Publique un comentario 
La disfunción mitocondrial y el estrés oxidativo en la enfermedad de Alzheimer
Texto completo:
PDFResumen
Objetivo: describir los efectos de la disfunción de la respiración mitocondrial, el estrés nitroso activo y a alteración en la homeostasis neuronal del Ca 2+ en la génesis del Alzheimer
Métodos: se realizó una investigación tipo revisión documental. Para identificar los documentos revisados se consultó la base bibliográfica PubMed/Medline. Se incluyeron los trabajos entre enero 2021 y 2023.
Desarrollo: la influencia que tienen algunos mecanismos celulares en la génesis del Alzheimer como la disfunción mitocondrial, las alteraciones de la homeostasis del calcio neuronal
Conclusiones: la etiología de la enfermedad de Alzheimer no ha sido completamente esclarecida; los mecanismos que se postulan para explicarla son la hipótesis de la cascada mitocondrial, la neurotoxicidad del péptido amiloide β, la dis-regulación del metabolismo neuronal del Ca 2+ y el desequilibrio de los procesos de fusión y fisión mitocondriales.
.
Palabras clave
Referencias
GBD 2016 Neurology Collaborators. Global, regional, and national burden of neurological disorders, 1990–2016: a systematic analysis for the Global burden of Disease Study 2016. Lancet Neurol. 2019; 18(5):459–80.
Cornutiu G. The epidemiological scale of Alzheimer's disease. J Clin Med Res. 2015; 7(9):657–66.
Moreira PI, Carvalho C, Zhu X, Smith M.A, Perry G et al. Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. Biochimica et Biophysica Acta . 2010; 1802: 2– 10.
Wang W, Fanpeng Z, Xiaopin MA, Perry G, Zhu X. Mitochondria dysfunction in the p:Aathogenesis of Alzheimer’s disease: recent advances. Molecular Neurodegeneration. 2020;5:30 https://doi.org/10.1186/s13024-020-00376-6
Memar MY, Ghotaslou R, Samiei M, Adibkia K. Antimicrobial use of reactive oxygen therapy: current insights Infection and Drug Resistance 2018; 11 567–576.
Sies H. Oxidative stress: A concept in redox biology and medicine. Redox Biol. 2015; 4, 180–183.
Santos S. Coronavirus (Covmediid-19) sepsis: revisiting mitochondrial dysfunction in pathogenesis, aging, inflammation, and mortality Inflammation Research. 2020; 69:1077–1085 https://doi.org/10.1007/s00011-020-01389-z
Van der Bliek AM, Sedensky MM, Morgan PG. Cell biology of the mitochondrion. Genetics. 2017; 207:843–71. https ://doi.org/10.1534/genet ics.117.30026 2.
Wimalawansa SJ, Vitamin D deficiency: Efects on oxidative stress, epigenetics, gene regulation, and aging.Biology 2019, 8, 30.
Zhang L, Wang X, Cueto R, Effia C, Zhang Y, Tand H, et al. Biochemical basis and metabolic interplay of redox regulation. RedoxBiology.2019; 6:
, https://doi.org/10.1016/j.redox.2019.101284.
Fakouri NB, Hansen TL, Desler C, Anugula S, Rasmussen, LJ. From powerhouse to perpetrator— Mitochondria in health and disease. Biology. 2019; 8: 35.
Fridovich I. Fundamental aspects of Reactive Oxygen Species, or What's the Matter with Oxygen? Annals of the New York Academy of Sciences Volume 893, Issue 1: OXIDATIVE/ENERGY METABOLISM IN NEURODEGENERATIVE DISORDERS Nov 1999 Pages xi-xiii, 1-439 page IRWIN FRIDOVICH https://doi.org/10.111 /j.1749-6632.1999.tb07814.xopen_in_new Publisher John Wiley & Sons, LtdISSN0077-8923eISSN1749-6632 Online 6 February 2006; Pages13 – 18.
Naviaux RK. Incomplete healing as a cause of aging: The role of mitochondria and the cell danger response. Biology 2019; 8: 27.
Butterfield DA, Halliwell B. Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease. Nat Rev Neurosci. 2019; 20(3):148–60.
Barcelos PD, Haas RH. Coq10 and aging. Biology 2019, 8, 28.
Sang S, Pan X, Chen Z, Zeng F, Pan S, Liu H, et al. Thiamine diphosphate reduction strongly correlates with brain glucose hypometabolism in Alzheimer’s disease, whereas amyloid deposition does not. Alzheimers Res Ther. 2018; 10(1):26.
Lopez J, Le Douce A, Logan AM, James G, Bonvento MP, Murphy A. et al. Complex I assembly into super-complexes determines differential mitochondrial ROS production in neurons and astrocytes, Proc. Natl. Acad. Sci. U.S.A. 2016; 113:13063–13068.
Hekimi S, Wang Noe A. Mitochondrial ROS and the effectors of the intrinsic apoptotic pathway in aging cells: the discerning killers!. Front. Genet. 2016; 7: 161.
Jones PD, Sies H. The redox code, Antioxidants Redox Signal. 2015; 23: 734–746.
Vida I, Martinez de Toda A, Garrido E, Carro JA, Molina S, de la Fuente M. Impairment of several immune functions and redox state in blood cells of Alzheimer's disease patients. Relevant role of neutrophils in oxidative stress. Frontiers in Immunology.2018 vol. 8: p. 1974-84.
Daiber A, Di Lisa F, Oelze M, Kroller S, Steven S, Schulz E, et al. Crosstalk of mitochondria with nadph oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function, Br. J. Pharmacol. 2017; 174: 1670–1689.
Kroller S, Steven S, Kossmann S, Scholz A, Daub S, Oelze M. et al. Molecular mechanisms of the crosstalk between mitochondria and nadph oxidase through reactive oxygen species-studies in white blood cells and in animal models. Antioxidants Redox Signal.2014; 20: 247–266.
Doughan AK, Harrison DG, Dikalov SI. Molecular mechanisms of angiotensin II-mediated mitochondrial dysfunction: linking mitochondrial oxidative damage and vascular endothelial dysfunction, Circ. Res.2008; 102: 488–496.
Mastroeni D, Khdour OM, Delvaux E, Nolz J, Olsen G, Berchtold N, et al. Nuclear but not mitochondrial-encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer’s disease. Alzheimers Dement. 2017;13 (5):510–9.
Radi R. Oxygen radicals, nitric oxide, and peroxynitrite: redox pathways in molecular medicine, Proc. Natl. Acad. Sci. U.S.A.2018; 115: 5839–5848.
Birnbaum JH, Wanner D, Gietl AF. Oxidative stress and altered mitochondrial protein expression in the absence of amyloid-β and tau pathology in iPSC-derived neurons from sporadic Alzheimer's
disease patients. Stem Cell Research.2018; vol. 27:121–130.
Monteiro dos Santos S, Rodrigues CF, Azulay C, Lima AR, Chagas M. Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer’s Disease? Oxidative Medicine and Cellular Longevity. 2019; Volume Article ID 8409329, 14 pages https://doi.org/10.1155/2019/8409329
Cadonic C, Golam Sabbir M,Albensi BC. Mechanisms of Mitochondrial Dysfunction in Alzheimer’s Disease Mol Neurobiol. 2016; 53:6078–6090,doi 10.1007/s12035-015-9515-5
Haas RH, Mitochondrial Dysfunction in Aging and Diseases of Aging Biology. 2019; 8 ( 48); doi: 10.3390/biology8020048.
Montgomery MK. Mitochondrial dysfunction and diabetes: Is mitochondrial transfer a friend or foe? Biology. 2019; 8( 33).
Weise CM, Chen K, Chen Y, Kuang X, Savage CR, Reiman EM, et al. Left lateralized cerebral glucose metabolism declines in amyloid-beta positive persons with mild cognitive impairment. Neuroimage Clin. 2018; 20:286–96.
Swerdlow RH. Mitochondria and mitochondrial cascades in Alzheimer’s disease. J Alzheimers Dis. 2018; 62 (3):1403–16.
Magalingam KB, Radhakrishnan A, Ping NS, Haleagrahara N, Current concepts of neurodegenerative mechanisms in Alzheimer's disease. BioMed Research International, 2018; Article ID 3740461, 12 pages.
Croteau E, Castellano CA, Fortier M, Bocti C, Fulop T, Paquet N, et al. A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s disease. Exp Gerontol. 2018; 107:18–26.
D’Souza AR, Minczuk M. Mitochondrial transcription and translation:overview. Essays Biochem. 2018; 62(3):309–20.
Weidling I, Swerdlow RH. Mitochondrial dysfunction and stress responses in Alzheimer’s disease. Biology 2019; 8 ( 39).
Swerdlow RH, Khan SM. A Mitochondrial cascade hypothesis for sporadic Alzheimer's disease. Med. Hypotheses.2004; 63:8–20.
Swerdlow RH, Khan SM. The Alzheimer's disease mitochondrial cascade hypothesis: An update. Exp. Neurol. 218 (2009) 308–315.
Santos RX, Correia SC, Wang X, Perry G, Smith MA, Moreira PI, Zhu X. Alzheimer’s disease: diverse aspects of mitochondrial malfunctioning. Int J Clin. Exp. Pathol. 2017;3(6):570–581.
Swerdlow RH. Mitochondria and mitochondrial cascades in Alzheimer’s disease. J Alzheimers Dis. 2018; 62(3):1403–16.
Bermejo P, Gomez P, Santos J, Pastor E, Gil P, Martin S. Determination of malonaldehyde in Alzheimer's disease: a comparative study of high-performance liquid chromatography and thiobarbituric acid test Gerontology.1997; 43:218–222.
Calvo M, Hernando E, Nunez L, Villalobos C. Amyloid beta oligomers increase ER-mitochondria Ca 2+ cross talk in young hippocampal neurons and exacerbate aging-induced intracellular Ca 2+ remodeling. Front. Cell Neurosci. 2019;13: 22 -7.
Sarasija S. et al. Presenilin mutations deregulate mitochondrial Ca 2+ homeostasis and metabolic activity causing neurodegeneration in Caenorhabditis elegans. eLife . 2018;7, https://doi.org/10.7554/eLife.33052 (2018)
Luongo TS. The mitochondrial Na + /Ca2 + exchanger is essential for Ca 2+ homeostasis and viability. Nature. 2017; 545: 93–97.
Lee KS. Altered ER-mitochondria contact impacts mitocondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models. Proc. Natl Acad. Sci. USA.2018; 115, E8844– E8853.
Devin PJ, Kolmetzky W, Tomar D, Di Meco A, Lombardi A.A. Impaired mitochondrial calcium efflux contributes to disease progression in models of Alzheimer’s disease. NATURE COMMUNICATIONS | 2019; 10:3885 | https://doi.org/10.1038/s41467-019-11813-6
Area E. A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease. Cell Death Dis.2018; 9, 335.
Paranjpe MD, Chen X, Liu M, Paranjpe I, Leal JP, Wang R, et al. The effect of ApoE epsilon4 on longitudinal brain region-specific glucose metabolism in patients with mild cognitive impairment: a FDG-PET study. Neuroimage Clin. 2019; 22:101795.
Caldwell CC, Yao J, Brinton G. Targeting the prodromal stage of Alzheimer’s disease: Bioenergetic and mitochondrial opportunities. Neurotherapeutics.2015; 12: 66-80.
Patel M. Targeting oxidative stress in central nervous system disorders. Trends Pharmacol Sci. 2016; 37: 768-778.
Enlaces refback
- No hay ningún enlace refback.
Esta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial 4.0 Internacional.
La revista está: Certificada por el CITMA
La revista es de acceso abierto y gratuito.