Cerebrospinal fluid levels of soluble amyloid precursor protein and β-amyloid 42 in patients with multiple sclerosis, neuromyelitis optica and clinically isolated syndrome

Journal of International Medical Research

Volumn 39, Issue 6, 2011, Pages 2402-2413

  Mai, W ^a   Hu, X ^b   Lu, Z ^b   Peng, F ^b   Wang, Y ^b  

^a THE FIFTH AFFILIATED HOSPITAL OF SUN YAT SEN UNIVERSITY   (China)

^b THE THIRD AFFILIATED HOSPITAL OF SUN YAT SEN UNIVERSITY   (China)

Author keywords

Amyloid precursor protein; Axonal damage; Clinically isolated syndrome; Multiple sclerosis; Neuromyelitis optica; amyloid 42

Indexed keywords

AMYLOID BETA PROTEIN[1-42]; AMYLOID PRECURSOR PROTEIN; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR;

ADULT; ARTICLE; BLOOD SAMPLING; BRAIN ATROPHY; CEREBROSPINAL FLUID ANALYSIS; CLINICAL EVALUATION; CLINICALLY ISOLATED SYNDROME; CONCENTRATION PROCESS; CONTROLLED STUDY; DISEASE DURATION; DRUG EFFECT; EXPANDED DISABILITY STATUS SCALE; FEMALE; HUMAN; MAJOR CLINICAL STUDY; MALE; MULTIPLE SCLEROSIS; MYELOOPTIC NEUROPATHY; NEUROLOGIC DISEASE; NEUROPROTECTION; PROTEIN CEREBROSPINAL FLUID LEVEL;

EID: 84555206079     PISSN: 03000605     EISSN: None     Source Type: Journal    
DOI: 10.1177/147323001103900641     Document Type: Article

References (43)

1. Kira J: Search for the pathogenesis of multiple sclerosis from the bedside. Rinsho Shinkeigaku 2008; 48: 931-933 [in Japanese, English abstract].
2. Trapp BD, Peterson J, Ransohoff RM, et al: Axonal transection in the lesions of multiple sclerosis. N Engl J Med 1998; 338: 278-285.
3. De Stefano N, Matthews PM, Antel JP, et al: Chemical pathology of acute demyelinating lesions and its correlation with disability. Ann Neurol 1995; 38: 901-909.
4. Matthews PM, De Stefano N, Narayanan S, et al: Putting magnetic resonance spectroscopy studies in context: axonal damage and disability in multiple sclerosis. Semin Neurol 1998; 18: 327-336.
5. Koo EH, Sisodia SS, Archer DR, et al: Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport. Proc Natl Acad Sci U S A 1990; 87: 1561-1565.
6. Kaether C, Skehel P, Dotti CG: Axonal membrane proteins are transported in distinct carriers: a two-color video microscopy study in cultured hippocampal neurons. Mol Biol Cell 2000; 11: 1213-1224.
7. Höglund K, Thelen KM, Syversen S, et al: The effect of simvastatin treatment on the amyloid precursor protein and brain cholesterol metabolism in patients with Alzheimer's disease. Dement Geriatr Cogn Disord 2005; 19: 256-265.
8. Olsson A, Höglund K, Sjögren M, et al: Measurement of α-and β-secretase cleaved amyloid precursor protein in cerebrospinal fluid from Alzheimer patients. Exp Neurol 2003; 183: 74-80.
9. Sennvik K, Fastbom J, Blomberg M, et al: Levels of α-and β-secretase cleaved amyloid precursor protein in the cerebrospinal fluid of Alzheimer's disease patients. Neurosci Lett 2000; 278: 169-172.
10. Kornek B, Storch MK, Weissert R, et al: Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions. Am J Pathol 2000; 157: 267-276.
11. Mancardi G, Hart B, Roccatagliata L, et al: Demyelination and axonal damage in a non-human primate model of multiple sclerosis. J Neurol Sci 2001; 184: 41-49.
12. Bitsch A, Schuchardt J, Bunkowski S, et al: Acute axonal injury in multiple sclerosis. Correlation with demyelination and inflammation. Brain 2000; 123: 1174-1183.
13. Kuhlmann T, Lingfeld G, Bitsch A, et al: Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time. Brain 2002; 125: 2202-2212.
14. Ferguson B, Matyszak MK, Esiri MM, et al: Axonal damage in acute multiple sclerosis lesions. Brain 1997; 120: 393-399.
15. Aboul-Enein F, Weiser P, Höftberger R, et al: Transient axonal injury in the absence of demyelination: a correlate of clinical disease in acute experimental autoimmune encephalomyelitis. Acta Neuropathol 2006; 111: 539-547.
16. Craner MJ, Hains BC, Lo AC, et al: Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE. Brain 2004; 127: 294-303.
17. Black JA, Newcombe J, Trapp BD, et al: Sodium channel expression within chronic multiple sclerosis plaques. J Neuropathol Exp Neurol 2007; 66: 828-837.
18. Mattsson N, Axelsson M, Haghighi S, et al: Reduced cerebrospinal fluid BACE1 activity in multiple sclerosis. Mult Scler 2009; 15: 448-454.
19. Valis M, Talab R, Stourac P, et al: Tau protein, phosphorylated tau protein and beta-amyloid42 in the cerebrospinal fluid of multiple sclerosis patients. Neuro Endocrinol Lett 2008; 29: 971-976.
20. Hein Née Maier K, Köhler A, Diem R, et al: Biological markers for axonal degeneration in CSF and blood of patients with the first event indicative for multiple sclerosis. Neurosci Lett 2008; 436: 72-76.
21. Polman CH, Reingold SC, Edan G, et al: Diagnostic criteria for multiple sclerosis: 2005 revisions to the "McDonald Criteria". Ann Neurol 2005; 58: 840-846.
22. Wingerchuk DM, Lennon VA, Pittock SJ, et al: Revised diagnostic criteria for neuromyelitis optica. Neurology 2006; 66: 1485-1489.
23. Pelidou SH, Giannopoulos S, Tzavidi S, et al: Multiple sclerosis presented as clinically isolated syndrome: the need for early diagnosis and treatment. Ther Clin Risk Manag 2008; 4: 627-630.
24. Link H, Kostulas V: Utility of isoelectric focusing of cerebrospinal fluid and serum on agarose evaluated for neurological patients. Clin Chem 1983; 29: 810-815.
25. You XF, Ye J, Li CJ, et al: Neuromyelitis optica IgG and related clinical features of patients with neuromyelitis optica. Zhonghua Yi Xue Za Zhi 2010; 90: 2477-2480 [in Chinese, English abstract].
26. Kim SM, Waters P, Vincent A, et al: Cerebrospinal fluid/serum gradient of IgG is associated with disability at acute attacks of neuromyelitis optica. J Neurol 2011; epub ahead of print.
27. Kuhle J, Leppert D, Petzold A, et al: Neurofilament heavy chain in CSF correlates with relapses and disability in multiple sclerosis. Neurology 2011; 76: 1206-1213.
28. Pelletier J, Suchet L, Witjas T, et al: A longitudinal study of callosal atrophy and interhemispheric dysfunction in relapsing-remitting multiple sclerosis. Arch Neurol 2001; 58: 105-111.
29. Fisher E, Rudick RA, Cutter G, et al: Relationship between brain atrophy and disability: an 8-year follow-up study of multiple sclerosis patients. Mult Scler 2000; 6: 373-377.
30. Pierce JE, Trojanowski JQ, Graham DI, et al: Immunohistochemical characterization of alterations in the distribution of amyloid precursor proteins and β-amyloid peptide after experimental brain injury in the rat. J Neurosci 1996; 16: 1083-1090.
31. Bramlett HM, Kraydieh S, Green EJ, et al: Temporal and regional patterns of axonal damage following traumatic brain injury: a beta-amyloid precursor protein immunocytochemical study in rats. J Neuropathol Exp Neurol 1997; 56: 1132-1141.
32. Wolozin B, Kellman W, Ruosseau P, et al: Decreased prevalence of Alzheimer disease associated with 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitors. Arch Neurol 2000; 57: 1439-1443.
33. Fassbender K, Simons M, Bergmann C, et al: Simvastatin strongly reduces levels of Alzheimer's disease β-amyloid peptides Aβ42 and Aβ40 in vitro and in vivo. Proc Natl Acad Sci USA 2001; 98:5856-5861.
34. Sjögren M, Gustafsson K, Syversen S, et al: Treatment with simvastatin in patients with Alzheimer's disease lowers both α-and β-cleaved amyloid precursor protein. Dement Geriatr Cogn Disord 2003; 16: 25-30.
35. Friedhoff LT, Cullen EI, Geoghagen NS, et al: Treatment with controlled-release lovastatin decreases serum concentrations of human β-amyloid (Aβ) peptide. Int J Neuropsycho-pharmacol 2001; 4: 127-130.
36. Simons M, Schwärzler F, Lütjohann D, et al: Treatment with simvastatin in normocholesterolemic patients with Alzheimer's disease: a 26-week randomized, placebo-controlled, double-blind trial. Ann Neurol 2002; 52: 346-350.
37. Höglund K, Wiklund O, Vanderstichele H, et al: Plasma levels of β-amyloid(1-40), β-amyloid(1-42), and total β-amyloid remain unaffected in adult patients with hypercholesterolemia after treatment with statins. Arch Neurol 2004; 61: 333-337.
38. Riekse RG, Li G, Petrie EC, et al: Effect of statins on Alzheimer's disease biomarkers in cerebrospinal fluid. J Alzheimers Dis 2006; 10: 399-406.
39. Turner PR, O'Connor K, Tate WP, et al: Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory. Prog Neurobiol 2003; 70: 1-32.
40. Trysberg E, Höglund K, Svenungsson E, et al: Decreased levels of soluble amyloid β-protein precursor and β-amyloid protein in cerebrospinal fluid of patients with systemic lupus erythematosus. Arthritis Res Ther 2004; 6: R129-R136.
41. Weggen S, Eriksen JL, Sagi SA, et al: Evidence that nonsteroidal anti-inflammatory drugs decrease amyloid β42 production by direct modulation of γ-secretase activity. J Biol Chem 2003; 278: 31831-31837.
42. Tokuda T, Oide T, Tamaoka A, et al: Prednisolone (30 -60 mg/day) for diseases other than AD decreases amyloid β-peptides in CSF. Neurology 2002; 58: 1415-1418.
43. Kulstad JJ, McMillan PJ, Leverenz JB, et al: Effects of chronic glucocorticoid administration on insulin-degrading enzyme and amyloid-beta peptide in the aged macaque. J Neuropathol Exp Neurol 2005; 64: 139-146.