18. Disease Progression Modeling and Subtyping, Part 1
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MIT 6.S897 Machine Learning for Healthcare, Spring 2019
Instructor: David Sontag
View the complete course: https://ocw.mit.edu/6-S897S19
YouTube Playlist: https://www.youtube.com/playlist?list=PLUl4u3cNGP60B0PQXVQyGNdCyCTDU1Q5j
Prof. Sontag discusses aspects of disease progression modeling, including staging, subtyping, and multi-task and unsupervised learning. The goals are to determine the patient’s place in the disease trajectory and how treatment may affect progression.
License: Creative Commons BY-NC-SA
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This video aims to educate undergraduate university students with at least one year of science background about how to disease progression and development is measured for ALS (Amyotrophic Lateral Sclerosis, also known as Lou Gehrig’s disease or motor neuron disease). Despite recent advances in research, there is currently no cure for ALS and much is still unknown about the disease. The number of individuals who die from ALS has increased to three per day in Canada. This video discusses ALS research relating to the measurement of disease progression.
Video by students from McMaster University’s Demystifying Medicine Seminar Series
Subscribe to the McMaster Demystifying Medicine YouTube channel: https://www.youtube.com/c/DemystifyingMedicine
This video is provided for general and educational information only. Please consult your health care provider for Information about your health.
Copyright McMaster University 2018
#DemystifyingMedicine #ALS
References
Armon, C., Graves, M.C., Moses, D., Forte, D.K. Sepulveda, L. Darby, S. & Smith, R. A. (2000). Linear estimates of disease progression predict survival in patients with amyotrophic lateral sclerosis. Muscle & Nerve, 23, 874-882.
Armon, C. & Brandstater, M.E. (1999). Motor unit number estimate-based rates of progression of ALS predict patient survival. Muscle & Nerve, 22, 1571-1575.
Czaplinski, A., Yen, A.A. & Appel, S.H. (2006). Forced vital capacity (FVC) as an indicator of survival and disease progression in an ALS clinic population. Journal of Neurology, Neurosurgery, and Psychiatry, 77, 390-392.
DeJesus-Hernandez, M., Mackenzie, I.R., Boeve, B.F., Boxer, A.L., Baker, M., Rutherford, N.J., […] & Rademakers, R. (2011). Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-Linked FTD and ALS. Neuron, 72, 245-256.
Freischmidt, A., Wieland, T., Richter, B., Ruf, W., Schaeffer, V., Muller, K., […] & Weishaupt, J.H. (2015). Haploinsufficiency of TBK1 causes familial ALS and front-temporal dementia. Nature Neuroscience, 18, 631-636.
Simon, N.G., Turner, M. R., Vucic, S., Al-Chalabi, A., Shefner, J., Lomen-Hoerth, C. & Kiernan, M.C. (2014). Quantifying disease progression amyotrophic lateral sclerosis. Annals of Neurology, 76, 643-657.
Wong, P.C., Pardo, C.A., Borchelt, D.R., Lee, M.K., Copeland, N.G., Jenkins, J.A., […] & Price, D.L. (1995). An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria. Neuron, 14, 1105-1116.
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