Skip to main navigation menu Skip to main content Skip to site footer
##common.pageHeaderLogo.altText##

Narrative Review

Vol. 3 No. 2 (1997)

Innate Inflammatory Reaction of the Brain in Alzheimer Disease

  • Edith G. McGeer, Ph.D.
  • Patrick L. McGeer, M.D.
DOI
https://doi.org/10.26443/mjm.v3i2.543
Submitted
November 6, 2020
Published
2020-12-01

Abstract

N/A

References

  1. McGeer PL, McGeer EG. The inflammatory system of brain:implications for therapy of Alzheimer and other neurodegenerative disorders. Brain Research Review 21(2):195- 218; 1995.
  2. McGeer PL, Schulzer M, McGeer EG. Arthritis and antiinflammatory agents as negative risk factors for Alzheimer disease: A review of seventeen epidemiological studies. Neurology 47(2):425-432; 1996.
  3. Selkoe DJ. Cell biology of the beta-amyloid protein and the genetics of Alzheimer’s disease. Cold Spring Harbor Symposia on Quantitative Biology 61:587-596; 1996.
  4. Iqbal K, Grundke-Iqbal I. Molecular mechanism of Alzheimer’s neurofibrillary degeneration and therapeutic intervention. Annals of the New York Academy of Sciences 777:132-138; 1996.
  5. Braak H, Braak E. Evolution of the neuropathology of Alzheimer’s disease. Acta Neurologica Scandinavica Supplementum 165:3-12; 1996.
  6. Brun A, Englund E. Regional pattern of degeneration in Alzheimer's disease: neuronal loss and histopathological grading. Histopathology 5(5):549-564; 1981.
  7. Metchnikoff E. Leaons sur la pathologie comparée de l’inflammation. Paris: Masson; 1892.
  8. Pike CJ, Cummings BJ, Monzavi R, Cotman CW. Beta-amyloid induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer’s disease. Neuroscience 63(2):517-531; 1994.
  9. Klegeris A, McGeer PL. Rat brain microglia and peritoneal macrophages show similar responses to respiratory burst stimulants. Journal of Neuroimmunology 53(1):83-90;1994.
  10. Klegeris A, Walker DG, McGeer PL. Activation of macrophages by Alzheimer b amyloid peptide. Biochemical and Biophysical Research Communications 199(2):984-991; 1994.
  11. Taupenot L, Ciesielski-Traska J, et al. Chromogranin A triggers a phenotypic transformation and the generation of nitric oxide in brain microglial cells. Neuroscience 72(2): 377-389; 1996.
  12. Klegeris A, McGeer PL. b-Amyloid protein enhances macrophage production of oxygen free radicals and glutamate. Journal of Neuroscience Research 49(2): 229-2357; 1997.
  13. McMillian MK, Vainio PJ, Tuominen RK. Role of protein kinase C in microglia-induced neurotoxicity in mesencephalic cultures. Journal of Neuropathology and Experimental Neurology 56(3):301-307; 1997.
  14. Giulian D, Haverkamp LJ, Yu JH, et al. Specific domains of b- amyloid from Alzheimer plaque elicit neuronal killing in human microglia. Journal of Neuroscience 16(19):6021-6037; 1996.
  15. Roher AE, Chaney MO, Kuo YM, et al. Morophology and toxicity of A-beta (1-42) derived from neuritic and vascular amyloid deposits of Alzheimer’s disease. Journal of Biological Chemistry 271(34):20631-20635;1996.
  16. Giulian D, Vaca K, Corpuz M. Brain glia release factors with opposing actions upon neuronal survival. Journal of Neuroscience 13(1):29-37; 1993.
  17. Shen Y, Li R, McGeer EG, McGeer PL. Neuronal expression of mRNAs for complement proteins of the classical pathway in Alzheimer brain. Brain Research 769(2):391-395; 1997.
  18. Terai K, McGeer EG, McGeer PL. Neurons express proteins of the classical complement pathway in Alzheimer disease. Brain Research 769(2):385-390; 1997.
  19. Veerhuis R, van der Valk P, Janssen I, et al. Complement activation in amyloid plaques in Alzheimer’s disease brains does not proceed further than C3. Virchows Archiv 426(6): 603-610;1995.
  20. McGeer PL, McGeer EG. Kawamata T, et al. Reactions of the immune system in chronic degenerative neurological diseases. Canadian Journal of Neurological Sciences 18(3 Suppl):376-379; 1991.
  21. Itagaki S, Akiyama H, Saito H, et al. Ultrastructural localization of complement membrane attack complex (MAC)-like immunoreactivity in brains of patients with Alzheimer’s disease. Brain Research 645(1-2):78-84; 1994.
  22. Webster S, Lue L-F, Brachova L, et al. Molecular and cellular characterization of the membrane attack complex, C5b-9, in Alzheimer’s disease. Neurobiology of Aging 18(4): 415-421;1997.
  23. McGeer EG, McGeer PL. Inflammatory cytokines in the CNS. CNS Drugs 7: 214-228; 1997.
  24. Terai K, Matsuo A, McGeer PL. Enhancement of immunoreactivity for NF-kB in the hippocampal formation and cerebral cortex of Alzheimer’s disease. Brain Research 735(1):159-168; 1996.
  25. Conner EM, Grisham MB. Inflammation, free radicals and antioxidants. Nutrition 12(4): 274-277; 1996.
  26. Helmes E, Merskey H, Fox H, et al. Patterns of deterioration in senile dementia of the Alzheimer type. Archives of Neurology 52(3):306-310; 1995.
  27. Ohm TG, Muller H, Braak H, et al. Close-meshed prevalence rates of different stages as a tool to uncover the rate of Alzheimer’s disease-related neurofibrillary changes, Neuroscience 64(1):209-217; 1995.
  28. Akiyama H, Tooyama I, Kondo H, et al. Early response of brain resident microglia to kainic acid-induced hippocampal lesions. Brain Research 635(1-2):257-268; 1994.
  29. Pasinetti GM, Johnson SA, Rozovsky I, et al. Complement C1qB and C4 mRNAs responses to lesioning in rat brain. Experimental Neurology 118(2):117-125; 1992.
  30. Jiang H, Burdick D, Glabe GG, et al. b-Amyloid activates complement by binding to a specific region of the collagen-like domain of the C1q A chain. Journal of Immunology 152(10):5050-5059; 1994.
  31. Rogers J, Cooper NR, Webster S, et al. Complement activation by b-amyloid in Alzheimer disease. Proceedings of the National Academy of Science USA 89(21):10016-10020; 1992.
  32. Gasque P, Thomas A, Fontaine M, et al. Complement activation on human neuroblastoma cell lines in vitro: route of activation and expression of functional complement regulatory proteins. Journal of Neuroimmunology 66(1-2):29-40; 1996.
  33. Shen Y, Halperin JA, Lee CM. Complement-mediated neurotoxicity is regulated by homologous restriction. Brain Research 671(2):282-292; 1995.
  34. Pasinetti GM. Inflammatory mechanisms in neurodegeneration in Alzheimer’s disease: the role of the complement system. Neurobiology of Aging 17(5):707-716; 1996.
  35. Agoropoulou C, Wing MG, Wood A. CD59 expression and complement susceptibility of human neuronal cell line (NTera2). Neuroreport 7(5):997-1004; 1996.
  36. McGeer PL, Walker DG, Akiyama H, et al. Detection of the membrane inhibitor of reactive lysis (CD59) in diseased neurons of Alzheimer brain. Brain Research 544(2):315-319; 1991.
  37. McGeer PL, Kawamata T, Walker DG. Distribution of clusterin in Alzheimer brain tissue. Brain Research 579(2):337-341;1992.
  38. Akiyama H, Kawamata T, Dedhar S, et al. Immunohistochemcial localization of vitronectin, its receptor and beta-3 integrin in Alzheimer brain tissue. Journal of Neuroimmunology 32(1):19-28; 1991.
  39. Walker DG, Yasuhara O, Patston PA, et al. Complement C1 inhibitor is produced by brain tissue and is cleaved in Alzheimer disease. Brain Research 675(1-2):75-82; 1995.
  40. Laskin DL, Pendino KJ. Macrophages and inflammatory mediators in tissue injury. Annual Review of Pharmacology and Toxicology 35:655-677; 1995.
  41. McGeer PL, Rogers J. Anti-inflammatory agents as a therapeutic approach to Alzheimer’s disease. Neurology 42(2):447-449; 1992.
  42. Rich JB, Rasmusson DX, Folstein MF, et al. Nonsteroidal antiinflammatory drugs in Alzheimer’s disease. Neurology 45(1):51-55; 1995.
  43. Doraiswamy PM, Krishen A, Stallone F, et al. (1996) NSAIDs and cognition in Alzheimer’s disease. Neurology 46(4):1194;1996.
  44. Rogers J, Kirby LC, Hempelman SR, et al. Clinical trial of indomethacin in Alzheimer’s disease. Neurology 43(8): 1609-1611; 1993.
  45. Ostbye T, Crosse E. Net economic costs of dementia in Canada. Canadian Medical Association Journal 151(10):1457-1464;1994.
  46. Stewart WF, Kawas C, Corrada M, et al. Risk of Alzheimer’s disease and duration of NSAID use. Neurology 48(3): 626-632;1997.

Downloads

Download data is not yet available.