medigraphic.com
Academia Mexicana de Neurología, A.C.

2019, Número 3

<< Anterior Siguiente >>

Rev Mex Neuroci 2019; 20 (3)


Inmunología de la enfermedad de Alzheimer

Sosa-García LI, Hernández-Jiménez J, Del Moral-Huerta DI, Duyckaerts C, Calderón-Garcidueñas AL

Idioma: Ingles.
Referencias bibliográficas: 59
Paginas: 162-170
Archivo PDF: 141.99 Kb.


RESUMEN

La enfermedad de Alzheimer (EA) es una patología neurodegenerativa multifactorial. La neuroinflamación es un evento temprano de las etapas presintomáticas en la EA y contribuye a su progresión. En este trabajo revisamos la participación de astrocitos, microglia y células de la barrera hematoencefálica, los mecanismos de muerte celular y los factores inflamatorios como las quimiocinas, los interferones y los receptores tipo Toll que participan en la progresión y la perpetuación de esta enfermedad. También se mencionan algunas de sus posibilidades pronósticas y terapéuticas. La identificación de los diferentes actores involucrados en la inflamación y de los principales mecanismos de daño podrían permitir el desarrollo de estrategias y tratamientos preventivos para combatir esta enfermedad devastadora.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Lewis J, Dickson DW. Propagation of tau pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies. Acta Neuropathol. 2016;131:27-48.

  2. Balin BJ, Hudson AP. Etiology and pathogenesis of late-onset alzheimer’s disease. Curr Allergy Asthma Rep. 2014;14:417.

  3. Gatz M, Reynolds CA, Fratiglioni L, et al. Role of genes and environments for explaining alzheimer disease. Arch Gen Psychiatry. 2006;63:168-74.

  4. International Genomics of Alzheimer’s Disease Consortium (IGAP). Convergent genetic and expression data implicate immunity in alzheimer’s disease. Alzheimers Dement. 2015;11:658-71.

  5. Heppner FL, Ransohoff RM, Becher B. Immune attack: the role of inflammation in alzheimer disease. Nat Rev Neurosci. 2015;16:358-72.

  6. Liu C, Cui G, Zhu M, Kang X, Guo H. Neuroinflammation in alzheimer’s disease: chemokines produced by astrocytes and chemokine receptors. Int J Clin Exp Pathol. 2014;7:8342-55.

  7. Birch AM. The contribution of astrocytes to alzheimer’s disease. Biochem Soc Trans. 2014;42:1316-20.

  8. Lee WJ, Liao YC, Wang YF, et al. Plasma MCP-1 and cognitive decline in patients with alzheimer’s disease and mild cognitive impairment: a two-year follow-up study. Sci Rep. 2018;8:1280.

  9. Zhao H, Wang Q, Cheng X, et al. Inhibitive effect of resveratrol on the inflammation in cultured astrocytes and microglia induced by Aβ1-42. Neuroscience. 2018;379:390-404.

  10. Bahniwal M, Little JP, Klegeris A. High glucose enhances neurotoxicity and inflammatory cytokine secretion by stimulated human astrocytes. Curr Alzheimer Res. 2017;14:731-41.

  11. Parkhurst CN, Yang G, Ninan I, et al. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor. Cell. 2013;155:1596-609.

  12. Melchior B, Puntambekar SS, Carson MJ. Microglia and the control of autoreactive T cell responses. Neurochem Int. 2006;49:145-53.

  13. Kierdorf K, Erny D, Goldmann T, et al. Microglia emerge from erythromyeloid precursors via pu.1-and irf8-dependent pathways. Nat Neurosci. 2013;16:273-80.

  14. Guedes JR, Lao T, Cardoso AL, El Khoury J. Roles of microglial and monocyte chemokines and their receptors in regulating alzheimer’s disease- associated amyloid-β and tau pathologies. Front Neurol. 2018; 9:549.

  15. Lanni C, Fagiani F, Racchi M, et al. Beta-amyloid short-and long-term synaptic entanglement. Pharmacol Res. 2019;139:243-60.

  16. Gay M, Evrard C, Descamps F, et al. A phenotypic approach to the discovery of compounds that promote non-amyloidogenic processing of the amyloid precursor protein: toward a new profile of indirect β-secretase inhibitors. Eur J Med Chem. 2018;159:104-25.

  17. Kirouac L, Rajic AJ, Cribbs DH, Padmanabhan J. Activation of ras-ERK signaling and GSK-3 by amyloid precursor protein and amyloid beta facilitates neurodegeneration in alzheimer’s disease. ENeuro. 2017; 4:ENEURO.0149-16.2017.

  18. Kim Y, Kim C, Jang HY, Mook-Jung I. Inhibition of cholesterol biosynthesis reduces γ-secretase activity and amyloid-β generation. J Alzheimers Dis. 2016;51:1057-68.

  19. Neumann U, Ufer M, Jacobson LH, et al. The BACE-1 inhibitor CNP520 for prevention trials in alzheimer’s disease. EMBO Mol Med. 2018; 10:e9316.

  20. Zhang H, Liu D, Huang H, Zhao Y, Zhou H. Characteristics of insulin-degrading enzyme in alzheimer’s disease: a meta-analysis. Curr Alzheimer Res. 2018;15:610-7.

  21. Kazkayasi I, Burul-Bozkurt N, Ismail MA, et al. Insulin deprivation decreases insulin degrading enzyme levels in primary cultured cortical neurons and in the cerebral cortex of rats with streptozotocin-induced diabetes. Pharmacol Rep. 2018;70:677-83.

  22. Shi Y, Holtzman DM. Interplay between innate immunity and alzheimer disease: APOE and TREM2 in the spotlight. Nat Rev Immunol. 2018; 18:759-72.

  23. Arboleda-Bustos CE, Ortega-Rojas J, Mahecha MF, et al. The p.R47H variant of TREM2 gene is associated with late-onset alzheimer disease in colombian population. Alzheimer Dis Assoc Disord. 2018;32:305-8.

  24. Wang Y, Ulland TK, Ulrich JD, et al. TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques. J Exp Med. 2016;213:667-75.

  25. Li JT, Zhang Y. TREM2 regulates innate immunity in alzheimer’s disease. J Neuroinflammation. 2018;15:107.

  26. Zheng H, Jia L, Liu CC, et al. TREM2 promotes microglial survival by activating wnt/β-catenin pathway. J Neurosci. 2017;37:1772-84.

  27. Jendresen C, Årskog V, Daws MR, Nilsson LN. The alzheimer’s disease risk factors apolipoprotein E and TREM2 are linked in a receptor signaling pathway. J Neuroinflammation. 2017;14:59.

  28. Tam WY, Ma CH. Bipolar/rod-shaped microglia are proliferating microglia with distinct M1/M2 phenotypes. Sci Rep. 2014;4:7279.

  29. Krbot K, Hermann P, Skorić MK, et al. Distinct microglia profile in creutzfeldt- jakob disease and alzheimer’s disease is independent of disease kinetics. Neuropathology. 2018;38:591-600.

  30. Streit WJ, Braak H, Xue QS, Bechmann I. Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in alzheimer’s disease. Acta Neuropathol. 2009;118:475-85.

  31. Medeiros R, Kitazawa M, Passos GF, et al. Aspirin-triggered lipoxin A4 stimulates alternative activation of microglia and reduces alzheimer disease- like pathology in mice. Am J Pathol. 2013;182:1780-9.

  32. Kirkland JL, Tchkonia T. Cellular senescence: a translational perspective. EBioMedicine. 2017;21:21-8.

  33. Bussian TJ, Aziz A, Meyer CF, et al. Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline. Nature. 2018; 562:578-82.

  34. Snyder HM, Corriveau RA, Craft S, et al. Vascular contributions to cognitive impairment and dementia including alzheimer’s disease. Alzheimers Dement. 2015;11:710-7.

  35. McFadyen JD, Kiefer J, Braig D, et al. Dissociation of C-reactive protein localizes and amplifies inflammation: evidence for a direct biological role of C-reactive protein and its conformational changes. Front Immunol. 2018;9:1351.

  36. Shibata M, Yamada S, Kumar SR, et al. Clearance of alzheimer’s amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier. J Clin Invest. 2000;106:1489-99.

  37. Jeynes B, Provias J. Evidence for altered LRP/RAGE expression in alzheimer lesion pathogenesis. Curr Alzheimer Res. 2008;5:432-7.

  38. Erickson MA, Banks WA. Blood-brain barrier dysfunction as a cause and consequence of alzheimer’s disease. J Cereb Blood Flow Metab. 2013;33:1500-13.

  39. Liu C, Chen K, Lu Y, Fang Z, Yu G. Catalpol provides a protective effect on fibrillary Aβ1-42 -induced barrier disruption in an in vitro model of the blood-brain barrier. Phytother Res. 2018;32:1047-55.

  40. Wong WB, Lin VW, Boudreau D, Devine EB. Statins in the prevention of dementia and alzheimer’s disease: a meta-analysis of observational studies and an assessment of confounding. Pharmacoepidemiol Drug Saf. 2013;22:345-58.

  41. Salech F, Ponce DP, SanMartín CD, et al. PARP-1 and p53 regulate the increased susceptibility to oxidative death of lymphocytes from MCI and AD patients. Front Aging Neurosci. 2017;9:310.

  42. Solleiro-Villavicencio H, Rivas-Arancibia S. Systemic th17/IL-17A response appears prior to hippocampal neurodegeneration in rats exposed to low doses of ozone. Neurologia. 2017. pii: S0213-4853(17) 30194-9.

  43. Derkow K, Rössling R, Schipke C, et al. Distinct expression of the neurotoxic microRNA family let-7 in the cerebrospinal fluid of patients with alzheimer’s disease. PLoS One. 2018;13:e0200602.

  44. Merlini M, Kirabali T, Kulic L, Nitsch RM, Ferretti MT. Extravascular CD3+ T cells in brains of alzheimer disease patients correlate with tau but not with amyloid pathology: an immunohistochemical study. Neurodegener Dis. 2018;18:49-56.

  45. SanMartin CD, Henriquez M, Chacon C, et al. Vitamin D increases aβ140 plasma levels and protects lymphocytes from oxidative death in mild cognitive impairment patients. Curr Alzheimer Res. 2018;15:561-9.

  46. Sommer A, Winner B, Prots I. The trojan horse-neuroinflammatory impact of T cells in neurodegenerative diseases. Mol Neurodegener. 2017;12:78.

  47. Ahmed ME, Iyer S, Thangavel R, et al. Co-localization of glia maturation factor with NLRP3 inflammasome and autophagosome markers in human alzheimer’s disease brain. J Alzheimers Dis. 2017;60:1143-60.

  48. Tammineni P, Cai Q. Defective retrograde transport impairs autophagic clearance in alzheimer disease neurons. Autophagy. 2017;13:982-4.

  49. Navarro V, Sanchez-Mejias E, Jimenez S, et al. Microglia in alzheimer’s disease: activated, dysfunctional or degenerative. Front Aging Neurosci. 2018;10:140.

  50. Shao BZ, Cao Q, Liu C. Targeting NLRP3 inflammasome in the treatment of CNS diseases. Front Mol Neurosci. 2018;11:320.

  51. Raikwar SP, Thangavel R, Dubova I, et al. Targeted gene editing of glia maturation factor in microglia: a novel alzheimer’s disease therapeutic target. Mol Neurobiol. 2019;56:378-93.

  52. Ciaramella A, Salani F, Bizzoni F, et al. The stimulation of dendritic cells by amyloid beta 1-42 reduces BDNF production in alzheimer’s disease patients. Brain Behav Immun. 2013;32:29-32.

  53. Janelidze S, Mattsson N, Stomrud E, et al. CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early alzheimer disease. Neurology. 2018;91:e867-77.

  54. Lin MS, Hung KS, Chiu WT, et al. Curcumin enhances neuronal survival in N-methyl-d-aspartic acid toxicity by inducing RANTES expression in astrocytes via PI-3K and MAPK signaling pathways. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35:931-8.

  55. Ransohoff RM, El Khoury J. Microglia in health and disease. Cold Spring Harb Perspect Biol. 2015;8:a020560.

  56. Xia MQ, Qin SX, Wu LJ, Mackay CR, Hyman BT. Immunohistochemical study of the beta-chemokine receptors CCR3 and CCR5 and their ligands in normal and alzheimer’s disease brains. Am J Pathol. 1998;153:31-7.

  57. Grimaldi LM, Zappalà G, Iemolo F, et al. A pilot study on the use of interferon beta-1a in early alzheimer’s disease subjects. J Neuroinflammation. 2014;11:30.

  58. Rubio-Araiz A, Finucane OM, Keogh S, Lynch MA. Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid. J Neuroinflammation. 2018;15:247.

  59. Sohrabifar N, Gharesouran J, Talebi M, Ghojazadeh M, Mohaddes Ardebili SM. Association of CLU and TLR2 gene polymorphisms with late- onset alzheimer disease in a Northwestern Iranian population. Turk J Med Sci. 2015;45:1082-6.




2020     |     www.medigraphic.com