NEUROINFLAMMATION IN ALZHEIMER’S DISEASE AND INVOLVEMENT OF INTERLEUKIN-1: A MECHANISTIC VIEW

Authors

  • Vivek Sharma Government College of Pharmacy, Rohru District Shimla (171 207) Himachal Pradesh, India

Abstract

Ageing is a universal biological fact and a natural process. It begins from the day we are born, or perhaps even before. Of the world’s 580 million elderly, 77 million (22% of total) live in India. The increasing life expectancy of Indians, in the last decade, is likely to result in an increase in age-related disorders like Alzheimer’s disease and Parkinson’s disease. Alzheimer’s disease, the most common disorder of geriatric population, is a chronic, progressive, untreatable neurodegenerative disorder characterized by apraxia, aphasia, agnosia and severe cognitive deficits. Several behavioural changes like anxiety, hallucinations, depression and delusions are also experienced. Lot of progress has been made regarding understanding the pathological pathways involved, yet the available therapy only provide symptomatic relief but do not stop progression of disease. Several of key areas have been recognised and out of them inflammation has been regarded as inseparable and crucial factor involved. Interleukin-1 is a key molecule in systemic immune responses in health and disease and has analogous roles in the brain where it contributes to neuronal degeneration by energy dysfunction and triggering production of other cytokines, nitric oxide and others. IL-1 over expression is also associated with rheumatoid arthritis, vascular dementia, diabetes mellitus, periodontitis, systemic sclerosis, autoimmune encephalomyelitis and cerebral infarction. Present review is an effort to present IL-1 as potential therapeutic target in treatment of Alzheimer’s disease by linking it with several of pathological factors like amyloidβ, neurofibrillary tangles, neuron loss and cholinergic dysfunction.

Keywords:

Alzheimer’s disease, cytokine, interleukin-1, microglia.

DOI

https://doi.org/10.25004/IJPSDR.2011.030403

References

1. Delay C, Sebastien SH. MicroRNAs and Alzheimer’s disease Mouse Models; Current Insights and Future Research Avenues. International Journal of Alzheimer’s disease. 2011; 46-49.
2. Samsam M. Role of Inflammation in Neurological and Psychiatric Disorders. Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry. 2010; 9:15-19.
3. Hebert LE et al. Alzheimer disease in the US population: prevalence estimates using the 2000 census. Arch Neurol. 2003; 60:119-1122.
4. Maier L. Neurobiological bases for Alzheimer’s disease. J Neurosci Nurs. 2000; 32: 117-125.
5. Kitazawa M, Tritia R, Yamasaki JK, Frank M. Microglia as a Potential Bridge between the Amyloidβ Peptide and Tau. Ann. N.Y. Acad. Sci. 2004; 85-103.
6. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole G M. Inflammation and Alzheimer’s disease. Neurobiology of Aging 2000; 383-421.
7. Glass CK, Saijo K, Winner B, Marchetto MC, Gage FH. Mechanisms underlying inflammation in neurodegeneration. Cell 2010; 918-34.
8. McNaull BB, Todd S, Mc Guinness B, Passmore AP. Inflammation and Anti-Inflammatory Strategies for Alzheimer's disease - A Mini-Review. Gerontology 2009; 56: 3-14.
9. Itagaki SP, McGeer L, Akiyama H, Zhu S, Selkoe D. Relationship of microglia and astrocytes to amyloid deposits of Alzheimer disease. J. Neuroimmunol. 1989; 173-182.
10. Mattiace LA, Davies P, Yen SH, Dickson DW. Microglia in cerebellar plaques in Alzheimer's disease. Acta Neuropathol. 1990; 493-498.
11. Dickson D, Lee WS, Mattiace L A, Yen SH, Brosman C. Microglia and cytokines in neurological disease with special reference to AIDS and Alzheimer's disease. Glia. 1993; 67:75-83.
12. McGeer PL, Rogers J. Anti-inflammatory agents as a therapeutic approach to Alzheimer's disease. Neurology. 1992; 42:447- 449.
13. Ehab E, Tuppo Hugo R, Arias. The role of inflammation in Alzheimer’s disease. The International Journal of Biochemistry & Cell Biology 2005; 37: 289-305.
14. Hortega del rio P, El ‘tercer elemento’ de los centros nerviosos, Poder fagocitario y movilidad de la microglia. Bol Soc Esp Biol An. 1919; 9:154-166.
15. Hopkins SJ, Rothwell NJ. Cytokines and the nervous system I, expression and recognition. Trends in Neuroscience. 1995; 18: 83-88.
16. Lee YB, Nagai A, Kim SU. Cytokines, chemokines, and cytokine receptors in human microglia, Journal of Neuroscience Research. 2002; 69: 94-103.
17. Cohen RM. The Role of the Immune System in Alzheimer’s disease. Winter. 2009; 2:17-21.
18. Rainero I, Bo M, Ferrero M, Valfre W, Vaula G, Pinessi L. Association between the interleukin-1alpha gene and Alzheimer's disease, a meta-analysis. Neurobiol Aging. 2004; 25: 1293-1298.
19. Yucesoy B, Peila R, White LR, Wu KM, Johnson VJ, Kashon ML, Luster MI, Launer LJ. Association of interleukin-1 gene polymorphisms with dementia in a community-based sample, the Honolulu-Asia Aging Study. Neurobiol Aging 2006; 27:211-217.
20. Lopez NJ, Jara L, Valenzuela CY. Association of interleukin-1 polymorphisms with periodontal disease. J Periodontol. 2005; 76: 234-243.
21. Kawaguchi Y. IL-1 alpha gene expression and protein production by fibroblasts from patients with systemic sclerosis. Clin Exp Immunol. 1994; 97: 445-450.
22. Sutton C, Brereton C, Keogh B, Mills KH, Lavelle EC. A crucial role for interleukin (IL)-1 in the induction of IL-17-producing T cells that mediate autoimmune encephalomyelitis. J Exp Med. 2006; 203:1685-1691.
23. Um JY, Jeong HJ, Park RK, Hong SH, Kim HM. Aspects of gene polymorphisms in cerebral infarction, inflammatory cytokines. Cell Mol Life Sci. 2005; 62: 824-833.
24. Gery I, Waksman BH. Potentiation of the T-lymphocyte response to mitogens, II, The cellular source of potentiating mediator(s). J Exp Med. 1972; 136:143-155.
25. Vicenova B, Vopalensky V, Burysek M. Emerging Role of Interleukin-1 in Cardiovascular Diseases. Physiol Res. 2009; 58: 481-498.
26. Ferrari D, Chiozzi P, Falzoni S, Hanau S, Di virgilio F. Purinergic modulation of interleukin-1 beta release from microglial cells stimulated with bacterial endotoxin. J Exp Med. 1997; 185:579-582.
27. Pelegrin P, Surprenant A. Pannexin-1 mediates large pore formation and interleukin-:1beta release by the ATP gated P2X7 receptor. EMBO J. 2006; 25: 5071-5082.
28. Mandinova A, Soldi R, Graziani I, Bagala C, Bellum S, Landriscina M, Tarantini F, Prudovsky I, Maciag T. S100A13 mediates the copper-dependent stress-induced release of IL-1alpha from both human U937 and murine NIH 3T3 cells. J Cell Sci. 2003; 116: 2687-2696.
29. Nicklin MJ, Weith A, Duff GW. A physical map of the region encompassing the human interleukin-1 alpha, interleukin-1 beta, and interleukin-1 receptor antagonist genes. Genomics. 1994; 19:382-4,
30. Kornman KS. Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging. Am J Clin Nutr. 2006; 83:475S-83S,
31. Griffin WST, Stanley L, Ling C, White L, MacLeod V, Perrot LJ. Brain interleukin I and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. Proceedings of the National Academy of Sciences USA. 1989; 86:7611-7615.
32. Schneider H, Pitossi F, Balschun D, Wagner A, Del Rey A, Besedovsky HO. A neuromodulatory role of interleukin-1beta in the hippocampus. Proc Nat Acad Sci USA. 1998; 95: 7778-7783.
33. Murray CA, Lynch MA. Evidence that increased hippocampal expression of the cytokine interleukin-1 beta is a common trigger for age- and stress-induced impairments in long-term potentiation. J Neurosci. 1998; 18:2974-2981.
34. Griffin WST, Sheng JG, Roberts GW, Mrak RE. Interleukin-1 expression in different plaque types in Alzheimer’s disease. J Neuropath Exp Neurol. 1995; 54:276-281.
35. Mrak RE, Griffin WST. The role of activated astrocytes and of the neurotrophic cytokine S100B in the pathogenesis of Alzheimer’s disease. Neurobiology of Aging. 2001a; 22: 915–922.
36. Mrak RE, Griffin WST. Interleukin-1, neuroinflammation, and Alzheimer’s disease. Neurobiology of Aging. 2001b; 903-908.
37. Li R, ShenY, Yang BL, Lue LF, Finch C, Rogers J. Estrogen enhances uptake of amyloid beta-protein by microglia derived from the human cortex. Journal of Neurochemistry. 2000; 75: 1447-1454.
38. Li Y, Barger SW, Liu L, Mrak RE, Griffin WST. S100_ induction of the pro-inflammatory cytokine interleukin-6 in neurons, implications for Alzheimer pathogenesis. Journal of Neurochemistry. 2000; 74:143-150.
39. Sheng JG, Mrak RE, Griffin WST. Glial-neuronal interactions in Alzheimer disease, progressive association of IL-1alpha + microglia and S100beta + astrocytes with neurofibril neurofibrillary tangles stages. Journal of Neuropathology and Experimental Neurology 1997; 56:285-290.
40. Whitehouse PJ, Price DL, Clark AW, Coyle JT, DeLong MR. Alzheimer disease, evidence for selective loss of cholinergic neurons in the nucleus basalis. Ann Neurol. 1981; 10:122-126.
41. Bartus RT, Dean RL, Beer B, Lippa AS. The cholinergic hypothesis of geriatric memory dysfunction. Science 1981; 217:408-417.
42. Flicker L. Acetylcholinesterase inhibitors for Alzheimer's disease. BMJ. 1999; 318: 615-6.
43. Salpeter M. Electron microscope radioautography as a quantitative tool in enzyme cytochemistry. The distribution of acetylcholinesterase at motor endplates of a vertebrate twitch muscle. J Cell Bio. 1967; 32: 379-389.
44. Hall ZW, Kelly RB. Enzymatic detachment of endplate acetylcholinesterase form muscle. Nat New Biol. 1971; 32:62-63.
45. Alvarez A, Opazo C, Alarcon R, Garrido J, Inestrosa NC. Acetylcholinesterase promotes the aggregation of amyloid-b-peptide fragments by forming a complex with the growing fibrils. J Mol Biol. 1971; 272:348-361.
46. Mori F, Lai C, Fusi F, Giacobini E. Cholinesterase inhibitors increase secretion of APPs in rat brain cortex. NeuroReport. 1995; 6:633-636.
47. Inestrosa NC, Alvarez A, Perez CA, Moreno RD, Vicente M, Linker C, Casanueva OI, Soto C, Garrido J. Acetylcholinesterase accelerate sassembly of amyloid-b-peptides into Alzheimer’s fibrils, possible role of the peripheral site of the enzyme. Neuron. 1996; 16: 881-891.
48. Li Y, Liu L, Kang J, Sheng JG, Barger SW, Mrak R E, Griffin WST. Neuronal-glial interactions mediated by interleukin-1 enhance neuronal acetylcholinesterase activity and mRNA expression. 2000; 20: 149-155.
49. Beeri R, Andres C, Lev-Lehman E, Timberg R, Huberman T, Shani M, Soreq H. Transgenic expression of human acetylcholinesterase induces progressive cognitive deterioration in mice. Curr Top Biol. 1995; 5:1063-1071.
50. Winkler J, Suhr ST, Gage FH, Thal LJ, Fisher LJ. Essential role of acetylcholine in spatial memor. Nature. 1995; 375:484-487.
51. Layer PG, Willbold E. Novel functions of cholinesterases in development, physiology and disease. Prog Histochem Cytochem. 1995; 29:1-99.
52. Sternfeld M, Ming GL, Song HJ, Sela K, Timberg R, Poo MM, Soreq H. Acetylcholinesterase enhances neurite growth and synapse development through alternative contributions of its hydrolytic capacity, core protein, and variable C termini. J Neurosci. 1998; 18:1240-1249.
53. Muller D, Wiegmann H, Langer U, Motzen-Lenz S, Nitsch RM. Lu 25–109, a combined m1 agonist and m2 antagonist, modulates regulated processing of the amyloid precursor protein of Alzheimer’s disease. J Neural Transm. 1998; 105:1029-1043.
54. Del Rey A, Besedovsky H. Interleukin-1 affects glucose homeostasis. Am J Physiol. 1987; 253:794-798.
55. Del Rey A, Besedovsky H. Antidiabetic effects of interleukin. Proc Natl Acad Sci USA. 1989; 86:5943-5947.
56. Del Rey A, Besedovsky HO. Metabolic and neuroendocrine effects of pro‐inflammatory cytokines. Eur J Clin Invest. 1992; 22: 10-15.
57. Del Rey A, Monge‐Arditi G, Besedovsky HO.Central and peripheral mechanisms contribute to the hypoglycemia induced by interleukin‐1. Ann N Y Acad Sci. 1998; 840: 153-161.
58. Del Rey A, Monge‐Arditi G, Klusman I, Besedovsky HO. Metabolic and endocrine effects of interleukin‐1 in obese, diabetic Zucker fa/fa rats. Exp Clin Endocrinol Diabetes 1996; 104: 317-326.
59. Braak H, Braak E, Strothjohann M. Abnormally phosphorylated tau protein related to the formation of neurofibrillary tangles and neuropil threads in the cerebral cortex of sheep and goat. Neurosci Lett. 1994; 171:1-4.
60. DeKosky ST, Scheff SW. Synapse loss in frontal cortex biopsies in Alzheimer’s disease, correlation with cognitive severity. Ann Neurol. 1990; 27:457- 464.
61. Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA, Katzman R. Physical basis of cognitive alterations in Alzheimer’s disease, synapse loss is the major correlate of cognitive impairment. Ann Neurol. 1991; 30:572-580.
62. Li Y, Liu L, Barger SW, Griffin WST. Interleukin-1 Mediates Pathological Effects of Microglia on Tau Phosphorylation and on Synaptophysin Synthesis in Cortical Neurons through a p38-MAPK Pathway. The Journal of Neuroscience 2003; 23(5): 1605-1611.
63. Xia Z, Dickens M, Raingeaud J, Davis RJ, Greenberg ME. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis. Science 1995; 270:1326-1331.
64. Kawasaki H, Morooka T, Shimohama S, Kimura J, Hirano T, Gotoh Y, Nishida E. Activation and involvement of p38 mitogen-activated protein kinase in glutamate-induced apoptosis in rat cerebellar granule cells. J Biol Chem. 1997; 272:18518-18521.
65. Sheng JG, Jones RA, Zhou XQ, McGinness JM, Van Eldik LJ, Mrak RE, Griffin WS. Interleukin-1 promotion of MAPK-p38 over expression in experimental animals and in Alzheimer’s disease, potential significance for tau protein phosphorylation. Neurochem Int. 2001; 39:341-348.
66. Scheff SW, Sparks DL, Price DA. Quantitative assessment of synaptic density in the outer molecular layer of the hippocampal dentate gyrus in Alzheimer’s disease. Dementia 1996; 7:226-232.
67. Mattson MP. Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives. Physiol Rev. 1997; 77:1081-1132.
68. Lee VM, Balin BJ, Otvos L Jr, Trojanowski JQ. A68, a major subunit of paired helical filaments and derivatized forms of normal tau. Science 1991; 251:675-678.
69. Wischik CM, Edwards PC, Lai RY, Roth M, Harrington CR. Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines. Proc Natl Acad Sci USA 1996; 93:11213-11218.
70. Buxbaum JD, Oishi M, Chen HI, Pinkas-Kramarski R, Jaffe EA, Gandy SE, Greengard P. Cholinergic agonists and interleukin 1 regulate processing and secretion of the Alzheimer beta/A4 amyloid protein precursor. Proc Natl Acad Sci USA 1992; 89:10075-10078.
71. Callahan LM, Coleman PD. Neurons bearing neurofibrillary tangles are responsible for selected synaptic deficits in Alzheimer’s disease. Neurobiol Aging 1995; 16:311-314.
72. DiPatre PL, Gelman BB. Microglial cell activation in aging and Alzheimer disease, partial linkage with neurofibrillary tangle burden in the hippocampus. J Neuropathol Exp Neurol. 1997; 56:143-149.
73. Sheng JG, Mrak RE, Griffin WST. Glial-neuronal interactions in Alzheimer disease, progressive association of IL-1alpha + microglia and S100beta + astrocytes with neurofibrillary tangles stages. Journal of Neuropathology and Experimental Neurology 1997; 56: 285-290.
74. Brenneman DE, Page SW, Schultzberg M, Thomas F H, Zelazowski P, Burnet P, Avidor R, Sternberg EM. A decomposition product of a contaminant implicated in L-tryptophan eosinophilia myalgia syndrome affects spinal cord neuronal cell death and survival through stereospecific, maturation and partly interleukin-1-dependent mechanisms. J Pharmacol Exp Ther. 1992; 266:1029-1035.
75. Zhu SG, Sheng JG, Jones RA, Brewer MM, Zhou XQ, Mrak RE, Griffin WST. Increased interleukin-1 converting enzyme expression and activity in Alzheimer disease. J Neuropathol Exp Neurobiol. 1999; 58: 582-587.
76. Chan SL, Griffin WST, Mattson MP. Evidence for Caspase-mediated cleavage of AMPA receptor subunits in neuronal apoptosis and Alzheimer’s disease. J Neurosci Res. 1999; 57: 315-323.
77. Sheng JG, Zhou XQ, Mrak RE, Griffin WST. Progressive neuronal injury associated with neurofibrillary tangle formation in Alzheimer’s disease. J Neuropathol Exp Neurol. 1998; 57:323-328.
78. Sheng JG, Mrak RE, Rovnaghi CR, Kozlowska E, Van Eldik LJ, Griffin WST. Human brain S100a and S100b mRNA expression increases with age, Pathogenic implications for Alzheimer’s disease. Neurobiol Aging.1996; 17:359-363.
79. Rossi F, Bianchini E. Synergistic induction of nitric oxide by hamyloid and cytokines in astrocytes, Biochem, Biophys Res Commun. 1996; 225: 474- 478.
80. Griffin WST, Sheng JG, Gentleman SM, Graham DI, Mrak RE, Roberts GW. Microglial interleukin-1 expression in human head injury, correlations with neuronal and neuritic βamyloid precursor protein expression. Neurosci Lett. 1994; 176:133-136.
81. Sheng JG, Boop FA, Mrak RE, Griffin WST. Increased neuronal βamyloid precursor protein expression in human temporal lobe epilepsy, association with interleukin-1 alpha immunoreactivity. J Neurochem. 1994; 63:1872-1879.
82. Stanley LC, Mrak RE, Woody RC, Perrot LJ, Zhang SX, Marshak DR, Nelson SJ, Griffin WST. Glial cytokines as neuropathogenic factors in HIV infection, pathogenic similarities to Alzheimer’s disease. J Neuropathol Exp Neurol. 1994; 53: 231-238.
83. Mackenzie IRA, Miller LA. Senile plaques in temporal lobe epilepsy. Acta Neuropathol. 1994; 87:504-510.
84. Esiri MM, Biddolph SC, Morris CS. Prevalence of Alzheimer plaques in AIDS. J Neurol Neurosurg Psychiatry 1998; 65: 29-33.

Published

01-10-2011
Statistics
Abstract Display: 150
PDF Downloads: 165
Dimension Badge

How to Cite

“NEUROINFLAMMATION IN ALZHEIMER’S DISEASE AND INVOLVEMENT OF INTERLEUKIN-1: A MECHANISTIC VIEW”. International Journal of Pharmaceutical Sciences and Drug Research, vol. 3, no. 4, Oct. 2011, pp. 287-91, https://doi.org/10.25004/IJPSDR.2011.030403.

Issue

Section

Review Article

How to Cite

“NEUROINFLAMMATION IN ALZHEIMER’S DISEASE AND INVOLVEMENT OF INTERLEUKIN-1: A MECHANISTIC VIEW”. International Journal of Pharmaceutical Sciences and Drug Research, vol. 3, no. 4, Oct. 2011, pp. 287-91, https://doi.org/10.25004/IJPSDR.2011.030403.

Similar Articles

1-10 of 197

You may also start an advanced similarity search for this article.