Growing up, I followed everything my big brother did, be it climbing mango trees or attempting to play football with my other male cousins (that did not work out well for me). I really look up to him so when he introduced me to the 1990’s X-Men cartoon which you may or may not be familiar with, it held a special place in my heart forever. Looking back on those days of coming home from school to hear the epic theme song just brings back really fond memories. Have you ever thought of some of the X-Men heroes who actually started off as villains? I can think of a few:
How about Gambit, who started off as a professional thief and had the ability to mentally generate, control and manipulate pure kinetic energy at his wish. He is of course an expert at card-throwing and hand-to-hand combat. He later joined the X-Men team where he met his love, Rogue.
If you read the comics you might remember Emma Frost who changed from one of the X-Men’s most dangerous adversaries to one of its most dominant members and leaders. She was a mutant with massive telepathic ability, and also had the ability to transform into an organic diamond state which as we know, has amazing strength and toughness. This also overpowered her telepathy.
Just like these villains turned superheroes, a protein that has previously been blamed for causing cancer cells to spread around the body is now being praised for its brain repair and protection function.
According to researchers at the University of Copenhagen mutations of a protein called S100A4 has forever been deemed a protein involved in metastasis (the spread of cancer from one organ to another). Scientists found that this protein is not typically found in our brain except when there’s shock or deterioration in the brain. However, after conducting experiments on mice where this protein was deleted, they found that the brains of the mice were not as protected and had a lesser ability to resist injury.
So what happened?
The scientists discovered that the S100A2 worked by signaling pathways inside neurons in metastasis.
When the protein S100A4 was deleted in the mice, it worsened the neuron loss after the brain trauma thus causing the oxidative cell damage to become greater and down regulating the neuroprotective protein metallothionein I + II. Two neurotrophic themes were identified in S100A4 which showed that they were neuroprotective in animal replicas of brain trauma. They found that S100A4 saves neurons via the Janus kinase/ STAT pathway and predominantly the inter-leukin 10 receptor. Their data introduced S100A4 as healing target in neurodegeneration, and thus the whole S100 family is currently being researched as a possibly significant aspect in central nervous system injury.
Research is being continued in the hope that they may be able to find an even better treatment for Alzheimer’s disease among other neurodegenerative diseases. Let’s keep our fingers crossed!
University of Copenhagen. 2012. “Reconsidering cancer’s bad guy.” ScienceDaily. Accessed March 24, 2013. http://www.sciencedaily.com/releases/2012/11/121116124644.htm