Derleme
BibTex RIS Kaynak Göster

ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ

Yıl 2024, Cilt: 48 Sayı: 1, 300 - 311, 20.01.2024
https://doi.org/10.33483/jfpau.1337722

Öz

Amaç: Bağışıklık sistemi, vücudu enfeksiyonlara karşı savunan, yabancı maddelere tepki oluşturan ve hastalık gibi durumlarda organizmayı koruyan bir sistemdir. Merkezi sinir sistemi bağışıklık yanıtları bakımından periferik organlardan farklı benzersiz bir yapıya sahiptir. Son yıllarda gerçekleştirilen kapsamlı araştırmalar, beyin ve bağışıklık sistemi arasında karmaşık bir etkileşim olduğunu göstermiştir. Beyin bağışıklık sistemi, merkezi sinir sistemi içinde yer alan bir dizi hücresel ve moleküler mekanizmadan ve bağışıklık hücreleri ve moleküllerinin yer aldığı bir dizi yapıdan oluşan kompleks bir sistemdir. Beyindeki kronik inflamasyonun birçok nörodejeneratif hastalıkta ilerleyici nöron ölümünde önemli bir rol oynayabileceği bilinmektedir. Son yıllarda başta kadınlar olmak üzere ileri yaş popülasyonu etkileyen Alzheimer hastalığı, kısa süreli hafıza, biliş ve günlük yaşam aktivitelerinde zorluklarla ilgili sorunlarla karakterize edilen ilerleyici, nörodejeneratif bir hastalıktır. Alzheimer hastalığı genetik, immün ve çevresel etmenleri de içerdiği düşünülen kompleks bir mekanizmayla ortaya çıkar. Bu hastalığın kesin bir tedavisi yoktur ve kullanılan ilaçlar ancak semptomları geciktirir. Kompleman sistem doğuştan gelen bağışıklık sisteminin bir parçasıdır. Bu sistemin üç farklı aktive edici yolu vardır ve nihai olarak hedef hücre lizisine neden olan bir membran saldırı kompleksinin oluşumuyla sonuçlanır.
Sonuç ve Tartışma: Bu derlemede kompleman sistemin merkezi sinir sisteminde işleyişine ve Alzheimer hastalığı gibi nörodejeneratif bozukluklara yol açan kronik nöroinflamasyona nasıl katkıda bulunduğuna dair bilgiler paylaşılması amaçlanmıştır.

Proje Numarası

none

Kaynakça

  • 1. Emmerling, M.R., Watson, M.D., Raby, C.A., Spiegel, K. (2000). The role of complement in Alzheimer's disease pathology. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1502(1), 158-171. [CrossRef]
  • 2. Veerhuis, R., Nielsen, H.M., Tenner, A.J. (2011). Complement in the brain. Molecular Immunology, 48(14), 1592-1603. [CrossRef]
  • 3. Crehan, H., Hardy, J., Pocock, J. (2012). Microglia, Alzheimer's disease, and complement. International Journal of Alzheimer's disease, 2012, 983640. [CrossRef]
  • 4. Ueno, M., Chiba, Y., Murakami, R., Matsumoto, K., Kawauchi, M., Fujihara, R. (2016). Blood-brain barrier and blood-cerebrospinal fluid barrier in normal and pathological conditions. Brain Tumor Pathology, 33(2), 89-96. [CrossRef]
  • 5. Morgan, B.P. (2018). Complement in the pathogenesis of Alzheimer's disease. Seminars in Immunopathology, 40(1), 113-124. [CrossRef]
  • 6. Montagne, A., Barnes, S.R., Sweeney, M.D., Halliday, M.R., Sagare, A.P., Zhao, Z., Toga, A.W., Jacobs, R. E., Liu, C.Y., Amezcua, L., Harrington, M.G., Chui, H.C., Law, M., Zlokovic, B.V. (2015). Blood-brain barrier breakdown in the aging human hippocampus. Neuron, 85(2), 296-302. [CrossRef]
  • 7. Varatharaj, A., Galea, I. (2017). The blood-brain barrier in systemic inflammation. Brain, Behavior, and Immunity, 60, 1-12. [CrossRef]
  • 8. Takeda, S., Sato, N., Morishita, R. (2014). Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy. Frontiers in Aging Neuroscience, 6, 171. [CrossRef]
  • 9. McGeer, E.G., McGeer, P.L. (1998). The importance of inflammatory mechanisms in Alzheimer disease. Experimental Gerontology, 33(5), 371-378. [CrossRef]
  • 10. Shinjyo, N., Kagaya, W., Pekna, M. (2021). Interaction between the complement system and ınfectious agents-A potential mechanistic link to neurodegeneration and dementia. Frontiers in Cellular Neuroscience, 15, 710390. [CrossRef]
  • 11. Mapunda, J.A., Tibar, H., Regragui, W., Engelhardt, B. (2022). How does the immune system enter the brain? Frontiers in Immunology, 13, 805657. [CrossRef]
  • 12. Shah, A., Kishore, U., Shastri, A. (2021). Complement system in Alzheimer's disease. International Journal of Molecular Sciences, 22(24), 13647. [CrossRef]
  • 13. WHO (World Health Organization) web site. (2023). Dementia. Available online: https://www.who.int/news-room/fact sheets/detail/dementia. Erişim tarihi: 27.03.2023.
  • 14. Kumar, P.J., Clark, M. (2011). Kumar & Clark’s Clinical Medicine, Saunders Elsevier, Edinburgh.
  • 15. Tenner A.J. (2020). Complement-mediated events in Alzheimer’s disease: Mechanisms and potential therapeutic targets. Journal of Immunology, 204(2), 306-315. [CrossRef]
  • 16. Livingston, G., Sommerlad, A., Orgeta, V., Costafreda, S.G., Huntley, J., Ames, D., Ballard, C., Banerjee, S., Burns, A., Cohen-Mansfield, J., Cooper, C., Fox, N., Gitlin, L.N., Howard, R., Kales, H.C., Larson, E. B., Ritchie, K., Rockwood, K., Sampson, E.L., Samus, Q., Schneider, L.S., Selbæk, G., Teri, L., Mukadam, N. (2017). Dementia prevention, intervention, and care. Lancet, 390(10113), 2673-2734. [CrossRef]
  • 17. Sala Frigerio, C., Wolfs, L., Fattorelli, N., Thrupp, N., Voytyuk, I., Schmidt, I., Mancuso, R., Chen, W.T., Woodbury, M.E., Srivastava, G., Möller, T., Hudry, E., Das, S., Saido, T., Karran, E., Hyman, B., Perry, V. H., Fiers, M., De Strooper, B. (2019). The major risk factors for Alzheimer’s disease: Age, sex, and genes modulate the microglia response to Aβ plaques. Cell Reports, 27(4), 1293-1306. [CrossRef]
  • 18. Shastri, A., Bonifati, D.M., Kishore, U. (2013). Innate immunity and neuroinflammation. Mediators of inflammation, 2013, 342931. [CrossRef]
  • 19. Liu, Y.P., Lin, H.I., Tzeng, S.F. (2005). Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture. Brain Research, 1054(2), 152-158. [CrossRef]
  • 20. Harms, A.S., Lee, J.K., Nguyen, T.A., Chang, J., Ruhn, K.M., Treviño, I., Tansey, M.G. (2012). Regulation of microglia effector functions by tumor necrosis factor signaling. Glia, 60(2), 189-202. [CrossRef]
  • 21. Jimenez, S., Baglietto-Vargas, D., Caballero, C., Moreno-Gonzalez, I., Torres, M., Sanchez-Varo, R., Ruano, D., Vizuete, M., Gutierrez, A., Vitorica, J. (2008). Inflammatory response in the hippocampus of PS1M146L/APP751SL mouse model of Alzheimer's disease: Age-dependent switch in the microglial phenotype from alternative to classic. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, 28(45), 11650-11661. [CrossRef]
  • 22. Zhang, L., Dong, Z.F., Zhang, J.Y. (2020). Immunomodulatory role of mesenchymal stem cells in Alzheimer's disease. Life Sciences, 246, 117405. [CrossRef]
  • 23. Yong, H.Y.F., Rawji, K.S., Ghorbani, S., Xue, M., Yong, V.W. (2019). The benefits of neuroinflammation for the repair of the injured central nervous system. Cellular & Molecular Immunology, 16(6), 540-546. [CrossRef]
  • 24. Lo, M.W., Woodruff, T.M. (2020). Complement: Bridging the innate and adaptive immune systems in sterile inflammation. Journal of Leukocyte Biology, 108(1), 339-351. [CrossRef]
  • 25. Aisen, P.S., Cummings, J., Jack, C.R., Jr, Morris, J.C., Sperling, R., Frölich, L., Jones, R.W., Dowsett, S.A., Matthews, B.R., Raskin, J., Scheltens, P., Dubois, B. (2017). On the path to 2025: Understanding the Alzheimer's disease continuum. Alzheimer's Research & Therapy, 9(1), 60. [CrossRef]
  • 26. Bonifati, D.M., Kishore, U. (2007). Role of complement in neurodegeneration and neuroinflammation. Molecular Immunology, 44(5), 999-1010. [CrossRef]
  • 27. Schartz, N.D., Tenner, A.J. (2020). The good, the bad, and the opportunities of the complement system in neurodegenerative disease. Journal of Neuroinflammation, 17(1), 354. [CrossRef]
  • 28. Velazquez, P., Cribbs, D.H., Poulos, T.L., Tenner, A.J. (1997). Aspartate residue 7 in amyloid beta-protein is critical for classical complement pathway activation: implications for Alzheimer's disease pathogenesis. Nature Medicine, 3(1), 77-79. [CrossRef]
  • 29. Shen, Y., Lue, L., Yang, L., Roher, A., Kuo, Y., Strohmeyer, R., Goux, W.J., Lee, V., Johnson, G.V., Webster, S.D., Cooper, N.R., Bradt, B., Rogers, J. (2001). Complement activation by neurofibrillary tangles in Alzheimer's disease. Neuroscience Letters, 305(3), 165-168. [CrossRef]
  • 30. Tenner, A.J., Stevens, B., Woodruff, T.M. (2018). New tricks for an ancient system: Physiological and pathological roles of complement in the CNS. Molecular Immunology, 102, 3-13. [CrossRef]
  • 31. Ricklin, D., Lambris, J.D. (2013). Complement in immune and inflammatory disorders: pathophysiological mechanisms. Journal of Immunology, 190(8), 3831-3838. [CrossRef]
  • 32. Morgan, B.P., Gasque, P. (1997). Extrahepatic complement biosynthesis: where, when and why? Clinical and Experimental Immunology, 107(1), 1-7. [CrossRef]
  • 33. Gasque, P., Neal, J.W., Singhrao, S.K., McGreal, E.P., Dean, Y.D., Van, B.J., Morgan, B.P. (2002). Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activities. Molecular Neurobiology, 25(1), 1-17. [CrossRef]
  • 34. Tang, S., Zhou, W., Sheerin, N.S., Vaughan, R.W., Sacks, S.H. (1999). Contribution of renal secreted complement C3 to the circulating pool in humans. Journal of Immunology, 162(7), 4336-4341.
  • 35. Zhou, W., Marsh, J.E., Sacks, S.H. (2001). Intrarenal synthesis of complement. Kidney International, 59(4), 1227-1235. [CrossRef]
  • 36. Johnson, S.A., Lampert-Etchells, M., Pasinetti, G.M., Rozovsky, I., Finch, C.E. (1992). Complement mRNA in the mammalian brain: responses to Alzheimer's disease and experimental brain lesioning. Neurobiology of Aging, 13(6), 641-648. [CrossRef]
  • 37. Rozovsky, I., Morgan, T.E., Willoughby, D.A., Dugichi-Djordjevich, M.M., Pasinetti, G.M., Johnson, S.A., Finch, C.E. (1994). Selective expression of clusterin (SGP-2) and complement C1qB and C4 during responses to neurotoxins in vivo and in vitro. Neuroscience, 62(3), 741-758. [CrossRef]
  • 38. Veerhuis, R., Janssen, I., Hoozemans, J.J., De Groot, C.J., Hack, C.E., Eikelenboom, P. (1998). Complement C1-inhibitor expression in Alzheimer's disease. Acta Neuropathologica, 96(3), 287-296. [CrossRef]
  • 39. Walker, D.G., McGeer, P.L. (1992). Complement gene expression in human brain: comparison between normal and Alzheimer disease cases. Brain research. Molecular Brain Research, 14(1-2), 109-116. [CrossRef]
  • 40. Singhrao, S.K., Neal, J.W., Morgan, B.P., Gasque, P. (1999). Increased complement biosynthesis by microglia and complement activation on neurons in Huntington's disease. Experimental Neurology, 159(2), 362-376. [CrossRef]
  • 41. Kishore, U., Gupta, S.K., Perdikoulis, M.V., Kojouharova, M.S., Urban, B.C., Reid, K.B. (2003). Modular organization of the carboxyl-terminal, globular head region of human C1q A, B, and C chains. Journal of Immunology, 171(2), 812-820. [CrossRef]
  • 42. Yang, L.B., Li, R., Meri, S., Rogers, J., Shen, Y. (2000). Deficiency of complement defense protein CD59 may contribute to neurodegeneration in Alzheimer's disease. The Journal of Neuroscience, 20(20), 7505-7509. [CrossRef]
  • 43. McGeer, P.L., Akiyama, H., Itagaki, S., McGeer, E.G. (1989). Activation of the classical complement pathway in brain tissue of Alzheimer patients. Neuroscience Letters, 107(1-3), 341-346. [CrossRef]
  • 44. Rogers, J., Cooper, N.R., Webster, S., Schultz, J., McGeer, P.L., Styren, S.D., Civin, W.H., Brachova, L., Bradt, B., Ward, P. (1992). Complement activation by beta-amyloid in Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America, 89(21), 10016-10020. [CrossRef]
  • 45. Berg, A., Zelano, J., Stephan, A., Thams, S., Barres, B.A., Pekny, M., Pekna, M., Cullheim, S. (2012). Reduced removal of synaptic terminals from axotomized spinal motoneurons in the absence of complement C3. Experimental Neurology, 237(1), 8-17. [CrossRef]
  • 46. Shi, Q., Colodner, K. J., Matousek, S.B., Merry, K., Hong, S., Kenison, J. E., Frost, J.L., Le, K. X., Li, S., Dodart, J.C., Caldarone, B.J., Stevens, B., Lemere, C.A. (2015). Complement C3-Deficient mice fail to display age-related hippocampal decline. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, 35(38), 13029-13042. [CrossRef]
  • 47. Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., Cole, G. (1996). Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice. Science, 274(5284), 99-102. [CrossRef]
  • 48. Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C. M., Perez-tur, J., Hutton, M., Buee, L., Harigaya, Y., Yager, D., Morgan, D., Gordon, M. N., Holcomb, L., Refolo, L., Zenk, B., Hardy, J., Younkin, S. (1996). Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1. Nature, 383(6602), 710-713. [CrossRef]
  • 49. Matsuoka, Y., Picciano, M., Malester, B., LaFrancois, J., Zehr, C., Daeschner, J. M., Olschowka, J.A., Fonseca, M.I., O'Banion, M.K., Tenner, A.J., Lemere, C.A., Duff, K. (2001). Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease. The American Journal of Pathology, 158(4), 1345-1354. [CrossRef]
  • 50. Holcomb, L., Gordon, M.N., McGowan, E., Yu, X., Benkovic, S., Jantzen, P., Wright, K., Saad, I., Mueller, R., Morgan, D., Sanders, S., Zehr, C., O'Campo, K., Hardy, J., Prada, C.M., Eckman, C., Younkin, S., Hsiao, K., Duff, K. (1998). Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. Nature Medicine, 4(1), 97-100. [CrossRef]
  • 51. Webster, S.D., Yang, A.J., Margol, L., Garzon-Rodriguez, W., Glabe, C.G., Tenner, A.J. (2000). Complement component C1q modulates the phagocytosis of Abeta by microglia. Experimental Neurology, 161(1), 127-138. [CrossRef]
  • 52. Fonseca, M.I., Zhou, J., Botto, M., Tenner, A.J. (2004). Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease. The Journal of Neuroscience: The Official Journal of The Society for Neuroscience, 24(29), 6457-6465. [CrossRef]
  • 53. Hong, S., Beja-Glasser, V.F., Nfonoyim, B.M., Frouin, A., Li, S., Ramakrishnan, S., Merry, K.M., Shi, Q., Rosenthal, A., Barres, B. A., Lemere, C.A., Selkoe, D.J., Stevens, B. (2016). Complement and microglia mediate early synapse loss in Alzheimer mouse models. Science, 352(6286), 712-716. [CrossRef]
  • 54. Zhou, J., Fonseca, M.I., Pisalyaput, K., Tenner, A.J. (2008). Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease. Journal of Neurochemistry, 106(5), 2080-2092. [CrossRef]
  • 55. Kolev, M.V., Ruseva, M.M., Harris, C.L., Morgan, B.P., Donev, R.M. (2009). Implication of complement system and its regulators in Alzheimer's disease. Current Neuropharmacology, 7(1), 1-8. [CrossRef]
  • 56. Györffy, B. A., Tóth, V., Török, G., Gulyássy, P., Kovács, R. Á., Vadászi, H., Micsonai, A., Tóth, M.E., Sántha, M., Homolya, L., Drahos, L., Juhász, G., Kékesi, K.A., Kardos, J. (2020). Synaptic mitochondrial dysfunction and septin accumulation are linked to complement-mediated synapse loss in an Alzheimer's disease animal model. Cellular and Molecular Life Sciences: CMLS, 77(24), 5243-5258. [CrossRef]
  • 57. Litvinchuk, A., Wan, Y.W., Swartzlander, D.B., Chen, F., Cole, A., Propson, N.E., Wang, Q., Zhang, B., Liu, Z., Zheng, H. (2018). Complement C3aR inactivation attenuates tau pathology and reverses an immune network deregulated in tauopathy models and Alzheimer’s disease. Neuron, 100(6), 1337-1353.e5. [CrossRef]

THE ROLE OF THE COMPLEMENT SYSTEM IN ALZHEIMER’S DISEASE

Yıl 2024, Cilt: 48 Sayı: 1, 300 - 311, 20.01.2024
https://doi.org/10.33483/jfpau.1337722

Öz

Objective: Immune system is a system that defends the body against infections, reacts to foreign substances, and protects the organism in conditions such as illness. The central nervous system has a unique structure that differs from peripheral organs in terms of immune responses. Extensive research in recent years has shown that there is a complex interaction between the brain and immune system. Brain immune system is a complex system consisting of a number of cellular and molecular mechanisms within the central nervous system and a set of structures in which immune cells and molecules take place. It is known that chronic inflammation in the brain may play an important role in progressive neuron death in many neurodegenerative diseases. Alzheimer's disease, which has been affecting the elderly population, especially women in recent years, is a progressive, neurodegenerative disease characterized by problems related to short-term memory, cognition and difficulties in daily living activities. Alzheimer's disease occurs with a complex mechanism thought to include genetic, immune and environmental factors. There is no definite cure for this disease and the drugs used only delay the symptoms. The complement system is part of the innate immune system. This system has three different activating pathways and results in the formation of a membrane attack complex that ultimately causes target cell lysis.
Result and Discussion: In this review, we aimed to share information about the functioning of the complement system in the central nervous system and how it contributes to chronic neuroinflammation that leads to neurodegenerative disorders such as Alzheimer’s disease.

Destekleyen Kurum

none

Proje Numarası

none

Kaynakça

  • 1. Emmerling, M.R., Watson, M.D., Raby, C.A., Spiegel, K. (2000). The role of complement in Alzheimer's disease pathology. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1502(1), 158-171. [CrossRef]
  • 2. Veerhuis, R., Nielsen, H.M., Tenner, A.J. (2011). Complement in the brain. Molecular Immunology, 48(14), 1592-1603. [CrossRef]
  • 3. Crehan, H., Hardy, J., Pocock, J. (2012). Microglia, Alzheimer's disease, and complement. International Journal of Alzheimer's disease, 2012, 983640. [CrossRef]
  • 4. Ueno, M., Chiba, Y., Murakami, R., Matsumoto, K., Kawauchi, M., Fujihara, R. (2016). Blood-brain barrier and blood-cerebrospinal fluid barrier in normal and pathological conditions. Brain Tumor Pathology, 33(2), 89-96. [CrossRef]
  • 5. Morgan, B.P. (2018). Complement in the pathogenesis of Alzheimer's disease. Seminars in Immunopathology, 40(1), 113-124. [CrossRef]
  • 6. Montagne, A., Barnes, S.R., Sweeney, M.D., Halliday, M.R., Sagare, A.P., Zhao, Z., Toga, A.W., Jacobs, R. E., Liu, C.Y., Amezcua, L., Harrington, M.G., Chui, H.C., Law, M., Zlokovic, B.V. (2015). Blood-brain barrier breakdown in the aging human hippocampus. Neuron, 85(2), 296-302. [CrossRef]
  • 7. Varatharaj, A., Galea, I. (2017). The blood-brain barrier in systemic inflammation. Brain, Behavior, and Immunity, 60, 1-12. [CrossRef]
  • 8. Takeda, S., Sato, N., Morishita, R. (2014). Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy. Frontiers in Aging Neuroscience, 6, 171. [CrossRef]
  • 9. McGeer, E.G., McGeer, P.L. (1998). The importance of inflammatory mechanisms in Alzheimer disease. Experimental Gerontology, 33(5), 371-378. [CrossRef]
  • 10. Shinjyo, N., Kagaya, W., Pekna, M. (2021). Interaction between the complement system and ınfectious agents-A potential mechanistic link to neurodegeneration and dementia. Frontiers in Cellular Neuroscience, 15, 710390. [CrossRef]
  • 11. Mapunda, J.A., Tibar, H., Regragui, W., Engelhardt, B. (2022). How does the immune system enter the brain? Frontiers in Immunology, 13, 805657. [CrossRef]
  • 12. Shah, A., Kishore, U., Shastri, A. (2021). Complement system in Alzheimer's disease. International Journal of Molecular Sciences, 22(24), 13647. [CrossRef]
  • 13. WHO (World Health Organization) web site. (2023). Dementia. Available online: https://www.who.int/news-room/fact sheets/detail/dementia. Erişim tarihi: 27.03.2023.
  • 14. Kumar, P.J., Clark, M. (2011). Kumar & Clark’s Clinical Medicine, Saunders Elsevier, Edinburgh.
  • 15. Tenner A.J. (2020). Complement-mediated events in Alzheimer’s disease: Mechanisms and potential therapeutic targets. Journal of Immunology, 204(2), 306-315. [CrossRef]
  • 16. Livingston, G., Sommerlad, A., Orgeta, V., Costafreda, S.G., Huntley, J., Ames, D., Ballard, C., Banerjee, S., Burns, A., Cohen-Mansfield, J., Cooper, C., Fox, N., Gitlin, L.N., Howard, R., Kales, H.C., Larson, E. B., Ritchie, K., Rockwood, K., Sampson, E.L., Samus, Q., Schneider, L.S., Selbæk, G., Teri, L., Mukadam, N. (2017). Dementia prevention, intervention, and care. Lancet, 390(10113), 2673-2734. [CrossRef]
  • 17. Sala Frigerio, C., Wolfs, L., Fattorelli, N., Thrupp, N., Voytyuk, I., Schmidt, I., Mancuso, R., Chen, W.T., Woodbury, M.E., Srivastava, G., Möller, T., Hudry, E., Das, S., Saido, T., Karran, E., Hyman, B., Perry, V. H., Fiers, M., De Strooper, B. (2019). The major risk factors for Alzheimer’s disease: Age, sex, and genes modulate the microglia response to Aβ plaques. Cell Reports, 27(4), 1293-1306. [CrossRef]
  • 18. Shastri, A., Bonifati, D.M., Kishore, U. (2013). Innate immunity and neuroinflammation. Mediators of inflammation, 2013, 342931. [CrossRef]
  • 19. Liu, Y.P., Lin, H.I., Tzeng, S.F. (2005). Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture. Brain Research, 1054(2), 152-158. [CrossRef]
  • 20. Harms, A.S., Lee, J.K., Nguyen, T.A., Chang, J., Ruhn, K.M., Treviño, I., Tansey, M.G. (2012). Regulation of microglia effector functions by tumor necrosis factor signaling. Glia, 60(2), 189-202. [CrossRef]
  • 21. Jimenez, S., Baglietto-Vargas, D., Caballero, C., Moreno-Gonzalez, I., Torres, M., Sanchez-Varo, R., Ruano, D., Vizuete, M., Gutierrez, A., Vitorica, J. (2008). Inflammatory response in the hippocampus of PS1M146L/APP751SL mouse model of Alzheimer's disease: Age-dependent switch in the microglial phenotype from alternative to classic. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, 28(45), 11650-11661. [CrossRef]
  • 22. Zhang, L., Dong, Z.F., Zhang, J.Y. (2020). Immunomodulatory role of mesenchymal stem cells in Alzheimer's disease. Life Sciences, 246, 117405. [CrossRef]
  • 23. Yong, H.Y.F., Rawji, K.S., Ghorbani, S., Xue, M., Yong, V.W. (2019). The benefits of neuroinflammation for the repair of the injured central nervous system. Cellular & Molecular Immunology, 16(6), 540-546. [CrossRef]
  • 24. Lo, M.W., Woodruff, T.M. (2020). Complement: Bridging the innate and adaptive immune systems in sterile inflammation. Journal of Leukocyte Biology, 108(1), 339-351. [CrossRef]
  • 25. Aisen, P.S., Cummings, J., Jack, C.R., Jr, Morris, J.C., Sperling, R., Frölich, L., Jones, R.W., Dowsett, S.A., Matthews, B.R., Raskin, J., Scheltens, P., Dubois, B. (2017). On the path to 2025: Understanding the Alzheimer's disease continuum. Alzheimer's Research & Therapy, 9(1), 60. [CrossRef]
  • 26. Bonifati, D.M., Kishore, U. (2007). Role of complement in neurodegeneration and neuroinflammation. Molecular Immunology, 44(5), 999-1010. [CrossRef]
  • 27. Schartz, N.D., Tenner, A.J. (2020). The good, the bad, and the opportunities of the complement system in neurodegenerative disease. Journal of Neuroinflammation, 17(1), 354. [CrossRef]
  • 28. Velazquez, P., Cribbs, D.H., Poulos, T.L., Tenner, A.J. (1997). Aspartate residue 7 in amyloid beta-protein is critical for classical complement pathway activation: implications for Alzheimer's disease pathogenesis. Nature Medicine, 3(1), 77-79. [CrossRef]
  • 29. Shen, Y., Lue, L., Yang, L., Roher, A., Kuo, Y., Strohmeyer, R., Goux, W.J., Lee, V., Johnson, G.V., Webster, S.D., Cooper, N.R., Bradt, B., Rogers, J. (2001). Complement activation by neurofibrillary tangles in Alzheimer's disease. Neuroscience Letters, 305(3), 165-168. [CrossRef]
  • 30. Tenner, A.J., Stevens, B., Woodruff, T.M. (2018). New tricks for an ancient system: Physiological and pathological roles of complement in the CNS. Molecular Immunology, 102, 3-13. [CrossRef]
  • 31. Ricklin, D., Lambris, J.D. (2013). Complement in immune and inflammatory disorders: pathophysiological mechanisms. Journal of Immunology, 190(8), 3831-3838. [CrossRef]
  • 32. Morgan, B.P., Gasque, P. (1997). Extrahepatic complement biosynthesis: where, when and why? Clinical and Experimental Immunology, 107(1), 1-7. [CrossRef]
  • 33. Gasque, P., Neal, J.W., Singhrao, S.K., McGreal, E.P., Dean, Y.D., Van, B.J., Morgan, B.P. (2002). Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activities. Molecular Neurobiology, 25(1), 1-17. [CrossRef]
  • 34. Tang, S., Zhou, W., Sheerin, N.S., Vaughan, R.W., Sacks, S.H. (1999). Contribution of renal secreted complement C3 to the circulating pool in humans. Journal of Immunology, 162(7), 4336-4341.
  • 35. Zhou, W., Marsh, J.E., Sacks, S.H. (2001). Intrarenal synthesis of complement. Kidney International, 59(4), 1227-1235. [CrossRef]
  • 36. Johnson, S.A., Lampert-Etchells, M., Pasinetti, G.M., Rozovsky, I., Finch, C.E. (1992). Complement mRNA in the mammalian brain: responses to Alzheimer's disease and experimental brain lesioning. Neurobiology of Aging, 13(6), 641-648. [CrossRef]
  • 37. Rozovsky, I., Morgan, T.E., Willoughby, D.A., Dugichi-Djordjevich, M.M., Pasinetti, G.M., Johnson, S.A., Finch, C.E. (1994). Selective expression of clusterin (SGP-2) and complement C1qB and C4 during responses to neurotoxins in vivo and in vitro. Neuroscience, 62(3), 741-758. [CrossRef]
  • 38. Veerhuis, R., Janssen, I., Hoozemans, J.J., De Groot, C.J., Hack, C.E., Eikelenboom, P. (1998). Complement C1-inhibitor expression in Alzheimer's disease. Acta Neuropathologica, 96(3), 287-296. [CrossRef]
  • 39. Walker, D.G., McGeer, P.L. (1992). Complement gene expression in human brain: comparison between normal and Alzheimer disease cases. Brain research. Molecular Brain Research, 14(1-2), 109-116. [CrossRef]
  • 40. Singhrao, S.K., Neal, J.W., Morgan, B.P., Gasque, P. (1999). Increased complement biosynthesis by microglia and complement activation on neurons in Huntington's disease. Experimental Neurology, 159(2), 362-376. [CrossRef]
  • 41. Kishore, U., Gupta, S.K., Perdikoulis, M.V., Kojouharova, M.S., Urban, B.C., Reid, K.B. (2003). Modular organization of the carboxyl-terminal, globular head region of human C1q A, B, and C chains. Journal of Immunology, 171(2), 812-820. [CrossRef]
  • 42. Yang, L.B., Li, R., Meri, S., Rogers, J., Shen, Y. (2000). Deficiency of complement defense protein CD59 may contribute to neurodegeneration in Alzheimer's disease. The Journal of Neuroscience, 20(20), 7505-7509. [CrossRef]
  • 43. McGeer, P.L., Akiyama, H., Itagaki, S., McGeer, E.G. (1989). Activation of the classical complement pathway in brain tissue of Alzheimer patients. Neuroscience Letters, 107(1-3), 341-346. [CrossRef]
  • 44. Rogers, J., Cooper, N.R., Webster, S., Schultz, J., McGeer, P.L., Styren, S.D., Civin, W.H., Brachova, L., Bradt, B., Ward, P. (1992). Complement activation by beta-amyloid in Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America, 89(21), 10016-10020. [CrossRef]
  • 45. Berg, A., Zelano, J., Stephan, A., Thams, S., Barres, B.A., Pekny, M., Pekna, M., Cullheim, S. (2012). Reduced removal of synaptic terminals from axotomized spinal motoneurons in the absence of complement C3. Experimental Neurology, 237(1), 8-17. [CrossRef]
  • 46. Shi, Q., Colodner, K. J., Matousek, S.B., Merry, K., Hong, S., Kenison, J. E., Frost, J.L., Le, K. X., Li, S., Dodart, J.C., Caldarone, B.J., Stevens, B., Lemere, C.A. (2015). Complement C3-Deficient mice fail to display age-related hippocampal decline. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, 35(38), 13029-13042. [CrossRef]
  • 47. Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., Cole, G. (1996). Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice. Science, 274(5284), 99-102. [CrossRef]
  • 48. Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C. M., Perez-tur, J., Hutton, M., Buee, L., Harigaya, Y., Yager, D., Morgan, D., Gordon, M. N., Holcomb, L., Refolo, L., Zenk, B., Hardy, J., Younkin, S. (1996). Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1. Nature, 383(6602), 710-713. [CrossRef]
  • 49. Matsuoka, Y., Picciano, M., Malester, B., LaFrancois, J., Zehr, C., Daeschner, J. M., Olschowka, J.A., Fonseca, M.I., O'Banion, M.K., Tenner, A.J., Lemere, C.A., Duff, K. (2001). Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease. The American Journal of Pathology, 158(4), 1345-1354. [CrossRef]
  • 50. Holcomb, L., Gordon, M.N., McGowan, E., Yu, X., Benkovic, S., Jantzen, P., Wright, K., Saad, I., Mueller, R., Morgan, D., Sanders, S., Zehr, C., O'Campo, K., Hardy, J., Prada, C.M., Eckman, C., Younkin, S., Hsiao, K., Duff, K. (1998). Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. Nature Medicine, 4(1), 97-100. [CrossRef]
  • 51. Webster, S.D., Yang, A.J., Margol, L., Garzon-Rodriguez, W., Glabe, C.G., Tenner, A.J. (2000). Complement component C1q modulates the phagocytosis of Abeta by microglia. Experimental Neurology, 161(1), 127-138. [CrossRef]
  • 52. Fonseca, M.I., Zhou, J., Botto, M., Tenner, A.J. (2004). Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease. The Journal of Neuroscience: The Official Journal of The Society for Neuroscience, 24(29), 6457-6465. [CrossRef]
  • 53. Hong, S., Beja-Glasser, V.F., Nfonoyim, B.M., Frouin, A., Li, S., Ramakrishnan, S., Merry, K.M., Shi, Q., Rosenthal, A., Barres, B. A., Lemere, C.A., Selkoe, D.J., Stevens, B. (2016). Complement and microglia mediate early synapse loss in Alzheimer mouse models. Science, 352(6286), 712-716. [CrossRef]
  • 54. Zhou, J., Fonseca, M.I., Pisalyaput, K., Tenner, A.J. (2008). Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease. Journal of Neurochemistry, 106(5), 2080-2092. [CrossRef]
  • 55. Kolev, M.V., Ruseva, M.M., Harris, C.L., Morgan, B.P., Donev, R.M. (2009). Implication of complement system and its regulators in Alzheimer's disease. Current Neuropharmacology, 7(1), 1-8. [CrossRef]
  • 56. Györffy, B. A., Tóth, V., Török, G., Gulyássy, P., Kovács, R. Á., Vadászi, H., Micsonai, A., Tóth, M.E., Sántha, M., Homolya, L., Drahos, L., Juhász, G., Kékesi, K.A., Kardos, J. (2020). Synaptic mitochondrial dysfunction and septin accumulation are linked to complement-mediated synapse loss in an Alzheimer's disease animal model. Cellular and Molecular Life Sciences: CMLS, 77(24), 5243-5258. [CrossRef]
  • 57. Litvinchuk, A., Wan, Y.W., Swartzlander, D.B., Chen, F., Cole, A., Propson, N.E., Wang, Q., Zhang, B., Liu, Z., Zheng, H. (2018). Complement C3aR inactivation attenuates tau pathology and reverses an immune network deregulated in tauopathy models and Alzheimer’s disease. Neuron, 100(6), 1337-1353.e5. [CrossRef]
Toplam 57 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Farmasotik Toksikoloji
Bölüm Derleme
Yazarlar

Anıl Yirün 0000-0002-4050-8832

Selinay Başak Erdemli Köse 0000-0001-8986-585X

Pınar Erkekoğlu 0000-0003-4713-7672

Proje Numarası none
Erken Görünüm Tarihi 3 Kasım 2023
Yayımlanma Tarihi 20 Ocak 2024
Gönderilme Tarihi 7 Ağustos 2023
Kabul Tarihi 5 Ekim 2023
Yayımlandığı Sayı Yıl 2024 Cilt: 48 Sayı: 1

Kaynak Göster

APA Yirün, A., Erdemli Köse, S. B., & Erkekoğlu, P. (2024). ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ. Journal of Faculty of Pharmacy of Ankara University, 48(1), 300-311. https://doi.org/10.33483/jfpau.1337722
AMA Yirün A, Erdemli Köse SB, Erkekoğlu P. ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ. Ankara Ecz. Fak. Derg. Ocak 2024;48(1):300-311. doi:10.33483/jfpau.1337722
Chicago Yirün, Anıl, Selinay Başak Erdemli Köse, ve Pınar Erkekoğlu. “ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University 48, sy. 1 (Ocak 2024): 300-311. https://doi.org/10.33483/jfpau.1337722.
EndNote Yirün A, Erdemli Köse SB, Erkekoğlu P (01 Ocak 2024) ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ. Journal of Faculty of Pharmacy of Ankara University 48 1 300–311.
IEEE A. Yirün, S. B. Erdemli Köse, ve P. Erkekoğlu, “ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ”, Ankara Ecz. Fak. Derg., c. 48, sy. 1, ss. 300–311, 2024, doi: 10.33483/jfpau.1337722.
ISNAD Yirün, Anıl vd. “ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University 48/1 (Ocak 2024), 300-311. https://doi.org/10.33483/jfpau.1337722.
JAMA Yirün A, Erdemli Köse SB, Erkekoğlu P. ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ. Ankara Ecz. Fak. Derg. 2024;48:300–311.
MLA Yirün, Anıl vd. “ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University, c. 48, sy. 1, 2024, ss. 300-11, doi:10.33483/jfpau.1337722.
Vancouver Yirün A, Erdemli Köse SB, Erkekoğlu P. ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ. Ankara Ecz. Fak. Derg. 2024;48(1):300-11.

Kapsam ve Amaç

Ankara Üniversitesi Eczacılık Fakültesi Dergisi, açık erişim, hakemli bir dergi olup Türkçe veya İngilizce olarak farmasötik bilimler alanındaki önemli gelişmeleri içeren orijinal araştırmalar, derlemeler ve kısa bildiriler için uluslararası bir yayım ortamıdır. Bilimsel toplantılarda sunulan bildiriler supleman özel sayısı olarak dergide yayımlanabilir. Ayrıca, tüm farmasötik alandaki gelecek ve önceki ulusal ve uluslararası bilimsel toplantılar ile sosyal aktiviteleri içerir.