Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü

Nilüfer Şahin Calapoğlu; Musatafa Calapoğlu

doi:10.17343/sdutfd.55343

Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü

Öz

İlerleyici hafıza kaybı, bilişsel yetmezlik ve davranış değişiklikleri ile karakterize Alzheimer hastalığı (AH), beyin yetmezliğinin etiolojik olarak heterojen bir grubunu oluştururken dünya üzerinde de 18 milyondan fazla insanı etkilemektedir. AH kortikal ve subkortikal bölgelerdeki nöronal kaybın yanı sıra b-amiloid (Ab) peptid üretiminin artışı, birikimi ve nörofibriler yumakların (NFT) oluşumu ile ilişkilidir. Doku hasarına karşı birçok farklı hücre tarafından salınan kemokinler ve reseptörlerinin birincil görevleri lökositlerin inflamasyon bölgesine migrasyonunu sağlamaktır. Yapılan son çalışmalar, AH beyni ile inflamatuvar süreçte yer alan kemokinlerin ilişkili olduğuna dikkat çekmektedirler. Bu derlemede, AH'de kemokin ve kemokin reseptörlerinin nöroinflamtuvar rolleri ile ilgili son gelişmeler üzerinde durulmaktadır. Anahtar Kelimeler: Alzheimer hastalığı, inflamasyon, kemokinler, kemokin reseptörleri Abstract The role of chemokine and chemokine receptors in alzheimer's disease Alzheimer's disease (AD) that is an etiologically heterogeneous form of brain failure affects more than 18 million people worldwide and is characterized by progressive memory loss, cognitive impairment and behavioral changes. The disease associated with neuronal loss in cortical and subcortical regions and increased production and accumulation of b-amyloid (Ab) peptide and neurofibrillary tangle (NFT) formation. Chemokines and their receptors are released by different cells in response to tissue injury and their primary function is the migration of leukocytes to inflammatory sides. Recent studies point out that the involvement of chemokines in the inflammatory process associated with AD brain. This review focuses on the recent progress regarding the neuroinflammatory roles of chemokines and chemokin receptor involvement in AD. Key words: Alzheimer's disease, inflammation, chemokines, chemokine receptors

Anahtar Kelimeler

Alzheimer hastalýðý, inflamasyon, kemokinler, kemokin reseptörleri

Kaynakça

O'Brien J, Ames D, Burns A. Dementia. Second edition. London: Arnold; 2000:405-15.
Alzheimers Association www.alz.org (Last update: 6/1/2009)
Alzheimer Europe www.dementia-in-europe.eu (Last update: 31/10/2006)
www.alzheimer.gen.tr
Selkoe DJ. Neuropathology and molecular biology of Alzheimer Disease. In Dementia Update. American Academy of Neurology 49th Annual Meeting, April 12-19, 1997 Boston, MA:1997, American Academy of Neurology Press, USA;1997:39-61.
Pike CJ, Walencewicz AJ, Glabe CG, Cotman CW. In vitro aging of beta-amyloid protein causes peptide aggregation and neurotoxicity. Brain Res 1991;563:3114.
Lorenzo A, Yankner BA. Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. Proc Natl Acad Sci 1994;91:122437.
Hartley DM, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM, et al. Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J Neurosci 1999;19:887684.

Geula C, Wu CK, Saroff D, Lorenzo A, Yuan M, Yankner BA. Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity. Nat Med 1998;4:82731.
Lue LF, Kuo YM, Roher AE, Brachova L, Shen Y, Sue L, et al. Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease. Am J Pathol 1999;155:85362.
McLean CA, Cherny RA, Fraser FW, Fuller SJ, Smith MJ, Beyreuther , et al. Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease. Ann Neurol 1999;46:8606.
Wang J, Dickson DW, Trojanowski JQ, Lee VM. The levels of soluble versus insoluble brain Abeta distinguish Alzheimer's disease from normal and pathologic aging. Exp Neurol 1999;158:32837
Clarkson AN, Sutherland BA, Appleton I. The biology and pathology of hypoxia-ischemia: an update. Arch Immunol Ther Exp 2005;53:21325.
Benveniste EN. Inflammatory cytokines within the central nervous system: sources, function, and mechanism of action. Am J Physiol Cell Physiol 1992;263:1-16.
Ramirez MR, Muraro F, Zylbersztejn DS, Abel CR, Arteni NS, Lavinsky D, et al. Neonatal hypoxiaischemia reduces ganglioside, phospholipid and cholesterol contents in the rat hippocampus. Neuroscience Research 2003;46(3):339-47.
Benveniste EN, Nguyen VT, O'Kecfe GM. Immunological aspects of microglia: relevance to Alzheimer's disease. Neurochem Int 2001;39:381-91.
Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer's disease. Neurobiol Aging 2000;21:383-421.
Kara Ý, Müdüroðlu A. [Ýnflamasyon ve Norodejeneratif Hastalýklar.] Türkiye Klinikleri J Med Sci 2008;28(Suppl):115-8.
Aisen PS. Anti-inflammatory therapy for Alzheimers disease. Neurobiol Aging 2000;21:4478.
Thal LJ. Anti-inflammatory drugs and Alzheimers disease. Neurobiol Aging 2000;21:44950.
Lindley IJD, Westwick J, Kunkel SL. Nomenclature announcement- the chemokines. Immunol Today 1993;14:24.
Bokoch GM: Chemoattractant signalling and leukocyte activation. Blood 1995;86:1649-60.
Ono SJ, Nakamura T, Miyazaki D, Ohbayashi M, Dawson M, Toda M. Chemokines. Roles in leukocyte development, trafficking and effector function. J Allergy Clin Immunol 2003;111:1185-99.
Çaðlar M, Kansu E. Kemokinler, kemokin reseptörleri ve inflamasyon. ANKEM Dergisi 2004;18(Ek2):164- 8.
Oppenheim JJ, Zachariae COC, Mukaida N, Matsushima K. Properties of the novel proinflammatory supergene intercrine cytokine family. Annu Rev Immunol 1991;9:617-48.
Baggiolini M, Loestscher P. Chemokines in inflammation and immunity. Immunol Today 2000;21:418-20.
Mackay CR. Chemokines: immunologys high impact factors. Nature Immunol 2001;2:95-101.
Murdoch C, Finn A. Chemokine receptors and their role in inflammation and infectious diseases. Blood 2000;95:3032-43.
Loetscher P, Seitz M, Baggiolini M, Moser M. Interleukin-2 regulates CC chemokine receptor expression and chemotactic responsiveness in T lymphocytes. J Exp Med 1996;184:569-77.
Bonecchi R, Galliera E, Borroni EM, Corsi MM, Locati M, Mantovani A. Chemokines and chemokine receptors: an overview. Front Biosci. 2009 Jan 1;14:540-51.
Wong MM, Fish EN. Chemokines:attractive mediators of the immune response. Sem Immunol 2003;15:5-14.
Glabinski AR, Ransohoff RM. Chemokines and chemokine receptors in CNS pathology. J Neurovirology 1999;5:312.
Xia MQ, Hyman BT. Chemokines/chemokine receptors in the central nervous system and Alzheimer's disease. J Neurovirology 1999;5:3241.
Smits HA, Rijsmus A, van Loon JH, Wat JWY, Verhoef J, Boven LA, et al. Amyloid-beta-induced chemokine production in primary human macrophages and astrocytes. J Neuroimmunol 2002;127:1608.
Lue LF, Rydel R, Brigham EF, Yang LB, Hampel H, Murphy GM, et al. Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro. Glia 2001;35:729.
Ishizuka K, Kimura T, Igata-yi R, Katsuragi S, Takamatsu J, Miyakawa T. Identification of monocyte chemoattractant protein-1 in senile plaques and reactive microglia of Alzheimer's disease. Psychiatry Clin Neurosci 1997;51:1358.
Xia MQ, Qin SX, Wu LJ, Mackay CR, Hyman BT. Immunohistochemical study of the beta-chemokine receptors CCR3 andCCR5 and their ligands in normal and Alzheimer's disease brains. Am J Pathol 1998;153:317.
Pola R, Flex A, Gaetani E, Proia AS, Papaleo P, Di Giorgio A, et al. Monocyte chemoattractant protein- 1 (MCP-1) gene polymorphism and risk of Alzheimers disease in Italians. Exp Gerontol 2004;39:1249-56.
Combarros O, Infante J, Llorca J, Pena N, Fernandez- Viadero C, Berciano J. The chemokine receptor CCR5- 32 gene mutation is not protective against Alzheimers disease. Neurosci Lett 2004;366(3):312-4.
Fenoglio C, Galimberti D, Lovati C, Guidi I, Gatti A, Fogliarino S, et al. MCP-1 in Alzheimers disease patients: A-2518G polymorphism and serum levels. Neurobiol Aging 2004;25(9):1169-73.
Combarros O, Infante J, Llorca J, Berciano J. No evidence for association of the monocyte chemoattractant protein-1(2518) gene polymorphism and Alzheimer disease. Neurosci Lett 2004;360:25-8.
Tamura Y, Sakasegawaa Y, Omia K, Kishidaa H, Asadad T, Kimura H, et al. Association study of the chemokine, CXC motif, ligand 1 (CXCL1) gene with sporadic Alzheimers disease in a Japanese population. Neurosci Lett 2005;379:149-51.
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 Alzheimers disease brains. Am J Pathol 1998;153:317.
Xia MQ, Bacskai BJ, Knowles RB, Qin SX, Hyman BT. Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP- 10 in reactive astrocytes: in vitro ERK1/2 activation and role in Alzheimers disease. J Neuroimmunol 2000;108:22735.
Xia M, Hyman BT. GROalpha/KC, a chemokine receptor CXCR2 ligand, can be a potent trigger for neuronal ERK1/2 and PI-3 kinase pathways and for tau hyperphosphorylation: a role in Alzheimers disease? J Neuroimmunol 2002;122:5564.
Streit WJ, Conde JR, HarrisonJK. Chemokines and Alzheimers disease. Neurobiol Aging 2001;22:90913.
Halks-Miller M, Schroeder ML, Haroutunian V, Moenning U, Rossi M, Achim C et al. CCR1 is an early and specific marker of Alzheimers disease. Ann Neurol 2003;54:63846.
CH. Kim SJ. Kim JD, Choi IS. Choi IH. Fas ligand and fas are expressed constitutively in human astrocyles and the expression increases with IL-1, IL-6, TNF-á, or IFN-g. J Immunol 1999;162:1889-95.
Tuppo E.E, Arias H.R. The role of inflammation in Alzheimers disease. The International Journal of Biochemistry & Cell Biology 2005; 37:289305.

Ayrıntılar

Birincil Dil

Türkçe

Konular

-

Bölüm

-

Yazarlar

Nilüfer Şahin Calapoğlu

Musatafa Calapoğlu Bu kişi benim

Yayımlanma Tarihi

30 Aralık 2009

Gönderilme Tarihi

1 Ocak 2010

Kabul Tarihi

-

Yayımlandığı Sayı

Yıl 2009 Cilt: 16 Sayı: 4

DOI

https://doi.org/10.17343/sdutfd.55343

IZ

https://izlik.org/JA83ZY96ND

Kaynak Göster

RIS / Bibtex

APA

Şahin Calapoğlu, N., & Calapoğlu, M. (2009). Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü. Medical Journal of Süleyman Demirel University, 16(4), 39-44. https://doi.org/10.17343/sdutfd.55343

AMA

1.Şahin Calapoğlu N, Calapoğlu M. Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü. SDÜ Tıp Fak Derg. 2009;16(4):39-44. doi:10.17343/sdutfd.55343

Chicago

Şahin Calapoğlu, Nilüfer, ve Musatafa Calapoğlu. 2009. “Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü”. Medical Journal of Süleyman Demirel University 16 (4): 39-44. https://doi.org/10.17343/sdutfd.55343.

EndNote

Şahin Calapoğlu N, Calapoğlu M (01 Aralık 2009) Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü. Medical Journal of Süleyman Demirel University 16 4 39–44.

IEEE

[1]N. Şahin Calapoğlu ve M. Calapoğlu, “Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü”, SDÜ Tıp Fak Derg, c. 16, sy 4, ss. 39–44, Ara. 2009, doi: 10.17343/sdutfd.55343.

ISNAD

Şahin Calapoğlu, Nilüfer - Calapoğlu, Musatafa. “Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü”. Medical Journal of Süleyman Demirel University 16/4 (01 Aralık 2009): 39-44. https://doi.org/10.17343/sdutfd.55343.

JAMA

1.Şahin Calapoğlu N, Calapoğlu M. Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü. SDÜ Tıp Fak Derg. 2009;16:39–44.

MLA

Şahin Calapoğlu, Nilüfer, ve Musatafa Calapoğlu. “Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü”. Medical Journal of Süleyman Demirel University, c. 16, sy 4, Aralık 2009, ss. 39-44, doi:10.17343/sdutfd.55343.

Vancouver

1.Nilüfer Şahin Calapoğlu, Musatafa Calapoğlu. Alzheimer hastalığında kemokin ve kemokin reseptörlerinin rolü. SDÜ Tıp Fak Derg. 01 Aralık 2009;16(4):39-44. doi:10.17343/sdutfd.55343