The spectrum of multiple sclerosis: New lessons from pathology

Current Opinion in Neurology

Volumn 18, Issue 3, 2005, Pages 221-224

  Brück, Wolfgang ^a   Stadelmann, Christine ^a  

^a UNIVERSITY OF GÖTTINGEN   (Germany)

Author keywords

Axons; Inflammation; Magnetic resonance imaging; MRI; Multiple sclerosis; Oligodendrocytes; Pathogenesis

Indexed keywords

ANNEXIN; CD8 ANTIGEN; CHEMOKINE RECEPTOR CCR1; CHEMOKINE RECEPTOR CCR5; CYCLOOXYGENASE 2; INDUCIBLE NITRIC OXIDE SYNTHASE; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 1; MYELIN; SODIUM CALCIUM EXCHANGE PROTEIN;

AXONAL INJURY; BRAIN CORTEX; CORRELATION ANALYSIS; DEMYELINATION; DIAGNOSTIC APPROACH ROUTE; EFFECTOR CELL; EXCITOTOXICITY; GENE EXPRESSION REGULATION; HUMAN; HYPOXIA; INFLAMMATION; MULTIPLE SCLEROSIS; NERVE FIBER; NEUROPROTECTION; NUCLEAR MAGNETIC RESONANCE IMAGING; OLIGODENDROGLIA; PATHOPHYSIOLOGY; QUANTITATIVE ANALYSIS; REGULATORY MECHANISM; REMYELINIZATION; REVIEW; RISK FACTOR;

EID: 20444489863     PISSN: 13507540     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.wco.0000169736.60922.20     Document Type: Review

References (40)

1. Lassmann H. Pathology of multiple sclerosis. In: Compston A, Ebers G, Lassmann H, et al., editors. McAlpine's multiple sclerosis. 3rd ed. London: Churchill Livingstone; 1998. pp. 323-358.
2. Prineas JW. The neuropathology of multiple sclerosis. In: Koetsier JC, editor. Demyelinating diseases. Amsterdam: Elsevier Science Publishers; 1985. pp. 213-257.
3. Lassmann H. Axonal injury in multiple sclerosis. J Neurol Neurosurg Psychiatry 2003; 74:695-697.
4. Brück W, Kuhlmann T, Stadelmann C. Remyelination in multiple sclerosis. J Neurol Sci 2003; 206:181-185.
5. Lassmann H, Brück W, Lucchinetti C. Heterogeneity of multiple sclerosis pathogenesis: implications for diagnosis and therapy. Trends Mol Med 2001; 7:115-121.
6. Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple slerosis. New Engl J Med 2000; 343:938-952.
7. Lucchinetti C, Brück W, Parisi J, et al. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination. Ann Neurol 2000; 47:707-717.
8. Barnett MH, Prineas JW. Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion. Ann Neurol 2004; 55:458-468. This paper raises an interesting hypothesis on the early development of MS lesions with the cardinal features of extensive oligodendrocyte apoptosis, microglial activation and absence of inflammation.
9. Trapp BD. Pathogenesis of multiple sclerosis: The eyes only see what the mind is prepared to comprehend. Ann Neurol 2004; 55:455-457.
10. Lucchinetti CF, Brück W, Lassmann H. Evidence for pathogenic heterogeneity in multiple sclerosis. Ann Neurol 2004; 56:308.
11. Mahad DJ, Trebst C, Kivisakk P, et al. Expression of chemokine receptors CCR1 and CCR5 reflects differential activation of mononuclear phagocytes in pattern II and pattern III multiple sclerosis lesions. J Neuropathol Exp Neurol 2004; 63:262-273. An important study confirming lesional heterogeneity in MS by showing differential chemokine-receptor expression on monocytes/macrophages depending on the lesional pattern of MS.
12. Vos CM, van Haastert ES, De Groot CJ, et al. Matrix metalloproteinase-12 is expressed in phagocytotic macrophages in active multiple sclerosis lesions. J Neuroimmunol 2003; 138:106-114.
13. Kirk J, Plumb J, Mirakhur M, McQuaid S. Tight junctional abnormality in multiple sclerosis white matter affects all calibres of vessel and is associated with blood-brain barrier leakage and active demyelination. J Pathol 2003; 201:319-327.
14. Rose JW, Hill KE, Watt HE, Carlson NG. Inflammatory cell expression of cyclooxygenase-2 in the multiple sclerosis lesion. J Neuroimmunol 2004; 149:40-49.
15. Hill KE, Zollinger LV, Watt HE, et al. Inducible nitric oxide synthase in chronic active multiple sclerosis plaques: distribution, cellular expression and association with myelin damage. J Neuroimmunol 2004; 151:171-179.
16. Höftberger R, Aboul-Enein F, Brück W, et al. Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions. Brain Pathol 2004; 14:43-50. Expression of MHC class I molecules may lead to direct cytotoxic attack of oligodendrocytes, axons and neurons.
17. + cells in the cerebrospinal fluid and blood of MS patients over a period of years.
18. DeLuca GC, Ebers GC, Esiri MM. Axonal loss in multiple sclerosis: a pathological survey of the corticospinal and sensory tracts. Brain 2004; 127:1009-1018. A clear study showing that axon loss in MS is tract- and size-specific.
19. Craner MJ, Lo AC, Black JA, et al. Annexin II/p11 is up-regulated in Purkinje cells in EAE and MS. Neuroreport 2003; 14:555-558.
20. Waxman SG, Craner MJ, Black JA. Na(+) channel expression along axons in multiple sclerosis and its models. Trends Pharmacol Sci 2004; 25:584-591.
21. Craner MJ, Newcombe J, Black JA, et al. Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. Proc Natl Acad Sci USA 2004; 101:8168-8173. This paper shows elegantly that altered expression of sodium channels ia associated with axonal degeneration in MS.
22. Kidd D, Barkhof F, McConnell R, et al. Cortical lesions in multiple sclerosis. Brain 1999; 122:17-26.
23. Bö L, Vedeler CA, Nyland HI, et al. Subpial demyelination in the cerebral cortex of multiple sclerosis patients. J Neuropathol Exp Neurol 2003; 62:723-732.
24. Bö L, Vedeler CA, Nyland H, et al. Intracortical multiple sclerosis lesions are not associated with increased lymphocyte infiltration. Mult Scler 2003; 9:323-331.
25. Peterson JW, Bö L, Mörk S, et al. Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions. Ann Neurol 2001; 50:389-400.
26. Kurnellas MP, Nicot A, Shull GE, Elkabes S. Plasma membrane calcium ATPase deficiency causes neuronal pathology in the spinal cord: a potential mechanism for neurodegeneration in multiple sclerosis and spinal cord injury. FASEB J 2005; 19:298-300. This study in experimental autoimmune encephalomyelitis points towards a novel mechanism of neuronal injury in MS.
27. Lassmann H, Reindl M, Rauschka H, et al. A new paraclinical CSF marker for hypoxia-like tissue damage in multiple sclerosis lesions. Brain 2003; 126:1347-1357.
28. Cannella B, Raine CS. Multiple sclerosis: Cytokine receptors on oligodendrocytes predict innate regulation. Ann Neurol 2004; 55:46-57. This paper shows extensive expression of cytokine receptors by oligodendrocytes related to Th1 as well as Th2 immune responses.
29. De Keyser J, Zeinstra E, Frohman E. Are astrocytes central players in the pathophysiology of multiple sclerosis? Arch Neurol 2003; 60:132-136.
30. Nicholas AP, Sambandam T, Echols JD, Tourtellotte WW. Increased citrullinated glial fibrillary acidic protein in secondary progressive multiple sclerosis. J Comp Neurol 2004; 473:128-136. An interesting biochemical analysis of the glial fibrillary acidic protein protein in MS lesions, with the hypothesis that this protein is biochemically altered in secondary progressive MS.
31. Satoh JI, Yamamura T, Arima K. The 14-3-3 protein ε isoform expressed in reactive astrocytes in demyelinating lesions of multiple sclerosis binds to vimentin and glial fibrillary acidic protein in cultured human astrocytes. Am J Pathol 2004; 165:577-592. This paper adds new support to the possible role of the 14-3-3 protein in the organization of the astrocyte intermediate filament network.
32. Barkhof F. The clinico-pathological paradox in multiple sclerosis revisited. Curr Opin Neurol 2002; 15:239-245.
33. Bö L, Geurts JJ, Ravid R, Barkhof F. Magnetic resonance imaging as a tool to examine the neuropathology of multiple sclerosis. Neuropathol Appl Neurobiol 2004; 30:106-117.
34. 't Hart BA, Vogels J, Bauer J, et al. Non-invasive measurement of brain damage in a primate model of multiple sclerosis. Trends Mol Med 2004; 10:85-91. A concise review of the model of experimental autoimmune encephalomyelitis in non-human primates.
35. Schmierer K, Scaravilli F, Barker GJ, et al. Stereotactic co-registration of magnetic resonance imaging and histopathology in post-mortem multiple sclerosis brain. Neuropathol Appl Neurobiol 2003; 29:596-601.
36. Schmierer K, Scaravilli F, Altmann DR, et al. Magnetization transfer ratio and myelin in postmortem multiple sclerosis brain. Ann Neurol 2004; 56:407-415. The authors demonstrate a clear correlation between pathological features of the MS lesion such as myelin and axon content with MTR and T1 contrast. They do not find a magnetic resonance correlate of gliosis.
37. Barkhof F, Brück W, De Groot CJ, et al. Remyelinated lesions in multiple sclerosis: magnetic resonance image appearance. Arch Neurol 2003; 60:1073-1081.
38. Pirko I, Johnson A, Gamez J, et al. Disappearing "T1 black holes" in an animal model of multiple sclerosis. Front Biosci 2004; 9:1222-1227.
39. Pirko I, Gamez J, Johnson AJ, et al. Dynamics of MRI lesion development In an animal model of viral-induced acute progressive CNS demyelination. Neuroimage 2004; 21:576-582.
40. Pirko I, Johnson A, Ciric B, et al. In vivo magnetic resonance imaging of immune cells in the central nervous system with superparamagnetic antibodies. FASEB J 2004; 18:179-182. A provocative paper showing in vivo imaging of immune cells in an animal model of MS.