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group_2_presentation_3_-_als [2016/03/29 13:07]
monachd 		group_2_presentation_3_-_als [2018/01/25 15:18] (current)
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   * 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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 {{:​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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