New Scientific Findings on Multiple Sclerosis Disease

Parsa, Naser; Hosseini, Zohreh .S

New Scientific Findings on Multiple Sclerosis Disease

Document Type : Promotion Article

Authors

Naser Parsa ¹
Zohreh .S Hosseini ²

¹ National Institutes of Health, Ministry of Health, USA

² Shahid Beheshti University of Medical Sciences, Iran.

Abstract

Multiple Sclerosis or Muscular Sclerosis (MS) is a chronic neurodegenerative disease that affects the central nervous system (brain, spinal cord) and optic nerve. During an MS attack, inflammation occurs in areas of the white matter of the central nervous system in random patches called plaques. This leads to destruction of fatty-protein (myelin) protecting nerve cell fibers in the brain and spinal cord. Myelin allows for the smooth, high speed transmission of electrochemical messages between the brain, spinal cord and the body. When myelin is damaged, neurological transmission of messages may be slowed, resulting in diminished function. MS is considered an autoimmune disease that most often affects young adults. The immune system attacks myelin and oligodendrocytes cells that make myelin. An increased incidence of MS has been observed over the past two decades. The most recent epidemiological features possibly associated with environmental risk factors such as a vitamin D deficit, low life-long ultraviolet radiation, viral infection, aging and the high-latitude locations. Several effective drugs and complimentary therapies have been provided for MS patients to slow down the progression of their disabling disease. Understanding the molecular mechanisms of this dreadful disease along with progression of stem cells research may bring hope for those who suffer from MS disease.

Keywords

20.1001.1.2008935.1391.02.2.3.5

References

[1].Rodriguez, M., Siva, A., Ward, J., et al. (1994).” Impairment, Disability, and Handicap in Multiple Sclerosis: A Population-based Study in Olmsted County Minnesota” . Neurology, Vol.44, PP. 28–33.
[2].Hauser, S.(1994).” Multiple Sclerosis and other Ddemyelinating Diseases In: Isselbacher K.J, Martin., J.B, Fauci A.S., et al, eds” . Harrison’s Principles of Internal Medicine, New York: McGraw-Hill, PP. 2287–2953.
[3].Oksenberg, J.R., Hauser, S.L.(2005).”Genetics of Multiple Sclerosis” .Neurology Clinic, Vol. 23, PP. 61–75.
[4].Bagert, B., Camplair, P., Bourdette, D.(2002).” Cognitive Dysfunction in Multiple Sclerosis: Natural History, Pathophysiology and Management ” . CNS Drugs, Vol.16, PP. 445–455.
[5].Weinshenker, BG., Bass, B., Rice, G.P,. et al. (1989).” The Natural History of Multiple Sclerosis: A Geographically Based Study, Clinical Course and Disability” . Brain, Vol.112, PP.133–146.
[6] Montalban, X., (2005).” Primary Progressive Multiple Sclerosis” .Current Opinion Neurology, Vol.18, PP. 261–266.
[7].Lublin, F.D., Reingold, SC.(1996).” Defining the Clinical Course of Multiple Sclerosis: Results of an International Survey” , National Multiple Sclerosis Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis. Neurology, Vol.46, PP. 907–911.
[8].Barkhof, F., Filippi, M., Miller, DH., et al.(1997). ”Comparison of MRI Criteria at First Presentation to Predict Conversion to Clinically Definite Multiple Sclerosis” . Brain, Vol.120, PP. 2059–2069.
[9]McDonald, W.I., Compston, A., Edan, G., et al.(2001).” Recommended Diagnostic Criteria for Multiple Sclerosis: Guidelines from the International Panel on the Diagnosis of Multiple Sclerosis” . Annual Neurology. Vol. 50, PP. 121–127.
[10].Poser, CM.(1987).” Diagnostic Criteria for Multiple Sclerosis: An Addendum” . Annual Neurology, Vol. 22, PP. 773.
[11].Tintore, M., Rovira, A., Martinez, M.J., et al.(2000).” Isolated Demyelinating Syndromes: Comparison of Different MR Imaging Criteria to Predict Conversion to Clinically Definite Multiple Sclerosis” . American Journal of Neuro-Radiology. Vol. 21, PP. 702–706.
[12].Bot, J.C., Barkhof, F., Lycklama, A., Nijeholt, G., et al.(2002).” Differentiation of Multiple Sclerosis from other Inflammatory Disorders and Cerebrovascular Disease: Value of Spinal MR Imaging. Radiology, Vol. 223, PP. 46–56.
[13].Pashenkov, M., Teleshova ,N., Link, H.(2003).” Inflammation in the Central Nervous System: the Role for Dendritic Cells” . Brain Pathology, Vol. 13, PP. 23–33.
[14]. Hafler, D.A., Slavik, J.M., Anderson, D.E., et al. (2005).” Multiple Sclerosis” . Immunol Review”, Vol. 204, PP. 208–231.
[15] Link,. H.(1998).” The Cytokine Storm in Multiple Sclerosis” . Multiple Sclerosis, Vol. 4, PP. 12–15.
[16] Lassmann, H.(1998).” Pathology of Multiple Sclerosis. In: Compston A, Ebers, G., Lassmann, H., et al, eds” . McAlpine’s Multiple Sclerosis. London: Churchill Livingstone, PP. 323–357.
[17] Steinman, L. (2001).” Multiple Sclerosis: A Two-Stage Disease” . Nature Immunology, Vol. 2, PP. 762– 764.
[18] Lassmann, H., Bruck, W., Lucchinett, C. (2001).”Heterogeneity of Multiple Sclerosis Pathogenesis: Implicationsfor Diagnosis and Therapy” , Trends Mol Med, Vol. 7, PP. 115–121.
[19]. Lassmann, H.(2003).” Hypoxia-like Tissue Injury as a Component of Multiple Sclerosis Lesions” . Neurol Sci. Vol. 206, PP. 187–191.
[20]Trapp, BD., Ransohoff, R., Rudick, R.(1999).” Axonal Pathology in Multiple sclerosis: Relationship to Neurologic Disability” . Curr Opin Neurol, Vol. 12, PP.295–302.
[21].Kapoor, R., Davies, M., Blaker, P.A., et al. (2003).” Blockers of Sodium and Calcium Entry Protect Axons from Nitric Oxide-Mediated Degeneration” . Annual Neurology, Vol. 53, PP. 174–180.
[22]. Werner, P., Pitt D., Raine, C.S.(2001). ” Multiple Sclerosis: Altered Glutamate Homeostasis in Lesions Correlates with Oligodendrocyte and Axonal Damage”. Annual Neurology, Vol. 50, PP. 169–180.
[23]Craner, M.J., Newcombe, J., Black, J.A., et al.(2004).” 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, Vol. 101, PP. 8168–8173.
[24].Bo. L., Vedeler, C.A., Nyland, H., et al.(2003).” Intracortical Multiple Sclerosis Lesions are not Associated with Increased Lymphocyte Infiltration” , Multiple Sclerosis, Vol. 9, PP. 323–331.
[25].Peterson ,J.W., Bo, L., Mork, S., et al.(2001).” Transected Neurites, Apoptotic Neurons, and Reduced Inflammation in Cortical Multiple Sclerosis Lesions”. Annaul Neurology, Vol. 50, PP. 389–400.
[26].Olek, M.J.(2010).”Treatment of Relapsing-RemittingMultiple Sclerosis in Adults. ( http://www. uptodate.com/home/index.html ).
[27].Cotran, R.S., Kumar, V., Collins, T. (Robbins):(1999).” Pathologic Basis of Disease” , Chapter 30, 6th edition, PP. 1326-1327.
[28]. Parsa, N., Gaidano, G., Mukherjee, A., Hauptschein, R., Lenoir, G., Dalla-Favera, R., et al.(1994).” Cytogenetic and Molecular Analysis of 6q Deletions in Burkitt’s Lymphoma Cell lines” . Genes Chromosomes Cancer, Vol. 9, No.1. PP. 13-18.
[29].Papanicolaou, G.J., Parsa, N., Meltzer, P.S., Trent, J.M.(1997).” Assignment of Interferon Gamma Receptor to Human Chromosome Bands 6q24.1- q24.2 by Fluorescence In Situ Hybridization FISH)” . Journal of Cytogenetics and Cell Genetics, Vol. 76, PP. 181-182.