2014, Number 1
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Rev Mex Cel Mad Med Biorreg 2014; 1 (1)
Comparative study about the application of stem cells derived from bone marrow and adipose tissue as an alternative for the treatment of multiple sclerosis
Rubio GG, Herrera LR, Miranda NJA, Morales HVP
Language: Spanish
References: 15
Page: 5-8
PDF size: 144.34 Kb.
ABSTRACT
Multiple sclerosis is an autoimmune disease in which the autologous T cells are activated and enter the central nervous system and attacking myelin producing a multifocal demyelinating to inflammatory and sometimes healing axonal loss and white matter. This can lead to severe disability and neurological defects. The therapies used so far as the beta interferon or glatiramer acetate are focused on reducing the harm caused by lymphoid cells themselves helping to delayed central nervous system degeneration. The stem cell therapy is a growing area of research that may contribute to additional treatment options, leading to more effective management of multiple sclerosis, unifying criteria block in the progression of the disease and promoting regeneration of damaged sites. As regeneration we understand the functional recovery of a damaged tissue. Two stem cell therapies currently used for treating multiple sclerosis are the hematopoietic stem cell transplantation and emerging therapy transplant mesenchymal stem cells. The proposed study is based on analysis of the patients before and after treatment with mesenchymal stem cells helping standardizing an effective procedure and innovative treatment for this disease.
REFERENCES
Compston A, Coles A. Multiplesclerosis. Lancet. 2002; 359: 1221-1231.
Ferguson B, Matyszak MK, Esiri MM, Perry VH. Axonal damage in acute multiplesclerosis lesions. Brain. 1997; 120: 393-399.
Bjartmar C, Kidd G, Mörk S, Rudick R, Trapp BD. Neurological disability correlates with spinal cord axonal loss and reduced N-acetyl aspartate in chronic multiple sclerosis patients. Ann Neurol. 2000; 48: 893-901.
Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mörk S, Bö L. Axonal transection in the lesions of multiple sclerosis. N Engl J Med. 1998; 338: 278-285.
Simon JH. From enhancing lesions to brain atrophy in relapsing MS. J Neuroimmunol. 1999; 98: 7-15.
Fisher E, Rudick RA, Simon JH, Cutter G, Baier M, Lee JC, Miller D et al. Eight-year follow-up study of brain atrophy in patients with MS. Neurology. 2002; 59: 1412-1420.
Evangelou N, Esiri MM, Smith S, Palace J, Matthews PM. Quantitative pathological evidence for axonal loss in normal appearing white matter in multiple sclerosis. Ann Neurol. 2000; 47: 391-395.
Sawcer S, Hellenthal G, Pirinen M, Spencer CC, Patsopoulos NA, Moutsianas L, Dilthey A et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature. 2011; 476: 214-219.
Raff MC, Whitmore AV, Finn JT. Axonal self-destruction and neurodegeneration. Science. 2002; 296: 868-871.
Chandran S, Hunt D, Joannides A, Zhao C, Compston A, Franklin RJ. Myelin repair: The role of stem and precursor cells in multiple sclerosis. Philos Trans R Soc B. 2008; 363: 171-183.
Raine CS, Cross AH. Axonal dystrophy as a consequence of long-term demyelination. Lab Invest. 1989; 60: 714-725.
Kornek B, Storch MK, Weissert R, Wallstroem E, Stefferl A, Olsson T 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.
Rodriguez, M. A function of myelin is to protect axons from subsequent injury: Implications for deficits in multiple sclerosis. Brain. 2003; 126: 751-752.
Patrikios P, Stadelmann C, Kutzelnigg A, Rauschka H, Schmidbauer M, Laursen H, Sorensen PS, Brück W, Lucchinetti C, Lassmann H. Remyelination is extensive in a subset of multiple sclerosis patients. Brain. 2006; 129: 3165-3472.
Patani R, Balaratnam M, Vora A, Reynolds R. Remyelination can be extensive in multiplesclerosis despite a long disease course. Neuropathol Appl Neurobiol. 2007; 33: 277-287.