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group_2_presentation_3_-_als [2016/03/29 13:00]
monachd 		group_2_presentation_3_-_als [2018/01/25 15:18] (current)
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 Jean- Marie Charcot (1825-1893) noted the first reports of the characteristics of ALS in 1874, and named the fatal syndrome based on what he found. ​ He was a noted French neurologist who explained how the central nervous system works and who has been called “the Father of Neurology”. (Rowland, 2001)  Jean- Marie Charcot (1825-1893) noted the first reports of the characteristics of ALS in 1874, and named the fatal syndrome based on what he found. ​ He was a noted French neurologist who explained how the central nervous system works and who has been called “the Father of Neurology”. (Rowland, 2001) 
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 +{{:​stephen_hawking_2.jpg|Figure 1: Famous physicist Stephen Hawking}} 
 +   ​Figure 1: Famous physicist Stephen Hawking 
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 Drs. Scarmeas, Shih, Stern, Ottoman, and Rowland recently published a scientific article, concluding that subjects with motor neuron diseases were more likely to be slim, or had once been serious athletes. Many famous people in US history have had ALS (Scarmeas, N. et al., 2002). For example: Drs. Scarmeas, Shih, Stern, Ottoman, and Rowland recently published a scientific article, concluding that subjects with motor neuron diseases were more likely to be slim, or had once been serious athletes. Many famous people in US history have had ALS (Scarmeas, N. et al., 2002). For example:
   * Lou Gehrig was a very famous Yankee baseball player ​   * Lou Gehrig was a very famous Yankee baseball player ​
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   * Stephen Hawking, the famous physicist   * Stephen Hawking, the famous physicist
   * Even some in the musical field were subjected to ALS; Dimitri Shostakovitch and Charles Mingus both vigorously practiced musical instruments   * Even some in the musical field were subjected to ALS; Dimitri Shostakovitch and Charles Mingus both vigorously practiced musical instruments
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 ====== Epidemiology ====== ====== Epidemiology ======
  
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-{{:​prevalence_of_als.gif|Figure ​1:The figure shows prevalence rates per 100,000 population for cases of amyotrophic lateral sclerosis in the United States, by age group, on the basis of data from the National ALS Registry for October 19, 2010-December 31, 2011. Prevalence rates were highest for persons aged 70-79 years and lowest for those aged 18-39 years.}}+{{:​prevalence_of_als.gif|Figure ​2:The figure shows prevalence rates per 100,000 population for cases of amyotrophic lateral sclerosis in the United States, by age group, on the basis of data from the National ALS Registry for October 19, 2010-December 31, 2011. Prevalence rates were highest for persons aged 70-79 years and lowest for those aged 18-39 years.}}
  
-   ​Figure ​1: The figure shows prevalence rates per 100,000 population for cases of amyotrophic lateral sclerosis in the United States, by age group, on the basis of data +   ​Figure ​2: The figure shows prevalence rates per 100,000 population for cases of amyotrophic lateral sclerosis in the United States, by age group, on the basis of data 
    from the National ALS Registry for October 19, 2010-December 31, 2011. Prevalence rates were highest for persons aged 70-79 years and lowest for those aged 18-39 years. Available at:     from the National ALS Registry for October 19, 2010-December 31, 2011. Prevalence rates were highest for persons aged 70-79 years and lowest for those aged 18-39 years. Available at: 
    ​http://​www.cdc.gov/​als.    ​http://​www.cdc.gov/​als.
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 {{:​als_pathophysiology.jpg|Figure 3: The pathophysiology of ALS}} {{:​als_pathophysiology.jpg|Figure 3: The pathophysiology of ALS}}
  
-   ​Figure 3: The Pathophysiology of ALS +   ​Figure 3: The Pathophysiology of ALS (Vucic et al, 2014)
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 Overall, ALS is a rapidly, progressing disease that greatly impacts the everyday functioning of the individual who has it. ALS destroys motor neurons which are an important link in the nervous system. It is through motor neurons that the brain sends messages to the voluntary muscles throughout the body which leads to the individual losing the ability to walk, talk and breath. ALS is now recognized to have multiple interacting causes, all sharing a common pathway leading to the destruction of the motor neurons. Glutamate excitotoxicity in ALS patients can be linked to mutant astrocytes that malfunction and this can be the target of potential therapies. Drug therapy has shown promising temporary effects and although more research needs to be done, there is the potential to use innovative stem cell therapeutics to introduce healthy astrocytes into neuronal regions for longer-term effects. ​ Overall, ALS is a rapidly, progressing disease that greatly impacts the everyday functioning of the individual who has it. ALS destroys motor neurons which are an important link in the nervous system. It is through motor neurons that the brain sends messages to the voluntary muscles throughout the body which leads to the individual losing the ability to walk, talk and breath. ALS is now recognized to have multiple interacting causes, all sharing a common pathway leading to the destruction of the motor neurons. Glutamate excitotoxicity in ALS patients can be linked to mutant astrocytes that malfunction and this can be the target of potential therapies. Drug therapy has shown promising temporary effects and although more research needs to be done, there is the potential to use innovative stem cell therapeutics to introduce healthy astrocytes into neuronal regions for longer-term effects. ​
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 +====== References ======
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 +Als society of canada. (2012). A Manual for People Living with ALS. (7th ed.). Retrieved 27 March, 2016, from https://​www.als.ca/​sites/​default/​files/​files/​ALS%20Manual/​2012%20Manual%20People%20Living%20With%20ALS%20-%20ENGLISH%20Final.pdf
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 +Cifra, A., Nani, F., & Nistri, A. (2011). Riluzole is a potent drug to protect neonatal rat hypoglossal motoneurons in vitro from excitotoxicity due to glutamate uptake block. European Journal of Neuroscience,​ 33, 899-913.
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 +Dall'​Igna,​ O., Bobermin, L., Souza, D., & Santos, A. (2013). Riluzole increases glutamate uptake by cultured C6 astroglial cells. International Journal of Developmental Neuroscience,​ 31, 482-486.
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 +Gijn, J. (2011). Charles Bell (1774–1842). Journal of Neurology J Neurol 258, 1189–1190.
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 +Gordon PH. Amyotrophic lateral sclerosis: pathophysiology,​ diagnosis and management. CNS Drugs. 2011;​25(1):​1-15.
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 +Guo W, Chen Y, Zhou X, et al. An ALS-associated mutation affecting TDP-43 enhances protein aggregation,​ fibril formation and neurotoxicity. Nat Struct Mol Biol. 2011;​18(7):​822-30.
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 +Foran, E., & Trotti, D. (2009). Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis. Antioxidants & Redox Signaling, 11(7)
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 +Hillel, A. D., Miller, R. M., Yorkston, K., McDonald, E., Norris, F. H., & Konikow, N. (1989). Amyotrophic lateral sclerosis severity scale. Neuroepidemiology,​ 8(3), 142-150.
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 +Kato S. Amyotrophic lateral sclerosis models and human neuropathology:​ similarities and differences. Acta Neuropathol. 2008;​115(1):​97-114.
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 +Kiernan, MC; Vucic, S; Cheah, BC; Turner, MR; Eisen, A; Hardiman, O; Burrell, JR; Zoing, MC (12 March 2011). "​Amyotrophic lateral sclerosis."​. Lancet 377 (9769): 942–55. doi:​10.1016/​s0140-
 +6736(10)61156-7. PMID 21296405.
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 +Kondo, T. et al. (2014). Focal transplantation of human iPSC-derived glial-rich neural progenitors improves lifespan of ALS mice. Stem Cell Reports, 3(2), 242-249.
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 +Mackenzie IR, Rademakers R, Neumann M. TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia. Lancet Neurol. 2010;​9(10):​995-1007.
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 +Majoor-krakauer D, Willems PJ, Hofman A. Genetic epidemiology of amyotrophic lateral sclerosis. Clin Genet. 2003;​63(2):​83-101.
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 +Mioshi, E., Hsieh, S., Caga, J., Ramsey, E., Chen, K., Lillo, P., ... & Kiernan, M. C. (2014). A novel tool to detect behavioural symptoms in ALS. Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration,​ 15(3-4), 298-304.
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 +Rowland LP (March 2001). "How amyotrophic lateral sclerosis got its name: the clinical-pathologic genius of Jean-Martin Charcot"​. Arch. Neurol. 58 (3): 512–5. doi:​10.1001/​archneur.58.3.512. PMID 11255459
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 +Saberi S, Stauffer JE, Schulte DJ, Ravits J. Neuropathology of Amyotrophic Lateral Sclerosis and Its Variants. Neurol Clin. 2015;​33(4):​855-76.
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 +Saccon RA, Bunton-stasyshyn RK, Fisher EM, Fratta P. Is SOD1 loss of function involved in amyotrophic lateral sclerosis?. Brain. 2013;136(Pt 8):2342-58.
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 +Scarmeas, N., Shih, T., Stern, Y., Ottman, R., & Rowland, L. P. (2002). Premorbid weight, body mass, and varsity athletics in ALS. Neurology, 59(5), 773-775.
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 +Turner, M. R., Parton, M. J., Shaw, C. E., Leigh, P. N., & Al-Chalabi, A. (2003). Prolonged survival in motor neuron disease: a descriptive study of the King’s database 1990–2002. Journal of Neurology, Neurosurgery & Psychiatry, 74(7), 995-997
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 +Wijesekera, L., & Leigh, P. (2009). Amyotrophic lateral sclerosis. Orphanet Journal of Rare Diseases, 4(3)
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