Aging: the inevitable… or so we thought. Don’t get too excited, aging is apart of every living organisms’ life, and it always will be. Besides growing old as a downside itself, the real worry of aging is all of the diseases that you grow prone too. But what if there was a way to change that? What if there was a way to grow old healthily? In this blog post, I am going to be explaining how cellular modifications can potentially change the future of aging forever.
In order to understand how to prevent aging, we must understand how aging occurs in the first place. One of the main causes of aging roots from the mitochondria. The mitochondria is the source of energy for the cell and is responsible for cellular respiration. It also is independent from the cell, so it has its own DNA known as mtDNA. As time goes on, exposure to toxic products within the cell begins to cause the mitochondria’s DNA (mtDNA) to mutate. The build up of this mutation in mtDNA eventually causes the cell to function improperly, causing respiratory chain disfunction and many cell degenerative diseases. Common diseases due to mtDNA mutations are Parkinson’s disease, Alzheimers, and Huntington’s disease. Mitochondrial dysfunction can also lead to the damaging of nerve function- another side effect of old age. In our AP Biology class, we learned about the significant role the mitochondria has on cell function and how it came to be apart of the cell through the Endosymbiont Theory. This theory mentions the mitochondria’s own DNA, which we are diving into today to understand the effects of genetic mutation in the mitochondria and how we might combat it.
Professor and disease research specialist Ming Guo dives into how we can achieve healthier aging by combating mtDNA mutation. The only way to do this would be to rid the cell of mutant mtDNA and restore mitochondrial function. In order to understand how to do this, Guo conducts an experiment with Professor Bruce Hay involving fruit flies. Fruit flies share 80% of their disease genetics with humans, making them a viable option to begin testing on. Guo observed that by forcing the cell into autophagy, the cell will remove damaged cell parts and therefore restore proper cell function. By starving the cell, the cell is forced to eat damaged parts of itself, including mutated mitochondrial DNA, in order to survive. The term “autophagy” can be broken in to two terms: “auto” and “phagy”. “Auto” refers to “self” and “phagy” means “eat”. In essence, autophagy means, “self eating”, as seen through the cells digestion of its own damaged parts. This gets inevitably prevents mutations of the cell that damage cognitive function and mobility that usually come with old age. In our AP Bio class, we also discussed autophagy, or the removal of waste from a cell through the use of lysosomes.
The findings of this study shed light on how to counter mtDNA mutation through triggering cellular processes, such as autophagy, at a more efficient level than the cell previously had. On average, triggering autophagy in a cell gets rid of 95% of its mutated mitochondrial DNA. Guo and Hay’s findings are only just the beginning. Now that it is understood how to prevent mitochondrial DNA mutation, scientists must discover specific drugs on how to activate the cellular processes in a way that is safe, easy to administer, and available to the public. The answer to healthy aging, and longer lasting cognitive function that goes with it, is just around the corner!
I chose this topic because aging is inevitable for everybody, therefore it is relevant to every single person. Also, being that my family has a history with age related diseases, this topic particularly interests me. Ever since I was a kid, I would hear things like “You’ll be able to live to 200 the way technology is advancing” all of the time. This discovery is a huge step on making that statement a reality. Hopefully aging will soon become a less dreadful concept and people will live to be happier and healthier.