Inflammation induces tau pathology in inclusion body myositis model via glycogen synthase kinase-3β

Annals of Neurology

Volumn 64, Issue 1, 2008, Pages 15-24

  Kitazawa, Masashi ^a   Trinh, Dan N ^a   LaFerla, Frank M ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID PRECURSOR PROTEIN; GLYCOGEN SYNTHASE KINASE 3BETA; INTERLEUKIN 1BETA; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; LITHIUM CHLORIDE; TUMOR NECROSIS FACTOR ALPHA;

ACUTE DISEASE; ARTICLE; CD8+ T LYMPHOCYTE; CHRONIC DRUG ADMINISTRATION; CHRONIC INFLAMMATION; CYTOTOXIC T LYMPHOCYTE; ENZYME INHIBITION; INCLUSION BODY MYOSITIS; INFLAMMATION; MUSCLE BIOPSY; NEUROPATHOLOGY; PRIORITY JOURNAL; PROTEIN LOCALIZATION; PROTEIN PHOSPHORYLATION; TAUOPATHY; TRANSGENIC MOUSE;

ANIMALS; BIOPSY; CD8-POSITIVE T-LYMPHOCYTES; CELLS, CULTURED; CHEMOTAXIS, LEUKOCYTE; CYTOKINES; DISEASE MODELS, ANIMAL; ENZYME ACTIVATION; ENZYME INHIBITORS; GLYCOGEN SYNTHASE KINASE 3; HUMANS; INFLAMMATION; LIPOPOLYSACCHARIDES; MICE; MICE, INBRED C3H; MICE, INBRED C57BL; MICE, TRANSGENIC; MUSCLE, SKELETAL; MYOSITIS, INCLUSION BODY; PHOSPHORYLATION; TAU PROTEINS;

EID: 48949086699     PISSN: 03645134     EISSN: None     Source Type: Journal    
DOI: 10.1002/ana.21325     Document Type: Article

References (40)

1. Beyenburg S, Zierz S, Jerusalem F. Inclusion body myositis: clinical and histopathological features of 36 patients. Clin Invest 1993;71:351-361.
2. Dalakas MC. Clinical, immunopathologic, and therapeutic considerations of inflammatory myopathies. Clin Neuropharmacol 1992;15:327-351.
3. Tawil R, Griggs RC. Inclusion body myositis. Curr Opin Rheumatol 2002;14:653-657.
4. Askanas V, Alvarez RB, Engel WK. beta-Amyloid precursor epitopes in muscle fibers of inclusion body myositis. Ann Neurol 1993;34:551-560.
5. Fukuchi K, Pham D, Han M, et al. Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy. Am J Pathol 1998;153:1687-1693.
6. Jin LW, Hearn MG, Ogburn CE, et al. Transgenic mice overexpressing the C-99 fragment of betaPP with an alpha-secretase site mutation develop a myopathy similar to human inclusion body myositis. Am J Pathol 1998;153:1679-1686.
7. Kitazawa M, Green KN, Caccamo A, LaFerla FM. Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice. Am J Pathol 2006;168:1986-1997.
8. Moussa CE, Fu Q, Kumar P, et al. Transgenic expression of beta-APP in fast-twitch skeletal muscle leads to calcium dyshomeostasis and IBM-like pathology. Faseb J 2006;20: 2165-2167.
9. Sugarman MC, Yamasaki TR, Oddo S, et al. Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle. Proc Natl Acad Sci U S A 2002; 99:6334-6339.
10. Askanas V, Mirabella M, Engel WK, et al. Apolipoprotein E immunoreactive deposits in inclusion-body muscle diseases. Lancet 1994;343:364-365.
11. Mirabella M, Alvarez RB, Bilak M, et al. Difference in expression of phosphorylated tau epitopes between sporadic inclusion-body myositis and hereditary inclusion-body myopathies. J Neuropathol Exp Neurol 1996;55:774-786.
12. Albrecht S, Bilbao JM. Ubiquitin expression in inclusion body myositis. An immunohistochemical study. Arch Pathol Lab Med 1993;117:789-793.
13. Askanas V, Engel WK, Alvarez RB, et al. Novel immunolocalization of alpha-synuclein in human muscle of inclusion-body myositis, regenerating and necrotic muscle fibers, and at neuromuscular junctions. J Neuropathol Exp Neurol 2000;59: 592-598.
14. Dalakas MC. Sporadic inclusion body myositis - diagnosis, pathogenesis and therapeutic strategies. Nat Clin Pract Neurol 2006;2:437-447.
15. Pruitt JN 2nd, Showalter CJ, Engel AG. Sporadic inclusion body myositis: counts of different types of abnormal fibers. Ann Neurol 1996;39:139-143.
16. Figarella-Branger D, Civatte M, Bartoli C, Pellissier JF. Cytokines, chemokines, and cell adhesion molecules in inflammatory myopathies. Muscle Nerve 2003;28:659-682.
17. Raju R, Vasconcelos O, Granger R, Dalakas MC. Expression of IFN-gamma-inducible chemokines in inclusion body myositis. J Neuroimmunol 2003;141:125-131.
18. De Bleecker JL, Meire VI, Declercq W, Van Aken EH. Immunolocalization of tumor necrosis factor-alpha and its receptors in inflammatory myopathies. Neuromuscul Disord 1999;9: 239-246.
19. Emslie-Smith AM, Arahata K, Engel AG. Major histocompatibility complex class I antigen expression, immunolocalization of interferon subtypes, and T cell-mediated cytotoxicity in myopathies. Hum Pathol 1989;20:224-231.
20. Nagaraju K, Raben N, Loeffler L, et al. Conditional upregulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. Proc Natl Acad Sci U S A 2000;97:9209-9214.
21. Querfurth HW, Suhara T, Rosen KM, et al. Beta-amyloid peptide expression is sufficient for myotube death: implications for human inclusion body myopathy. Mol Cell Neurosci 2001;17: 793-810.
22. Sugarman MC, Kitazawa M, Baker M, et al. Pathogenic accumulation of APP in fast twitch muscle of IBM patients and a transgenic model. Neurobiol Aging 2006;27:423-432.
23. Kitazawa M, Oddo S, Yamasaki TR, et al. Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease. J Neurosci 2005;25:8843-8853.
24. Sheng JG, Bora SH, Xu G, et al. Lipopolysaccharide-induced- neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid beta peptide in APPswe transgenic mice. Neurobiol Dis 2003;14:133-145.
25. Nakashima H, Ishihara T, Suguimoto P, et al. Chronic lithium treatment decreases tau lesions by promoting ubiquitination in a mouse model of tauopathies. Acta Neuropathol (Berl) 2005; 110:547-556.
26. Noble W, Planel E, Zehr C, et al. Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo. Proc Natl Acad Sci U S A 2005;102: 6990-6995.
27. Caccamo A, Oddo S, Tran LX, Laferla FM. Lithium reduces tau phosphorylation but not A{beta} or working memory deficits in a transgenic model with both plaques and tangles. Am J Pathol 2007;170:1669-1678.
28. Nakano S, Akiguchi I, Nakamura S, et al. Aberrant expression of cyclin-dependent kinase 5 in inclusion body myositis. Neurology 1999;53:1671-1676.
29. Wilczynski GM, Engel WK, Askanas V. Cyclin-dependent kinase 5 colocalizes with phosphorylated tau in human inclusion-body myositis paired-helical filaments and may play a role in tau phosphorylation. Neurosci Lett 2000;293:33-36.
30. Leroy K, Yilmaz Z, Brion JP. Increased level of active GSK-3beta in Alzheimer's disease and accumulation in argyrophilic grains and in neurones at different stages of neurofibrillary degeneration. Neuropathol Appl Neurobiol 2007;33:43-55.
31. Feyt C, Kienlen-Campard P, Leroy K, et al. Lithium chloride increases the production of amyloid-beta peptide independently from its inhibition of glycogen synthase kinase 3. J Biol Chem 2005;280:33220-33227.
32. Su Y, Ryder J, Li B, et al. Lithium, a common drug for bipolar disorder treatment, regulates amyloid-beta precursor protein processing. Biochemistry 2004;43:6899-6908.
33. Gotz J, Chen F, van Dorpe J, Nitsch RM. Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils. Science 2001;293:1491-1495.
34. Lewis J, Dickson DW, Lin WL, et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science 2001;293:1487-1491.
35. Eto M, Kouroedov A, Cosentino F, Luscher TF. Glycogen synthase kinase-3 mediates endothelial cell activation by tumor necrosis factor-alpha. Circulation 2005;112:1316-1322.
36. Briemberg HR, Amato AA. Dermatomyositis and polymyositis. Curr Treat Options Neurol 2003;5:349-356.
37. Di Martino SJ, Kagen LJ. Newer therapeutic approaches: inflammatory muscle disorders. Rheum Dis Clin North Am 2006;32:121-128, ix.
38. Caccamo A, Oddo S, Sugarman MC, et al. Age- and region-dependent alterations in Abeta-degrading enzymes: implications for Abeta-induced disorders. Neurobiol Aging 2005;26:645-654.
39. Malicdan MC, Noguchi S, Nonaka I, et al. A Gne knockout mouse expressing human V572L mutation develops features similar to distal myopathy with rimmed vacuoles or hereditary inclusion body myopathy. Hum Mol Genet 2007;16:115-128.
40. Weihl CC, Miller SE, Hanson PI, Pestronk A. Transgenic expression of inclusion body myopathy associated mutant p97/ VCP causes weakness and ubiquitinated protein inclusions in mice. Hum Mol Genet 2007;16:919-928.