Evaluación de la administración de coenzima Q10 para atenuar las respuestas oxidativas de la agregación β-amiloide en modelos de enfermedad de Alzheimer: Revisión sistemática de la literatura
DOI:
https://doi.org/10.33448/rsd-v10i2.12751Palabras clave:
Enfermedad de Alzheimer; Estrés Oxidativo; Coenzima Q10.Resumen
El objetivo de este estudio fue evaluar los efectos de la administración de CoQ10 sobre la atenuación de las respuestas oxidativas por la agregación de β-amiloide en modelos de la enfermedad de Alzheimer. El presente trabajo es una revisión sistemática de la literatura, consistente en pasos establecidos por estrategias de búsqueda, identificación, selección y elegibilidad de estudios. CoQ10 o ubi-quinona y ubidecarenona, es una provitamina sintetizada de forma endógena, esta ha sido utilizada en ensayos clínicos para evaluar su potencial de neuroprotección y antioxidación. Los hallazgos mostraron que la CoQ10 tiene efectos antioxidantes y disminuye la deposición intracelular del compuesto beta-amiloide, ejerciendo un alivio oxidativo y un efecto antiapoptótico. La administración de CoQ10 demostró resultados significativos en la atenuación de las respuestas oxidativas de la agregación de β-amiloide en modelos de EA.
Citas
Attia, H., Albuhayri, S., Alaraidh, S., Alotaibi, A., Yacoub, H., Mohamad, R., & Al-Amin, M. (2020). Biotin, coenzyme Q10, and their combination ameliorate aluminium chloride-induced Alzheimer's disease via attenuating neuroinflammation and improving brain insulin signaling. Journal of biochemical and molecular toxicology, e22519. Advance online publication.
Beal, M. F. (2004). Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and coenzyme Q 10 as a potential treatment. Journal of bioenergetics and biomembranes, v. 36, n. 4, p. 381-386.
Bezprozvanny, I., & Mattson, M. P. (2008). Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease. Trends in neurosciences, v. 31, n. 9, p. 454-463.
Bonakdar, R. A., & Guarneri, E. (2005). Coenzyme Q10. American family physician, v. 72, n. 6, p. 1065-1070.
Chen, Z., & Zhong, C. (2014). Oxidative stress in Alzheimer’s disease. Neuroscience bulletin, v. 30, n. 2, p. 271-281.
Choi, H., Park, H. H., Koh, S. H., Choi, N. Y., Yu, H. J., Park, J., Lee, Y. J., & Lee, K. Y. (2012). Coenzyme Q10 protects against amyloid beta-induced neuronal cell death by inhibiting oxidative stress and activating the P13K pathway. Neurotoxicology, 33(1), 85–90.
Choi, JH., Ryu, YW., & Seo, JH. (2005). Biotechnological production and applications of coenzyme Q 10. Applied microbiology and biotechnology, v. 68, n. 1, p. 9-15.
Cioffi, F., Adam, R. H. I., & Broersen, K. (2019). Molecular mechanisms and genetics of oxidative stress in Alzheimer’s disease. Journal of Alzheimer's Disease, n. Preprint, p. 1-37.
Ciulla, M., Marinelli, L., Cacciatore, I., & Stefano, A. D. (2019). Role of Dietary Supplements in the Management of Parkinson's Disease. Biomolecules, 9(7), 271.
Darvesh, A. S., Carroll, R. T., Bishayee, A., Geldenhuys, W. J., & Van der Schyf, C. J. (2010). Oxidative stress and Alzheimer's disease: dietary polyphenols as potential therapeutic agents. Expert review of neurotherapeutics, 10(5), 729–745.
De Felice, F. G., Velasco, P. T., Lambert, M. P., Viola, K., Fernandez, S. J., Ferreira, S. T., & Klein, W. L. (2007). Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. The Journal of biological chemistry, 282(15), 11590–11601.
Díaz-Casado, M. E., Quiles, J. L., Barriocanal-Casado, E., González-García, P., Battino, M., López, L. C., & Varela-López, A. (2019). The Paradox of Coenzyme Q10 in Aging. Nutrients, 11(9), 2221.
Dumont, M., Kipiani, K., Yu, F., Wille, E., Katz, M., Calingasan, N. Y., Gouras, G. K., Lin, M. T., & Beal, M. F. (2011). Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease. Journal of Alzheimer's disease : JAD, 27(1), 211–223.
Durán-Prado, M., Frontiñán, J., Santiago-Mora, R., Peinado, J. R., Parrado-Fernández, C., Gómez-Almagro, M. V., Moreno, M., López-Domínguez, J. A., Villalba, J. M., & Alcaín, F. J. (2014). Coenzyme Q10 protects human endothelial cells from β-amyloid uptake and oxidative stress-induced injury. PloS one, 9(10), e109223.
Eratne, D., Loi, S. M., Farrand, S., Kelso, W., Velakoulis, D., & Looi, J. C. (2018). Alzheimer's disease: clinical update on epidemiology, pathophysiology and diagnosis. Australasian psychiatry : bulletin of Royal Australian and New Zealand College of Psychiatrists, 26(4), 347–357.
Farlow, M. R. (1998). Etiology and pathogenesis of Alzheimer’s disease. American journal of health-system pharmacy, v. 55, n. suppl_2, p. S5-S10.
Fernández, S. S. M., & Ribeiro, S. M. L. (2018). Nutrition and Alzheimer disease. Clinics in geriatric medicine, v. 34, n. 4, p. 677-697.
Folkers, K. (1996). Relevance of the Biosynthesis of Coenzyme Q10and of the Four Bases of DNA as a Rationale for the Molecular Causes of Cancer and a Therapy. Biochemical and biophysical research communications, v. 224, n. 2, p. 358-361.
Fouad, G. I. (2020). Combination of Omega 3 and Coenzyme Q10 Exerts Neuroprotective Potential Against Hypercholesterolemia-Induced Alzheimer's-Like Disease in Rats. Neurochemical Research, p. 1-14.
Frontiñán-Rubio, J., Sancho-Bielsa, F. J., Peinado, J. R., LaFerla, F. M., Giménez-Llort, L., Durán-Prado, M., & Alcain, F. J. (2018). Sex-dependent co-occurrence of hypoxia and β-amyloid plaques in hippocampus and entorhinal cortex is reversed by long-term treatment with ubiquinol and ascorbic acid in the 3 × Tg-AD mouse model of Alzheimer's disease. Molecular and cellular neurosciences, 92, 67–81.
Granick, B., Neubauer, D., & Dermarderosian, A. (1996). The Lawrence review of natural products. St. Louis: Facts and Comparisons, p. 1-3.
Gustafson, D. R., Skoog, I., Rosengren, L., Zetterberg, H., & Blennow, K. (2007). Cerebrospinal fluid beta-amyloid 1-42 concentration may predict cognitive decline in older women. Journal of neurology, neurosurgery, and psychiatry, 78(5), 461–464.
Gutierrez-Mariscal, F. M., Arenas-de Larriva, A. P., Limia-Perez, L., Romero-Cabrera, J. L., Yubero-Serrano, E. M., & López-Miranda, J. (2020). Coenzyme Q10 Supplementation for the Reduction of Oxidative Stress: Clinical Implications in the Treatment of Chronic Diseases. International journal of molecular sciences, 21(21), 7870.
Hidaka, T., Fujii, K., Funahashi, I., Fukutomi, N., & Hosoe, K. (2008). Safety assessment of coenzyme Q10 (CoQ10). BioFactors (Oxford, England), 32(1-4), 199–208.
Huang, X. G., Yee, B. K., Nag, S., Chan, S. T., & Tang, F. (2003). Behavioral and neurochemical characterization of transgenic mice carrying the human presenilin-1 gene with or without the leucine-to-proline mutation at codon 235. Experimental neurology, 183(2), 673–681.
Kamat, P. K., Kalani, A., Rai, S., Swarnkar, S., Tota, S., Nath, C., & Tyagi, N. (2016). Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies. Molecular neurobiology, 53(1), 648–661.
Kamat, P. K., Rai, S., Swarnkar, S., Shukla, R., Ali, S., Najmi, A. K., & Nath, C. (2013). Okadaic acid-induced Tau phosphorylation in rat brain: role of NMDA receptor. Neuroscience, 238, 97–113.
Karakahya, R. H., & Özcan, T. Ş. (2020). Salvage of the retinal ganglion cells in transition phase in Alzheimer’s disease with topical coenzyme Q10: is it possible?. Graefe's Archive for Clinical and Experimental Ophthalmology, v. 258, n. 2, p. 411-418.
Komaki, H., Faraji, N., Komaki, A., Shahidi, S., Etaee, F., Raoufi, S., & Mirzaei, F. (2019). Investigation of protective effects of coenzyme Q10 on impaired synaptic plasticity in a male rat model of Alzheimer's disease. Brain research bulletin, 147, 14–21.
Lee, J., Boo, J. H., & Ryu, H. (2009). The failure of mitochondria leads to neurodegeneration: Do mitochondria need a jump start?. Advanced drug delivery reviews, v. 61, n. 14, p. 1316-1323.
Littarru, G. P. & Tiano, L. (2010). Clinical aspects of coenzyme Q10: an update. Nutrition, v. 26, n. 3, p. 250-254.
Lockwood, K., Moesgaard, S., & Folkers, K. (1994). Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochemical and biophysical research communications, v. 199, n. 3, p. 1504-1508.
López-Lluch, G., Del Pozo-Cruz, J., Sánchez-Cuesta, A., Cortés-Rodríguez, A. B., & Navas, P. (2019). Bioavailability of coenzyme Q10 supplements depends on carrier lipids and solubilization. Nutrition (Burbank, Los Angeles County, Calif.), 57, 133–140.
Lovell, M. A., & Markesbery, W. R. (2007). Oxidative damage in mild cognitive impairment and early Alzheimer's disease. Journal of neuroscience research, v. 85, n. 14, p. 3036-3040.
Manzano-León, N., & Mas-Oliva, J. (2006). Oxidative stress, β-amiloide peptide and Alzheimer´ s disease. Gaceta medica de Mexico, v. 142, n. 3, p. 229-238.
Manzar, H., Abdulhussein, D., Yap T. E., & Cordeiro, M. F. (2020). Cellular Consequences of Coenzyme Q10 Deficiency in Neurodegeneration of the Retina and Brain. International Journal of Molecular Sciences, v. 21, n. 23, p. 9299.
Organização Mundial De Saúde (OMS). Global Dementia Observatory. Organização Mundial De Saúde. 2017.
Pereira, A. S., Shitsuka, D. M., Parreira, F. J., & Shitsuka, R. (2018). Metodologia da pesquisa científica.
Prangthip, P., Kettawan, A., Posuwan, J., Okuno, M., & Okamoto, T. (2016). An Improvement of Oxidative Stress in Diabetic Rats by Ubiquinone-10 and Ubiquinol-10 and Bioavailability after Short- and Long-Term Coenzyme Q10 Supplementation. Journal of dietary supplements, 13(6), 647–659
Rai, S., Kamat, P. K., Nath, C., & Shukla, R. (2014). Glial activation and post-synaptic neurotoxicity: the key events in Streptozotocin (ICV) induced memory impairment in rats. Pharmacology, biochemistry, and behavior, 117, 104–117.
Roberson, E. D., Halabisky, B., Yoo, J. W., Yao, J., Chin, J., Yan, F., Wu, T., Hamto, P., Devidze, N., Yu, G. Q., Palop, J. J., Noebels, J. L., & Mucke, L. (2011). Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(2), 700–711.
Sohal, R. S., & Forster, M. J. (2007). Coenzyme Q, oxidative stress and aging. Mitochondrion, v. 7, p. S103-S111.
Tönnies, E., & Trushina, E. (2017). Oxidative stress, synaptic dysfunction, and Alzheimer’s disease. Journal of Alzheimer's Disease, v. 57, n. 4, p. 1105-1121.
Wadsworth, TL, Bishop, JA, Pappu, AS, Woltjer, RL, & Quinn, JF (2008). Avaliação da coenzima Q como estratégia antioxidante na doença de Alzheimer. Journal of Alzheimer's disease: JAD , 14 (2), 225-234.
Wang, Z., Yang, L., & Zheng, H. (2012). Role of APP and Aβ in synaptic physiology. Current Alzheimer research, 9(2), 217–226.
Yang, X., Yang, Y., Li, G., Wang, J., & Yang, E. S. (2008). Coenzyme Q10 attenuates beta-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutation. Journal of molecular neuroscience : MN, 34(2), 165–171.
Yang, X., Dai, G., Li, G., & Yang, E. S. (2010). Coenzyme Q10 reduces beta-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer's disease. Journal of molecular neuroscience : MN, 41(1), 110–113.
Descargas
Publicado
Cómo citar
Número
Sección
Licencia
Derechos de autor 2021 Francisco Emanoel Alves de Araújo; João Matheus Caé da Rocha; Bruna Jéssica Dantas de Lucena; Sarah Vitória Gomes de Sousa; Maria Raquel Araújo de Sousa; Lucas Emmanuel Rocha de Moura Marques; João Lindemberg Bandeira de Lima; Kellyson Lopes da Silva Macedo; Salvador Viana Gomes Junior
Esta obra está bajo una licencia internacional Creative Commons Atribución 4.0.
Los autores que publican en esta revista concuerdan con los siguientes términos:
1) Los autores mantienen los derechos de autor y conceden a la revista el derecho de primera publicación, con el trabajo simultáneamente licenciado bajo la Licencia Creative Commons Attribution que permite el compartir el trabajo con reconocimiento de la autoría y publicación inicial en esta revista.
2) Los autores tienen autorización para asumir contratos adicionales por separado, para distribución no exclusiva de la versión del trabajo publicada en esta revista (por ejemplo, publicar en repositorio institucional o como capítulo de libro), con reconocimiento de autoría y publicación inicial en esta revista.
3) Los autores tienen permiso y son estimulados a publicar y distribuir su trabajo en línea (por ejemplo, en repositorios institucionales o en su página personal) a cualquier punto antes o durante el proceso editorial, ya que esto puede generar cambios productivos, así como aumentar el impacto y la cita del trabajo publicado.
