Life with ALS
Due to the decrease in strength and an increase in spasticity (rigidity or stiffness) of muscles, fatigue and lack of energy is very common after the onset of Amyotrophic Lateral Sclerosis. This outcome is fairly predictable even though the progressiveness of the disease is not. If one with ALS learns how to conserve their energy, extreme exhaustion will play a lesser role in the symptoms they experience After diagnosis, patients survive between 3 to 5 years, where about 25% can live even longer than that. Soon thereafter, one with ALS will lose the ability to care for themselves and function completely, but some reassurance perhaps exists due to the fact that their mind is not effected. The illness does not strip someone of who they are, but only the actions they are capable of. Nonetheless, finding better treatments and searching for a cure are of the utmost importance to the scientific community and those who have been affected by ALS. Simply spreading knowledge of the disease is the first step along the rode to ending the continued suffering of thousands of victims.
Ongoing Research
A plethora of research is making significant progress all throughout the plane of ALS, yet any sort of cure is still unknown. Investigations into glutamate inhibition have revealed other potential obstacles for ALS treatment. The most prevalent of these obstacles is the presence of SOD1 (Cu/Zn superoxide dismutase), which even in the company of glutamate inhibitors, seems to cause a significant mitochondrial dysfunction and motor neuron degeneration. In addition, oxidative damage, protein misfolding, general mitochondrial dysfunction, and defective axonal transport are also potential causes of neuron degeneration. Studies into mitochondria functioning also have helped to describe why SOD1 mutant proteins accumulate and selectively damage motor neurons. For instance, experimentation has led to the theory that the build up of mutant SOD1 replaces the normal SOD1 in the mitochondria of healthy cells. Further studies are already underway with the hopes of further discoveries.
(Pathogenesis of Amyotrophic Lateral Sclerosis. Digital image. World Journal of Biological Chemistry. Baishideng Publishing Group Co., Limited., 26 May 2010. Web. 3 Nov. 2012. <http://www.wjgnet.com/1949-8454/full/v1/i5/WJBC-1-62-g001.htm>.)
Due to ongoing research in rats, lots of information has been recently published about the affects of a mutation in the TAR DNA binding protein 43 (TDP-43) in sporadic and inherited Amyotrophic Lateral Sclerosis. TDP-43 is a cellular protein that has been known to bind RNA and DNA, as well as regulate gene expression via transcription, regulate gene splicing, and stabilize mRNA. As seen in the picture below, part a shows how the protein resides in the nucleus although having the ability to move out to the cytoplasm. In part b, it shows that the protein has been kicked out of the nucleus completely and starts to accumulate in the cytoplasm. This is the result of pathophysiological issues. Researchers, when experimenting with rats, have seen that when they express mutant TDP-43 in just their motor neurons alone, it causes a significant loss of spinal motor neurons. Conversely, rats expressing the disease gene in various neurons and muscle cells don’t lose as many spinal motor neurons, but still are subject to serious atrophy (wasting away) in muscles. Through resolving at this data, a new problem arose in the research community. Interestingly enough, they found that when transgene expression is turned off, the rats with small amounts of motor neuron loss were able to substantially recover much of the motor function. On the other hand, rats with a significant amount of motor neuron loss were not readily able to recovery much motor function, yet they did moderately. Not only did they find that the TDP-43 mutation is indicative of ALS progression, degeneration can also be partially reversed, but only as seen in the rat species thus far.
Genetic Mutation via TDP-43
(Chen-Plotkin, Alice S., Virginia M. Lee, and John Q. Trojanowski. TAR DNA-binding Protein 43. Digital image. Nature Reviews Neurology. Nature Publishing Group, Apr. 2010. Web. 6 Dec. 2012. <http://www.nature.com/nrneurol/journal/v6/n4/fig_tab/nrneurol.2010.18_F1.html>.)
Relating back to the possible treatments, it has been shown that a 100 mg daily dose of riluzole has increased survival of ALS patients for about 2 to 3 months.
Riluzole Structural Formula
(RxList. Rilutek Structural Formula. Digital image. Rilutek (Riluzole) Drug Information. RxList – The Internet Drug Index, 04 Aug. 2009. Web. 6 Dec. 2012. <http://www.rxlist.com/rilutek-drug.htm>.)
Amyotrophic Lateral Sclerosis (ALS) 
I know it’s a small issue, but the “affected” in the first paragraph should be “effected”.
Also, it feels a little incongruent that everywhere else it’s referred to as ALS and you’re using the whole disease name here.
I really like this wiki and think it is informational however on this page I would recommend additional pictures to add color. I feel your color scheme and appearance are effective as they do not distract from the text but this page I felt was a little bland compared to your others. I really liked the line, “The illness does not strip someone of who they are, but only the actions they are capable of.” It provided the best understanding of the diseases profound effect on life.