Bardini P, Santoro G, Davit A, Di Simone D, et al. Dehydroepiandrosterone reduces expression and activity of BACE in NT2 neurons exposed to oxidative stress. Neurobiol Dis 2003 ;14(2):291–301.

  11. 11.Gao J, Sun H-Y, Zhu Z-R, Ding Z, Zhu L. Antioxidant effects of dehydroepiandrosterone are related to up- regulation of thioredoxin in SH-SY5Y cells. Acta Biochim Biophys Sin (Shanghai) 2005;37(2):119–25.

  12. 12.Takahashi H, Nakajima A, Sekihara H. Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) inhibit the apoptosis in human peripheral blood lymphocytes. J Steroid Biochem Mol Biol 2004 ;88(3):261–4.

  13. 13.González-Polo RA, Soler G, Rodríguezmartín A, Morán JM, Fuentes JM. Protection against MPP+ neurotoxicity in cerebellar granule cells by antioxidants. Cell Biol Int 2004;28(5):373–80.

  14. 14.Kalivendi SV, Kotamraju S, Cunningham S, Shang T, Hillard CJ, Kalyanaraman B. 1-Methyl-4- phenylpyridinium (MPP+)-induced apoptosis and mitochondrial oxidant generation: role of transferrin- receptor-dependent iron and hydrogen peroxide. Biochem J 2003 1;371(Pt 1):151–64.

  15. 15.Drechsel DA, Liang L-P, Patel M. 1-methyl-4-phenylpyridinium-induced alterations of glutathione status in immortalized rat dopaminergic neurons. Toxicol Appl Pharmacol 2007 1;220(3):341–8.

  16. 16.Xu Q, Kanthasamy AG, Reddy MB. Neuroprotective effect of the natural iron chelator, phytic acid in a cell culture model of Parkinson’s disease. Toxicology 2008 ;(1-2):101–8.

  17. 17.Tian Y-Y, Jiang B, An L-J, Bao Y-M. Neuroprotective effect of catalpol against MPP(+)-induced oxidative stress in mesencephalic neurons. Eur J Pharmacol 2007 30;568(1-3):142–8.

  18. 18.Pain S, Barrier L, Deguil J, Milin S, Piriou A, Fauconneau B, et al. A cell-permeable peptide inhibitor TAT- JBD reduces the MPP+-induced caspase-9 activation but does not prevent the dopaminergic degeneration in substantia nigra of rats. Toxicology 2008 14;243(1-2):124–37.

  19. 19.Rubio-Osornio M, Montes S, Pérez-Severiano F, Aguilera P, Floriano-Sánchez E, Monroy-Noyola A, et al. Copper reduces striatal protein nitration and tyrosine hydroxylase inactivation induced by MPP+ in rats. Neurochem Int 2009 ;54(7):447–51.

  20. 20.Ferro MM, Bellissimo MI, Anselmo-Franci JA, Angellucci MEM, Canteras NS, Da Cunha C. Comparison of bilaterally 6-OHDA- and MPTP-lesioned rats as models of the early phase of Parkinson’s disease: histological, neurochemical, motor and memory alterations. J Neurosci Methods 2005 15;148(1):78–87.

  21. 21.Leng A, Yee BK, Feldon J, Ferger B. Acoustic startle response, prepulse inhibition, and spontaneous locomotor activity in MPTP-treated mice. Behav Brain Res 2004 5;154(2):449–56.

  22. 22.Boll MC, Sotelo J, Otero E, Alcaraz-Zubeldia M, Rios C. Reduced ferroxidase activity in the cerebrospinal fluid from patients with Parkinson’s disease. Neurosci Lett 1999 23;265(3):155–8.

  23. 23.Dexter DT, Wells FR, Lee AJ, Agid F, Agid Y, Jenner P, et al. Increased nigral iron content and alterations in other metal ions occurring in brain in Parkinson’s disease. Journal of neurochemistry 1989;52(6):1830–6.

  24. 24.Alcaraz-Zubeldia M, Montes S, Rıos C. Participation of manganese-superoxide dismutase in the neuroprotection exerted by copper sulfate against 1-methyl 4-phenylpyridinium neurotoxicity. Brain research bulletin 2001;55(2):277–9.

  25. 25.Braak H, Rüb U, Del Tredici K. Cognitive decline correlates with neuropathological stage in Parkinson’s disease. J Neurol Sci 2006 ;248(1-2):255–8.

  26. 26.Burn DJ, Tröster AI. Neuropsychiatric complications of medical and surgical therapies for Parkinson’s disease. J Geriatr Psychiatry Neurol 2004;17(3):172–80.

  27. 27.Rees PM, Fowler CJ, Maas CP. Sexual function in men and women with neurological disorders. Lancet 2007 ;369(9560):512–25.

  28. 28.Vallée M, Mayo W, Le Moal M. Role of pregnenolone, dehydroepiandrosterone and their sulfate esters on learning and memory in cognitive aging. Brain Res Rev 2001;37(1):301–12.

  29. 29.Lewis SJG, Slabosz A, Robbins TW, Barker RA, Owen AM. Dopaminergic basis for deficits in working memory but not attentional set-shifting in Parkinson’s disease. Neuropsychologia 2005;43(6):823–32.

  30. 30.Maia AF, Pinto AS, Barbosa ER, Menezes PR, Miguel EC. Obsessive-compulsive symptoms, obsessive-compulsive disorder, and related disorders in Parkinson’s disease. J Neuropsychiatry Clin Neurosci 2003;15(3):371–4.

  31. 31.Weintraub D, Siderowf AD, Potenza MN, Goveas J, Morales KH, Duda JE, et al. Association of dopamine agonist use with impulse control disorders in Parkinson disease. Arch Neurol 2006 ;63(7):969–73.

  32. 32.Valls-Solé J, Muñoz JE, Valldeoriola F. Abnormalities of prepulse inhibition do not depend on blink reflex excitability: a study in Parkinson’s disease and Huntington’s disease. Clin Neurophysiol 2004;115(7):1527–36.

  33. 33.Bradley KC, Boulware MB, Jiang H, Doerge RW, Meisel RL, Mermelstein PG. Changes in gene expression within the nucleus accumbens and striatum following sexual experience. Genes Brain Behav 2005;4(1):31–44.

  34. 34.O’Neill M, Brown VJ. The effect of striatal dopamine depletion and the adenosine A2A antagonist KW- 6002 on reversal learning in rats. Neurobiol Learn Mem 2007 ;88(1):75–81.

  35. 35.Campbell LE, Hughes M, Budd TW, Cooper G, Fulham WR, Karayanidis F, et al. Primary and secondary neural networks of auditory prepulse inhibition: a functional magnetic resonance imaging study of sensorimotor gating of the human acoustic startle response. Eur J Neurosci 2007 ;26(8):2327–33.

  36. 36.Pittenger C, Fasano S, Mazzocchi-Jones D, Dunnett SB, Kandel ER, Brambilla R. Impaired bidirectional synaptic plasticity and procedural memory formation in striatum-specific cAMP response element-binding protein-deficient mice. J Neurosci 2006 ;26(10):2808–13.




2020     |     www.medigraphic.com