AP Biology class blog for discussing current research in Biology

Author: cellanie

Will Scientists Crack the Impossible Code of Human Anti-Aging?

Have you ever wondered why humans age? Why we can’t stay alive forever? Or is it even possible to? According to a recent article from Scientific American, scientists are actively researching what lifestyle choices and diets can lead to a longer life.

Firstly, before we dive into that, let me explain why the article says we age and what causes cells to lose their ability to regenerate. The article says that cells are constantly being damaged in our body, from UV rays to poor nutrition, which causes them to regenerate to become healthy again. Regenerating cells divide into new healthy ones by making copies of their chromosomes, which contain DNA. But this is where the aging process begins. Each time a cell divides, the end or caps of the chromosome, called telomeres, shrink, and when they become too short, the cells cannot divide further. This cell state is called senescence. This state of the cell is dangerous, so we secrete chemicals to activate our immune system and eliminate them, but when our body does not destroy them, they cause neighboring cells to go into this state as well. If the senescence cells keep spreading to their neighbors, the body and brain work slower, causing our body to deteriorate, become susceptible to disease, and die.


This is where the scientists come in! According to the article, experts often believe in the popular disposable soma theory. This theory indicates that our bodies have limited lifetime energy and that humans use a good amount of it to do reproductive functions. So, if you choose not to reproduce, you could live a longer life. Is that not a hard choice? Children or a longer life? I know I wish there could be a happy medium! But, according to experts, if people try to reach a compromise, they risk mutations and major issues in decedents. Therefore, it is hard to combat the aging of humans from this perspective, not only for ethical reasons but also on the subject of time. In an article by Antonello Lorenzini, he states that time and environmental pressures cause constraints for us to repair damaged cells and reproduce in the limited window we have. Therefore, we as humans must maximize the time and energy we have as it is imperative for our aging process not to slow down at an earlier stage of our lives.

Since this approach did not work, researchers in the article looked at the perspective of targeting short telomeres and preventing cells from entering senescence. Yet, there is a problem in both of these ideas as well. People with long telomeres have more telomerase, which is the enzyme that keeps telomeres long; the problem with this is that cancer cells can use this telomerase to multiply unchecked. As well as this, people with longer telomeres tend to have a more likely chance of getting cancer and brain tumors as well. Is a longer life worth a higher chance of getting cancer? Personally, I do not think so. So researchers also tried to prevent cells from going into a senescent state, but they had a similar problem. The cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells.


Next, researchers looked at ideas for extending our lifespan through caloric restriction. A study from Nature displayed that people who ate 15% fewer calories had less body aging. This is also shown in the research from AARP, which said researchers at the National Institutes of Health found that adults who had 12% less caloric intake over two years opened biological pathways associated with healthy aging. But, back to the original article from Scientific American, it says this must be done carefully. Caloric restriction may extend life span but also may cause side effects, such as decreasing gray matter in the brain. So, as researchers try to find a solution that does not cause any harm to us as a species beyond a balanced diet and exercise, aging will not stop anytime soon. (Very sad, I know.)

Diet-ge013ccb43 1920

Lastly, I want to connect this to something we learned in AP Biology this year. In this unit, we discuss cell division and the cell cycle. This relates to the topic of anti-aging/aging because of the cell reproduction rate and the ability of the cell to replicate. As said above, as the cells are damaged, they must replicate. This process starts with interphase, where the cell will go through the G1, S, and G2 phases or the growing and replicating phases. The cell has normal functions, copies DNA, and doubles its organelles in preparation for mitosis. Next, it will move into mitosis, where it will divide the nucleus through kinetochore and nonkinetochore, and finally go into the stage of cytokinesis, where the cytoplasm is split. This can further relate to the topic through the telomeres and the telomerase. As said above, people with more telomerase can have a higher chance of getting cancer because the cancer can multiply unchecked. They can multiply unchecked because most cancer cells use telomerase to divide indefinitely, as it will continue to replicate and not die, which causes tumors to form. So, suppose our normal cells start to use telomerase. In that case, our cells will act similarly in replication to cancer, and our bodies will not be able to tell the difference.

Most cells only divide when given a chemical signal, but cancer cells do not obey this. They will divide even though they did not receive a chemical signal. In AP Bio, we learned that cancer cells also do not have the signal to stop replicating, which is where the telomerase comes in. Since cancer cells do not receive the signal to stop copying and they have long and reconstructing telomerase that allows them to do this, they will never die.

As well as this, we can link the idea from the senescent state – the cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells – to this as well. If genes are damaged when they are targeting aging cells, this can cause oncogenes to form. Oncogenes will cause the cells to divide when no signal is sent. This would lead to tumors because of the rapid cell replication. Similarly, suppose a mutation damages the tumor suppressor in the cell. In that case, there will be nothing stopping the oncogenes from replicating, allowing them to do what cancer does and replicate non-stop. Therefore, the process of anti-aging and cancer remarkably coincide as the very thing that we want to use for anti-aging is something that causes cancer to be able to divide indefinitely. That is pretty amazing and crazy to me! How can something in our bodies allow that to happen? What do you think?

Subvariant EG.5 is on the rise and dominating the U.S!

Since COVID’s peak in 2020, what has been going on? Is it still on the rise? According to a recent article from LiveScience, the omicron subvariant of Eris, or EG.5.1, has been the leading cause of new COVID-19 cases in the U.S. In this research article, the data from a model of the Centers for Disease Control and Prevention (CDC) , from July 23 to August 5 of 2023, EG.5 was 17.3%  of the new cases of COVID-19, which had previously only been 11.9% two weeks prior. Personally, seeing that jump in percentage within two weeks worries me about what harm this subvariant could cause. Additionally, more recently, EG.5 had a higher percentage of infection than any other omicron subvariant in the XBB lineage!

Map of countries with confirmed SARS-CoV-2 Omicron variant cases

But the real question is, what is EG.5? How is it a subvariant, and why is it dominating the U.S.? Well, EG.5 was derived from a branch of omicron, an XBB variant. Yet, how it differs from omicron is what makes it EG.5 and what is allowing it to become so prevalent. EG.5 has a mutation in its spike protein that helps evade the body’s immune system. This spike protein called S:F456L may not only be able to escape our immune system, but the mutation in its subvariant Eris, EG.5.1, has an additional spike change, S:Q52H, that can be beneficial for the virus itself. To further the idea that the virus is harmful, the World Health Organization currently lists the variant as “under monitoring.” The article says that the genetics of the virus, EG.5, can theoretically boost its transmissibility, meaning that this virus is more easily spread than past variants. This article, to some relief, does not have enough evidence of it yet. Still, according to Johns Hopkins, the mutation is known to avoid the immunity you get after infection or vaccination. I think the idea that the virus is benefiting itself while infecting millions of people is, to say the least, cause for worry. Knowing that this immune system-bypassing virus could infect my grandparents or fellow students is unthinkable.

Spike omicron mutations top

After hearing that, I wanted to know what that means. Is there going to be another outbreak? But there is no need to worry. In this article, using the Washington Post, it is displayed that EG.5 is only different because it has more ability to enter the cells and does not seem to be more lethal than other variants. Dr.K Srinath Reddy proposed that it had the same effect on the human body. As of July 2023, a variant XBB.1.16 was still more prevalent globally than EG.5, and the subvariant only accounted for 11.6%, previously 6.2% in June 2023, of the sampled SARS-CoV-2 sequences. Even though EG.5 is only 11.6%, it is still on the rise and will still infect more people in every country, so it is essential to know your options. According to YaleMedicine, updated vaccines such as Pfizer and Moderna are not a perfect match for eradicating this subvariant and that the vaccine was aimed for a close relative called XBB.1.5. But, the CDC states that the updated vaccines, since XBB.1.5 and EG.5 are so similar, should give a reasonable degree of protection and that the genetic code among omicron subvariants allows for cross-protection.

COVID-19 Vaccine vial and syringe - US Census

Now, as an AP Bio student, this change of structure in COVID is something we have talked about a lot recently. We discussed how the SARS-CoV0-2 virus comprises five main parts: spike proteins, membrane proteins, viral genome, nucleocapsid protein, and envelope protein. To explain these briefly, the spike proteins, membrane proteins, and envelope proteins are on the virus’s surface. The nucleocapsid protein protects the RNA, the viral genome. For this particular variant, I want to speak about the spike proteins and how, in AP Biology, we learned that these spike proteins recognize membrane-bound proteins of human cells and bind to them. Since this is an omicron variant, it follows a Receptor-Mediated Endocytosis pathway, a form in which receptor proteins on the surface capture and encapsulate specific molecules. This makes it more infectious. Once the omicron virus senses the membrane-bound protein of ACE2, it can enter the cell. This works because the omicron variant uses the ACE2 protein to become an endosome, enter the cell by endocytosis, and then break through Receptor-Mediated Endocytosis.

Contrary to the more extended version for SARS-CoV-2, how a transmembrane protease serine 2 cuts the spike protein in a specific location to which the protein will then undergo changes to insert itself into the cell membrane, the omicron version skips these steps to be able to go straight into the cell. The ability to skip these steps also connects to my article because it says the EG.5 subvariant can enter cells even more quickly. At this faster rate, this process can be hazardous and can spread much more quickly, causing more death and destruction. Therefore, learning this in AP Biology and how this process works allowed me to realize how bad this variant can be if the cross-protection is insufficient! But, please, if you are an AP Bio student like me, let me know what you think. Do you think this is more dangerous than portrayed? What do you think we should be doing!?

Unlocking Our Ancient Past: Exploring the Genetic Legacy of Extinct Cousins DNA

Have you ever wondered where we came from? Who we were? What genes truly lie within us, our mothers, fathers? According to a recent research article from ScienceDaily, Neanderthal genetics is one of them, and the genes still affect human life today. In this research article, the researchers from multi-institution teams, including Cornell University, have shown that Neanderthal genes comprise about 1 to 4% of the genome of present-day humans, mostly of those whose ancestors migrated out of Africa. These genomes are not surprising to the scientific community, but their effect on today’s society in human bodies is remarkable. Through a new plethora of computational genetic tools, researchers found the genetic effects of interbreeding between humans of non-African ancestry and Neanderthals that took place 50,000 years ago, as well as the effects on present-day human life. 

Close up of a Neanderthal in a museum

 In a study published in eLife, researchers reported that some Neanderthal genes are essential for specific traits in modern humans. Using an extensive dataset from the UK Biobank consisting of hereditary and trait information of nearly 300,000 Brits, the researchers examined more than 235,000 genetic variants likely to have originated from Neanderthals. They found that 4,303 of those differences in DNA play a vital role in modern humans and influence 47 distinct genetic traits. These genetic traits can include how fast someone can burn calories or a person’s natural immune resistance to certain diseases. Isn’t that unbelievable? How did something from so many years ago affect such a critical part of our lives? Even though they lived thousands of years ago, we all have a part of the Neanderthals in our genetics.

In another article by U.S.News, the idea of immune resistance through our body’s fight against COVID-19 is displayed. The results show that some people who have increased genes from their Neanderthal ancestors may have an increased likelihood of suffering severe forms of COVID-19. These genes, haplotype, increase the risks of hospitalization and not recovering from the virus, showing that having these traits while being able to burn calories fast may cause harm to us as well. As appealing as it might sound, I know it does to me that Neanderthal genes can help in various ways; it is also quite scary. The risk factors of diabetes, heart problems, and obesity can lead to death when mixed with the virus and the gene itself lingering within us. Since these genes are a part of our fundamental hereditary units and will continue to pass down from generation to generation, with all of these effects, this investigation commenced and evolved into an important and crucial step toward understanding where we came from and who we are. Therefore, these traits affect the lives of humans every day in COVID as well as provide multiple factors of traits that we live with every day, not even knowing where they came from.

Hospital HallwayNovel Coronavirus SARS-CoV-2

As an AP Bio student, in Unit 1, we talked about the parts of the cell along with the DNA that is within the cell. These cells are deeply related to what this topic is about, as the process in which genes work revolves around the cell that it is in. First, it starts with transcription, which is the process in which the genetic material is stored in DNA and replicated into a molecule of messenger RNA. The information goes from the DNA in the nucleus to the cytoplasm to carry out protein synthesis. In the cytoplasm, ribosomes make the proteins that create these specific effects mentioned above. Each gene carries instructions for the proteins that determine your features, such as eye color, hair color, height, and, in this case, immune resistance. These two must connect with each other to fully understand how these genes are still here thousands of years later. The answer is that the genetic material has been carried down for this time through each and every ancestor we have had. It’s pretty scary, if you ask me.

Diagram of a gene on a chromosome CRUK 020

I am not the only one who believes that these causes of our ancestral genes are threatening. If you are like me and want to continue learning about this, reach out! As well as anyone with first-hand knowledge of the research or possible medical intervention, please comment! Share your knowledge with me. The custom software discussed in the ScienceDaily link from UCLA is available for free download and use by anyone interested in further research. So, if you are an AP Bio student like I am or just interested in the genes defining us, even though they are from thousands of years ago, join the conversation. These traits and genes are just being figured out, as most of the work started in September 2023. No matter what fears you may have, to leave you with a sense of comfort after a long list of possible effects, modern human genes are prevailing over successive generations. Therefore, this research, although evolving with us, must continue.

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