Falla mitocondrial oxidativa inducida por estrés y sustancias vasoactivas como los iniciadores dominantes de la patología favorecen la reclasificación de la enfermedad de Alzheimer como una Vasocognopatía

Oxidative stress-induced mitochondrial failure and vasoactive substances as key initiators of pathology favor the reclassification of Alzheimer Disease as a vasocognopathy

Publicado 2008-12-31

Abrir | Descargar
PDF FLIP HTML
Número
Vol. 6 Núm. 10 (2008)
Sección
Articulo de Revisión
Cómo citar
morales et al., ludis. (2008). Falla mitocondrial oxidativa inducida por estrés y sustancias vasoactivas como los iniciadores dominantes de la patología favorecen la reclasificación de la enfermedad de Alzheimer como una Vasocognopatía. REVISTA NOVA , 6(10). https://doi.org/10.22490/24629448.408
DOI

https://doi.org/10.22490/24629448.408
Dimensions
PlumX
Licencia

Licencia Creative Commons
NOVA por http://www.unicolmayor.edu.co/publicaciones/index.php/nova se distribuye bajo una Licencia Creative Commons Atribución-NoComercial-SinDerivar 4.0 Internacional.

Así mismo,  los autores mantienen sus derechos de propiedad intelectual sobre los artículos.  

ludis morales et al.
    Mostrar biografía de los autores
    La enfermedad de Alzheimer y el accidente cerebrovascular son dos causas que conducen a la demencia relativa a la edad. El aumento de la evidencia apoya la idea de que la hipoperfusión crónica es sobre todo responsable de la patogénesis que es la base de ambos procesos de la enfermedad. La hipoperfusión se asocia al desequilibrio oxidativo, en gran parte debido a las especies reactivas del oxígeno, que se asocian a otros desórdenes degenerativos relativos a la edad. Evidencia reciente indica que un estímulo crónico de lesión induce la hipoperfusión vista en la microcirculación de las regiones vulnerables del cerebro. Esto conduce a la falta de energía, manifestada por daño a la ultraestructura mitocondrial. Los trastornos mitocondriales conducen a la formación de una gran cantidad de mitocondrias “hipoxicas” electrón-densas y causan la sobreproducción de deleciones en el ADN mitocondrial (mtADN), debidas muy probablemente a la ruptura de la doble hélice. Además, estas anormalidades mitocondriales coexisten con la actividad redox incrementada, peroxidación lipídica y la oxidación del ARN, que son características bien establecidas de la patología de Alzheimer, antes de la aparición de los depósitos del b-amiloide.   En la enfermedad de Alzheimer, el estrés oxidativo ocurre dentro de los varios compartimientos celulares y dentro de ciertos tipos de células más que en otros, a saber el endotelio vascular, que se asocia a daño aterosclerótico, así como en las neuronas piramidales y glia. Es interesante que estas células vulnerables demuestran deleciones del mtADN y marcadores de estrés oxidativo solamente en las regiones que están cercanamente relacionadas a los vasos dañados. Esta evidencia sugiere fuertemente que la hipoperfusión crónica induce la acumulación de los productos del estrés oxidativo. Además, las lesiones de la pared vascular del cerebro se correlacionan linealmente con el grado de daño celular neuronal y glial. Por lo tanto, concluimos que la hipoperfusión crónica es un iniciador clave del estrés oxidativo en varias células parénquimales del cerebro, y las mitocondrias parecen ser blancos primarios para el daño de cerebro en la enfermedad de Alzheimer. En este trabajo, delineamos el papel de la acumulación continua de los productos del estrés oxidativo, tales como una abundancia de productos de óxido nítrico (vía la sobreexpresión de NO sintasa inducible y/o neuronal (iNOS y nNOS respectivamente) y de acumulación del peroxinitrito, como factores secundarios pero acelerantes que comprometen la barrera hematoencefálica. Si éste resulta ser el caso, las intervenciones farmacológicas que apuntan a la hipoperfusion crónica pudieran mejorar las características dominantes de la demencia neurodegenerativa.    

    Visitas del artículo 220 | Visitas PDF 98

    Descargas

    Los datos de descarga todavía no están disponibles.
    1. Ballinger SW. Mitochondrial dysfunction in cardiovascular disease. Free Radic Biol Med. 2005;38:1278-1295.
    2. Aliev G, Gasimov E, Obrenovich ME, Fischbach K, Shenk JC, Smith MA, Perry G. Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: implication in the pathogenesis of Alzheimer’s disease. Vasc Health Risk Manag. 2008;4:721-730.
    3. Aliev G, Shenk JC, Fischbach K, Perry G. Stem cell niches as clinical targets: the future of anti-ischemic therapy? Nat Clin Pract Cardiovasc Med. 2008;5:590-591.
    4. Aliev G, Cobb C, Pacheco G, Shenk JC, Moreira PI, Fischbach K, Morales L, Gasimov E, Perry G. The Role of Oxidative Stress and Vasoactive Substances in the Pathophysiology of Alzheimer’s Disease. In: BioMarkers for Early Diagnosis of Alzheimer’s Disease, ISBN 978-1-60456-991-9 Editors: Daniela Galimberti and Elio Scarpini, 2008 Nova Science Publishers, Inc. Chapter IX, pg. 241-265.
    5. Obrenovich ME, Morales LA, Cobb C, Shenk JC, Méndez GM, Fischbach K, Smith MA, Qasimov E, Perry G, Aliev G. Insights into cerebrovascular complications and Alzheimer disease through the selective loss of GRK2 regulation. J. Cell Mol Med. 2008;12:1-13.
    6. Aliev G. Is non-genetic Alzheimer’s disease a vascular disorder with neurodegenerative consequences? J Alzheimers Dis. 2002;4:513-516.
    7. de la Torre JC. Alzheimer’s disease: how does it start? J Alzheimers Dis. 2002;4:497-512.
    8. Aliev G, Cirillo R, Salvatico E, Paro M, Prosdocimi M. Changes in vessel ultrastructure during ischemia and reperfusion of rabbit hindlimb: implications for therapeutic intervention. Microvasc Res. 1993;46:65-76.
    9. de la Monte SM, Wands JR. Molecular indices of oxidative stress and mitochondrial dysfunction occur early and often progress with severity of Alzheimer’s disease. J Alzheimers Dis. 2006;9:167-181.
    10. Malinski T. Nitric oxide and nitroxidative stress in Alzheimer’s disease. J Alzheimers Dis. 2007;11:207-218.
    11. Moreira PI, Honda K, Liu Q, Santos MS, Oliveira CR, Aliev G, Nunomura A, Zhu X, Smith MA, Perry G. Oxidative Stress: the old enemy in Alzheimer’s disease pathophysiology. Curr Alzheimer Res. 2005;2:403-408.
    12. Moreira PI, Zhu X, Lee HG, Honda K, Smith MA, Perry G. The (un)balance between metabolic and oxidative abnormalities and cellular compensatory responses in Alzheimer disease. Mech Ageing Dev. 2006;127:501-506.
    13. De Jong GI, De Vos RA, Steur EN, Luiten PG. Cerebrovascular hypoperfusion: a risk factor for Alzheimer’s disease? Animal model and postmortem human studies. Ann N Y Acad Sci. 1997;826:56-74.
    14. de la Torre JC. Hemodynamic consequences of deformed microvessels in the brain in Alzheimer’s disease. Ann N Y Acad Sci. 1997;826, 75-91.
    15. Friston KJ, Frackowiak RS. Cerebral function in aging and Alzheimer’s disease: the role of PET. Electroencephalogr Clin Neurophysiol Suppl. 1991;42: 355-365.
    16. Kumar A, Schapiro MB, Haxby JV, Grady CL, Friedland RP. Cerebral metabolic and cognitive studies in dementia with frontal lobe behavioral features. J Psychiatr Res. 1990;24:97-109.
    17. Galle J, Bengen J, Schollmeyer P, Wanner C. Impairment of endothelium-dependent dilation in rabbit renal arteries by oxidized lipoprotein(a). Role of oxygen-derived radicals. Circulation. 1995;92:1582-1589.
    18. de la Torre JC. Critically attained threshold of cerebral hypoperfusion: the CATCH hypothesis of Alzheimer’s pathogenesis. Neurobiol Aging. 2000;21:331-342.
    19. Meguro K, Blaizot X, Kondoh Y, Le Mestric C, Baron JC, Chavoix C.Ml. Neocortical and hippocampal glucose hypometabolism following neurotoxic lesions of the entorhinal and perirhinal cortices in the non-human primate as shown by PET. Implications for Alzheimer’s disease. Brain.1999;122( Pt 8):1519-1531.
    20. Beal MF. Aging, energy, and oxidative stress in neurodegenerative diseases. Ann Neurol. 1995;38: 357-366.
    21. Jagust WJ, Friedland RP, Budinger TF, Koss E, Ober B. Longitudinal studies of regional cerebral metabolism in Alzheimer’s disease. Neurology. 1998;38:909-912.
    22. Markesbery WR, Carney JM.. Oxidative alterations in Alzheimer’s disease. Brain Pathol. 1999; 9:133-146.
    23. Aliev G, Liu J, Shenk JC, Fischbach K, Pacheco GJ, Chen SG, Obrenovich ME, et al. Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats. J Cell Mol Med. 2008. in press.
    24. de la Torre JC, Stefano GB. Evidence that Alzheimer’s disease is a microvascular disorder: the role of constitutive nitric oxide. Brain Res Brain Res Rev. 2000;34:119-136.
    25. Crack PJ, Taylor JM. Reactive oxygen species and the modulation of stroke. Free Radic Biol Med. 2005;38:1433-1444.
    26. Lambeth JD. Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy. Free Radic Biol Med. 2007;43:332-347.
    27. Maulik N, Das DK. Redox signaling in vascular angiogenesis. Free Radic Biol Med. 2002;33:1047-1060.
    28. Lum H, Roebuck KA. Oxidant stress and endothelial cell dysfunction. Am J Physiol Cell Physiol. 2001;280:C719-741.
    29. Coyle JT, Puttfarcken P. Oxidative stress, glutamate, and neurodegenerative disorders. Science. 1993;262:689-695.
    30. Smith MA, Perry G, Richey PL, Sayre LM, Anderson VE, Beal MF, Kowall N. Oxidative damage in Alzheimer’s. Nature. 1996;382:120-121.
    31. Smith MA, Petot GJ, Perry G. Diet and oxidative stress: a novel synthesis of epidemiological data on Alzheimer’s disease. J Alzheimers Dis. 1999;1:203-206.
    32. Smith MA, Richey Harris PL, Sayre LM, Beckman JS, Perry G. Widespread peroxynitrite-mediated damage in Alzheimer’s disease. J Neurosci. 1997;17:2653-2657.
    33. Smith MA, Vasák M, Knipp M, Castellani RJ, Perry G. Dimethylargininase, a nitric oxide regulatory protein, in Alzheimer disease. Free Radic Biol Med. 1998;25:898-902.
    34. Prelli F, Castaño EM, van Duinen SG, Bots GT, Luyendijk W, Frangione B. Different processing of Alzheimer’s beta-protein precursor in the vessel wall of patients with hereditary cerebral hemorrhage with amyloidosis-Dutch t Biochem Biophys Res Commun. 1988;151:1150-1155.
    35. Lovell MA, Xie C, Markesbery WR. Decreased glutathione transferase activity in brain and ventricular fluid in Alzheimer’s disease. Neurology. 1998;51:1562-1566.
    36. Prasad MR, Lovell MA, Yatin M, Dhillon H, Markesbery WR. P Regional membrane phospholipid alterations in Alzheimer’s disease. Neurochem Res.1998;23:81-88.
    37. Markesbery WR. Oxidative stress hypothesis in Alzheimer’s disease. Free Radic Biol Med. 1997;23:134-147.
    38. Mecocci P, MacGarvey U, Kaufman AE, Koontz D, Shoffner JM, Wallace DC, Beal MF. Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain. Ann Neurol. 1993;34:609-616.
    39. Mecocci P, MacGarvey U, Beal MF. Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease. Ann Neurol. 1994;36:747-751.
    40. Mecocci P, Beal MF, Cecchetti R, Polidori MC, Cherubini A, Chionne F, Avellini L, Romano G, Senin U. Mitochondrial membrane fluidity and oxidative damage to mitochondrial DNA in aged and AD human brain. Mol Chem Neuropathol. 1997;31:53-64.
    41. Nunomura A, Perry G, Hirai K, Aliev G, Takeda A, Chiba S, Smith MA. Neuronal RNA oxidation in Alzheimer’s disease and Down’s syndrome. Ann N Y Acad Sci.1999;893:362-364.
    42. Nunomura A, Perry G, Pappolla MA, Wade R, Hirai K, Chiba S, Smith MA.). RNA oxidation is a prominent feature of vulnerable neurons in Alzheimer’s disease. J Neurosci. 1999;19:1959-1964.
    43. Nunomura A, Perry G, Aliev G, Hirai K, Takeda A, Balraj EK, Jones PK, et al. (2001). Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol. 2001;60:759-767.
    44. Aliev G, Smith MA, Seyidov D, Neal ML, Lamb BT, Nunomura A, Gasimov EK, et al. The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer’s disease. Brain Pathol. 2002;12: 21-35.
    45. Smith MA, Taneda S, Richey PL, Miyata S, Yan SD, Stern D, Sayre LM, Monnier VM, Perry G. Advanced Maillard reaction end products are associated with Alzheimer disease pathology. Proc Natl Acad Sci U S A.1994;9:5710-5714.
    46. Sayre LM, Zelasko DA, Harris PL, Perry G, Salomon RG, Smith MA. 4-Hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer’s disease. J Neurochem.1997;68:2092-2097.
    47. Perry G, Nunomura A, Hirai K, Takeda A, Aliev G, Smith MA. Oxidative damage in Alzheimer’s disease: the metabolic dimension. Int J Dev Neurosci. 2000;18:417-421.
    48. Cirillo R, Aliev G, Hornby EJ, Prosdocimi M. Endothelium as a therapeutical target in peripheral occlusive arterial diseases: consideration for pharmacological interventions. Pharmacol Res. 1994;29:293-311.
    49. Cirillo R, Aliev G, Hornby EJ, Prosdocimi M. Effect of cloricromene during ischemia and reperfusion of rabbit hindlimb: evidence for an involvement of leukocytes in reperfusion-mediated tissue and vascular injury. J Cardiovasc Pharmacol. 1992;20:969-975.
    50. Granger DN, Benoit JN, Suzuki M, Grisham MB. Leukocyte adherence to venular endothelium during ischemia-reperfusion. Am J Physiol. 1989;257:G683-688.
    51. Sala A, Aliev GM, Rossoni G, Berti F, Buccellati C, Burnstock G, Folco G, Maclouf J. Morphological and functional changes of coronary vasculature caused by transcellular biosynthesis of sulfidopeptide leukotrienes in isolated heart of rabbit. Blood. 1996;87:1824-1832.
    52. Salvatico E, Aliev GM, Novello D, Prosdocimi M. Functional depression of isolated perfused rat heart mediated by activated leukocytes: protective effect of cloricromene. J Cardiovasc Pharmacol.1994;24:638-647.
    53. Matz RL, Schott C, Stoclet JC, Andriantsitohaina R. Age-related endothelial dysfunction with respect to nitric oxide, endothelium-derived hyperpolarizing factor and cyclooxygenase products. Physiol Res. 2000;49: 11-18.
    54. Aliev G, Burnstock G. Watanabe rabbits with heritable hypercholesterolaemia: a model of atherosclerosis. Histol Histopathol. 1998;13:797-817.
    55. Aliev G, Mironov A, Cirillo R, Mironov A Jr, Gorelova E, Prosdocimi M.Evidence for the presence of early vascular lesions in newborn Watanabe heritable hyperlipidemic (WHHL) rabbits. Atherosclerosis. 1993;101:17-24.
    56. Stewart-Lee AL, Ferns GA, Anggård EE. Differences in onset of impaired ndothelial responses and in effects of vitamin E in the hypercholesterolemic rabbit carotid and renal arteries. J Cardiovasc Pharmacol.1995;25:906-913.
    57. Kalaria RN. The role of cerebral ischemia in Alzheimer’s disease. Neurobiol Aging. 2000;21: 321-330.
    58. Kalaria RN, Ballard C. Overlap between pathology of Alzheimer disease and vascular dementia. Alzheimer Dis Assoc Disord.1999;13 Suppl 3:S115-123.
    59. Price JM, Sutton ET, Hellermann A, Thomas T. beta-Amyloid induces cerebrovascular endothelial dysfunction in the rat brain. Neurol Res. 1997;19: 534-538.
    60. Iadecola C, Zhang F, Niwa K, Eckman C, Turner SK, Fischer E, Younkin S, et al. SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein. Nat Neurosci.1999;2:157-161.
    61. Niwa K, Carlson GA, Iadecola C. Exogenous A beta1-40 reproduces cerebrovascular alterations resulting from amyloid precursor protein overexpression in mice. J Cereb Blood Flow Metab.2000;20:1659-1668.
    62. Grammas P, Moore P, Weigel PH. Microvessels from Alzheimer’s disease brains kill neurons in vitro. Am J Pathol. 1999;154:337-342.
    63. Stewart PA, Hayakawa K, Akers MA, Vinters HV. A morphometric study of the blood-brain barrier in Alzheimer’s disease. Lab Invest. 1992;67:734-742.
    64. Aliev G, Seyidova D, Neal ML, Shi J, Lamb BT, Siedlak SL, Vinters HV, et al. Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice. Ann N Y Acad Sci. 2002;977:45-64.
    65. Aliev G, Smith MA, Vinters HV, et al. Mitochondrial abnormalities mark vulnerable neurons in Alzheimer disease. J Neuropathol Exp Neurol.1998;58: 511.
    66. Vinters HV, Miller BL, Pardridge WM. Brain amyloid and Alzheimer disease. Ann Intern Med. 1988;109:41-54.
    67. Etiene D, Kraft J, Ganju N, Gomez-Isla T, Gemelli B, Hyman BT, Hedley-Whyte ET, Wands JR, De La Monte SM. Cerebrovascular Pathology Contributes to the Heterogeneity of Alzheimer’s Disease. J Alzheimers Dis. 1998;1:119-134.
    68. Hock BJ Jr, Lamb BT. Transgenetic mouse models of Alzheimer’s disease. Trends.Genet. 2001;17:S7-12.
    69. Jakobovits A, Lamb BT, Peterson KR. Production of transgenic mice with yeast artificial chromosomes. Methods Mol Biol. 2000;136:435-453.
    70. Kulnane LS, Lamb BT. Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice. Neurobiol Dis. 2001;8:982-992.
    71. Octave JN. The amyloid peptide precursor in Alzheimer’s disease. Acta Neurol Belg. 1995;95:197-209.
    72. Selkoe DJ. Cell biology of the amyloid beta-protein precursor and the mechanism of Alzheimer’s disease. Annu Rev Cell Biol. 1994;10:373-403.
    73. Crawford JG. Alzheimer’s disease risk factors as related to cerebral blood flow: additional evidence. Med Hypotheses. 1998;50:25-36.
    74. Lindahl B, Lindahl U. Amyloid-specific heparan sulfate from human liver and spleen. J Biol Chem. 1997;272:26091-26094.
    75. Kisilevsky R. Amyloid beta threads in the fabric of Alzheimer’s disease. Nat Med. 1998;4:772-773.
    76. Klionsky DJ. Autophagy: from phenomenology to molecular understanding in less than a decade. Nat Rev Mol Cell Biol. 2007;8:931-937.
    77. Boland B, Nixon RA. Neuronal macroautophagy: from development to degeneration. Mol Aspects Med.2006;27: 503-519.
    78. Zheng L, Roberg K, Jerhammar F, Marcusson J, Terman A. Autophagy of amyloid beta-protein in differentiated neuroblastoma cells exposed to oxidative stress. Neurosci Lett. 2006;394:184-189.
    79. Kalaria RN. The blood-brain barrier and cerebrovascular pathology in Alzheimer’s disease. Ann N Y Acad Sci. 1999;893:113-125.
    80. Kawai M, Kalaria RN, Harik SI, Perry G. The relationship of amyloid plaques to cerebral capillaries in Alzheimer’s disease. Am J Pathol. 1990;137:1435-1446.
    81. Iwamoto N, Nishiyama E, Ohwada J, Arai H. Distribution of amyloid deposits in the cerebral white matter of the Alzheimer’s disease brain: relationship to blood vessels. Acta Neuropathol (Berl).1997;93: 334-340.
    82. Perry G, Smith MA, McCann CE, Siedlak SL, Jones PK, Friedland RP. Cerebrovascular muscle atrophy is a feature of Alzheimer’s disease. Brain Res. 1989;791:63-66.
    83. Perry G, Smith MA. The case for vascular abnormalities in AD. Curr Alzheimer Res. 1998;3:181-186.
    84. Joachim CL, Morris JH, Selkoe DJ.Diffuse senile plaques occur commonly in the cerebellum in Alzheimer’s disease. Am J Pathol. 1989;135:309-319.
    85. Coria F, Castaño E, Prelli F, Larrondo-Lillo M, van Duinen S, Shelanski ML, Frangione B. Isolation and characterization of amyloid P component from Alzheimer’s disease and other types of cerebral amyloidosis. Lab Invest. 1988;58:454-458.
    86. Tagliavini F, Ghiso J, Timmers WF, Giaccone G, Bugiani O, Frangione B. Coexistence of Alzheimer’s amyloid precursor protein and amyloid protein in cerebral vessel walls. Lab Invest. 1990;62:761-767.
    87. Thomas AJ, Morris CM, Ferrier IN, Kalaria RN. Distribution of amyloid beta 42 in relation to the cerebral microvasculature in an elderly cohort with Alzheimer’s disease. Ann N Y Acad Sci. 2000;903:83-88.
    88. Hofman A, Ott A, Breteler MM, Bots ML, Slooter AJ, van Harskamp F, van Duijn CN, Van Broeckhoven C, Grobbee DE. Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer’s disease in the Rotterdam Study. Lancet. 1997;349:151-154.
    89. Skoog I, Kalaria RN, Breteler MM. Vascular factors and Alzheimer disease. Alzheimer Dis Assoc Disord. 1999; Suppl 3:S106-114.
    90. Aliev G, Burnstock G. Watanabe rabbits with heritable hypercholesterolaemia: a model of atherosclerosis. Histol Histopathol. 1997;13:797-817.
    91. Smith JD, Breslow JL.. The emergence of mouse models of atherosclerosis and their relevance to clinical research. J Intern Med. 1997;242:99-109.
    92. Roses AD. On the metabolism of apolipoprotein E and the Alzheimer diseases. Exp Neurol. 1995;132:149-156.
    93. Ellis RJ, Olichney JM, Thal LJ, Mirra SS, Morris JC, Beekly D, Heyman A. Cerebral amyloid angiopathy in the brains of patients with Alzheimer’s disease: the CERAD experience, Part XV. Neurology. 1996;46:1592-1596.
    94. Kuo YM, Emmerling MR, Bisgaier CL, Essenburg AD, Lampert HC, Drumm D, Roher AE. Elevated low-density lipoprotein in Alzheimer’s disease correlates with brain abeta 1-42 levels. Biochem Biophys Res Commun.1998; 252:711-715.
    95. Montine TJ, Montine KS, Swift LL. Central nervous system lipoproteins in Alzheimer’s disease. Am J Pathol. 1997;151:1571-1575.
    96. Grant WB. Dietary links to Alzheimer’s disease: 1999 update. J Alzheimers Dis. 1999;1197-201.
    97. Refolo LM, Malester B, LaFrancois J, Bryant-Thomas T, Wang R, Tint GS, Sambamurti K, Duff K, Pappolla MA. Hypercholesterolemia accelerates the Alzheimer’s amyloid pathology in a transgenic mouse model. Neurobiol Dis. 2000;7: 321-331.
    98. Moreira PI, Siedlak SL, Wang X, Santos MS, Oliveira CR, Tabaton M, Nunomura A, et al. Autophagocytosis of mitochondria is prominent in Alzheimer disease. J Neuropathol Exp Neurol. 2007;66:525-532.
    99. Sparks DL. Coronary artery disease, hypertension, ApoE, and cholesterol: a link to Alzheimer’s disease? Ann N Y Acad Sci.1997;826:128-146.
    100. Sparks DL, Kuo YM, Roher A, Martin T, Lukas RJ. Alterations of Alzheimer’s disease in the cholesterol-fed rabbit, including vascular inflammation. Preliminary observations. Ann N Y Acad Sci. 2000;903:335-344.
    101. Acuña-Castroviejo D, Martín M, Macías M, Escames G, León J, Khaldy H, Reiter RJ. Melatonin, mitochondria, and cellular bioenergetics. J Pineal Res. 2001;30: 65-74.
    102. Castellani R, Hirai K, Aliev G, Drew KL, Nunomura A, Takeda A, Cash AD, et al. Role of mitochondrial dysfunction in Alzheimer’s disease. J Neurosci Res. 2002;70:357-360.
    103. Fiskum G, Murphy AN, Beal MF. Mitochondria in neurodegeneration: acute ischemia and chronic neurodegenerative diseases. J Cereb Blood Flow Metab. 1999;19:351-369.
    104. Schulz JB, Matthews RT, Klockgether T, Dichgans J, Beal MF. The role of mitochondrial dysfunction and neuronal nitric oxide in animal models of neurodegenerative diseases. Mol Cell Biochem. 1997;174:193-197.
    106. Hirai K, Aliev G, Nunomura A, Fujioka H, Russell RL, Atwood CS, Johnson AB, et al. Mitochondrial abnormalities in Alzheimer’s disease. J Neurosci. 2001;21:3017-3023.
    107. Beckman KB, Ames BN. The free radical theory of aging matures. Physiol Rev. 1998;78:547-581.
    108. Beckman KB, Ames BN. Mitochondrial aging: open questions. Ann N Y Acad Sci. 1998;854:118-127.
    109. Beckman KB, Ames BN. Endogenous oxidative damage of mtDNA. Mutat Res. 1999;424:51-58.
    110. Wallace DC. Mitochondrial diseases in man and mouse. Science. 1999;283:1482-1488.
    111. Bonilla E, Tanji K, Hirano M, Vu TH, DiMauro S, Schon EA. Mitochondrial involvement in Alzheimer’s disease. Biochim Biophys Acta. 1999;1410:171-182.
    112. Al-Abdulla NA, Martin LJ. Apoptosis of retrogradely degenerating neurons occurs in association with the accumulation of perikaryal mitochondria and oxidative damage to the nucleus. Am J Pathol. 1998;153:447-456.
    113. Wallace DC. Mitochondrial DNA in aging and disease. Sci Am. 1997;277:40-47.
    114. Aliev G, Shi J, Perry G, et al. Neuronal mitochondrial abnormalities in yeast artificial chromosome (YAC) transgenic mice overexpressing amyloid precursor protein (APP). Society for Neuroscience Abstracts Book. 2000.30.
    115. Aliev G, Smith MA, Turmaine M, Neal ML, Zimina TV, Friedland RP, Perry G, LaManna JC, Burnstock G. Atherosclerotic lesions are associated with increased immunoreactivity for inducible nitric oxide synthase and endothelin-1 in thoracic aortic intimal cells of hyperlipidemic Watanabe rabbits. Exp Mol Pathol. 2001;71:40-54.
    116. Shi J, Perry G, Berridge MS, Aliev G, Siedlak SL, Smith MA, LaManna JC, Friedland RP. Labeling of cerebral amyloid beta deposits in vivo using intranasal basic fibroblast growth factor and serum amyloid P component in mice. J Nucl Med. 2002;43:1044-1051.
    117. Aliev G, Smith MA, de la Torre JC, Perry G. Mitochondria as a primary target for vascular hypoperfusion and oxidative stress in Alzheimer’s disease. Mitochondrion. 2004;4: 649-663.
    118. Aliev G, Smith MA, Seyidov D, Neal ML, Lamb BT, Nunomura A, Gasimov EK, et al. The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer’s disease. Brain Pathol. 2002;12: 21-35.
    119. de la Torre JC, Aliev G. Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changes. J Cereb Blood Flow Metab. 2005;25:663-672.
    120. Obrenovich ME, Smith MA, Siedlak SL, Chen SG, de la Torre JC, Perry G, Aliev G. Overexpression of GRK2 in Alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesions. Neurotox Res. 2006;10:43-56.
    121. Shenk JC, Gasimov E, Liu J, Fischbach K, Puchowicz M, Xu K, Obrenovich ME, Smith MA, et al. (2008). ApoE4 overexpression initiates age-dependent brain hypoperfusion, mitochondrial lesions and cognitive impairment that can be prevented by feeding mice acetyl-L-Carnitine and R-Lipoic acid. J Neurol Sci. 2008. In press.
    122. Shi J, Perry G, Aliev G, Smith MA, Ashe KH, Friedland RP. Serum amyloid P is not present in amyloid beta deposits of a transgenic animal model. Neuroreport. 1999;10:3229-3232.
    123. Aliyev A, Chen SG, Seyidova D, Smith MA, Perry G, de la Torre J, Aliev G. Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer’s disease. J Neurol Sci. 2005;229-230:285-292.
    124. Moreira PI, Nunomura A, Nakamura M, Takeda A, Shenk JC, Aliev G, Smith MA, Perry G. Nucleic acid oxidation in Alzheimer disease. Free Radic Biol Med. 2006;44:1493-1505.
    125. Moreira PI, Siedlak SL, Wang X, Santos MS, Oliveira CR, Tabaton M, Nunomura A, et al. Increased Autophagic Degradation of Mitochondria in Alzheimer Disease. Autophagy. 2007;3:614-615.
    126. -------------------------------------------------------------------------------
    127. DOI: http://dx.doi.org/10.22490/24629448.408
    Tutoriales

    Autores:

    ¿Cómo enviar un artículo?

    Par evaluador:

    ¿Cómo evaluar un artículo?

    Información

    Palabras clave

    Perfil de Google Scholar

    Hace parte de
     
    Más leídos en los últimos 30 días

    Número actual

    Sistema OJS 3.4.0.5 - Metabiblioteca |