Multiple sclerosis: Difference between revisions

No edit summary
No edit summary
Line 1: Line 1:
'''Please have patience as I edit this page over the next week! Thank you!'''--[[User:Kirsten Eldredge|Kirsten Eldredge]] 04:06, 21 April 2012 (IDT)
'''Please have patience as I edit this page over the next week! Thank you!'''--[[User:Kirsten Eldredge|Kirsten Eldredge]] 04:06, 21 April 2012 (IDT)


'''Multiple sclerosis (MS)'''- an autoimmune disease that effects every patient differently based on the neurologic lesions found throughout the body. While some can go through their lives with relatively mild symptoms and short periods of relapse, others can become incapacitated within years or even months. Defined by Nylander and Hafler, MS is a "multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual."<ref name="MS Nylander & Hafler">PMID:22466660</ref> While the effects of the disease are well known, and various treatments exist for the disease, the exact identity of an antigen or infectious agent that causes the initiation of a myriad of symptoms is unknown. There are three ways in which MS is categorized: relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS). In RRMS, the patient experiences periods of time in which the symptoms considerably increase, although the neurological function of the patient usually returns to normal after the episode. Those with SPMS have symptoms like RRMS, but do not return to normal neurological function after the episode, rather they sustain the neurological damage (such as permanently losing the use of an arm). In PPMS, the patient has an initial episode that never ends. That is, once the symptoms begin, there is no relapse in the neurological degradation. Rather, a constant autoimmune attack on the patient's body causes increasingly severe symptoms, and sometimes death. Taking a biochemical look at the pathology and some of the various treatments that exist for MS helps in the understanding that MS is no longer a diagnosis which is hopeless, but is in fact full of hopeful and helpful treatments.  
'''Multiple sclerosis (MS)'''- an autoimmune disease that effects every patient differently based on the neurologic lesions found throughout the body. While some can go through their lives with relatively mild symptoms and short periods of relapse, others can become incapacitated within years or even months. Defined by Nylander and Hafler, MS is a "multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual."<ref name="MS Nylander & Hafler">PMID:22466660</ref> While the effects of the disease are well known, and various treatments exist for the disease, the exact identity of an antigen or infectious agent that causes the initiation of a myriad of symptoms is unknown. There are three ways in which MS is categorized: relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS). In RRMS, the patient experiences periods of time in which the symptoms considerably increase, although the neurological function of the patient usually returns to normal after the episode. Those with SPMS have symptoms like RRMS, but do not return to normal neurological function after the episode, rather they sustain the neurological damage (such as permanently losing the use of an arm). In PPMS, the patient has an initial episode that never ends. That is, once the symptoms begin, there is no relapse in the neurological degradation. Rather, a constant autoimmune attack on the patient's body causes increasingly severe symptoms, and sometimes death. Taking a biochemical look at the immunopathology and some of the various treatments that exist for MS helps in the understanding that MS is no longer a diagnosis which is hopeless, but is in fact full of hopeful and helpful treatments.  


<StructureSection load='1ifa' size='500' side='right' caption='Click on the green links to the left to see key structural features of Interferon Beta (PDB entry [[1ifa]])' scene='Multiple_sclerosis/Interferon_beta/1'>== Pathology==
<StructureSection load='1ifa' size='500' side='right' caption='Click on the green links to the left to see key structural features of Interferon Beta (PDB entry [[1ifa]])' scene='Multiple_sclerosis/Interferon_beta/1'>
== Immunopathology==


Many antigens have been investigated to determine whether they are the cause of T cell problems including: <scene name='Multiple_sclerosis/Mbp/1'>myelin basic protein</scene> (MBP, [[1bx2]]) with a peptide shown; <scene name='Multiple_sclerosis/Plp/1'>proteolipid protein</scene> (PLP, [[2xpg]]) with peptide shown; <scene name='Multiple_sclerosis/Mog/1'>oligodendrocyte glycoprotein</scene> (MOG, [[3csp]]); oligodendroglia-specific enzyme transaldolase, and heat shock protein alphabeta-crystallin.
Classical MS pathology has been characterized by white matter plaques which are typically located in the subcortical or periventricular white matter, optic nerve sheaths, brainstem, and spinal cord. The lesions that occur in these regions are generally identified by perivascular infiltrates that contain clonally expanded <scene name='Multiple_sclerosis/Cd8tcell/1'>CD8+ T cells</scene> (two ectodomains shown, [[3qzw]], as well as a smaller amount of <scene name='Multiple_sclerosis/Cd4tcell/1'>CD4+ T cells</scene> ([[3t0e]]), <scene name='Multiple_sclerosis/Monocyte/1'>monocytes</scene> ([[2ra4]]), and rare <scene name='Multiple_sclerosis/B_cell/1'>B cells</scene> ([[4e96]]), and <scene name='Multiple_sclerosis/Plasma_cell/1'>plasma cells</scene> ([[2wq9]]). Many antigens have been investigated to determine whether they are the cause of T cell problems including: <scene name='Multiple_sclerosis/Mbp/1'>myelin basic protein</scene> (MBP, [[1bx2]]) with a peptide shown; <scene name='Multiple_sclerosis/Plp/1'>proteolipid protein</scene> (PLP, [[2xpg]]) with peptide shown; <scene name='Multiple_sclerosis/Mog/1'>oligodendrocyte glycoprotein</scene> (MOG, [[3csp]]); oligodendroglia-specific enzyme transaldolase, and heat shock protein alphabeta-crystallin.




Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Kirsten Eldredge