AP Biology class blog for discussing current research in Biology

Tag: anti-aging

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.)

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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?

Of Mice and Menin; New Research Provides Answers to Aging

A Decline in Hypothalamic Menin Drives the Aging Process, and Dietary Supplement can Reverse it in Mice

A new study published by Lige Leng of Xiamen University, Xiamen, China, and colleagues on March 16th, 2023 reveals a possible link between the decline in hypothalamic Menin and aging. These findings revealed a previously unknown driver of physiological aging, and now suggest that the addition of a simple amino acid may reduce age-related changes.

“We speculate that the decline of Menin expression in the hypothalamus with age may be one of the driving factors of aging, and Menin may be the key protein connecting the genetic, inflammatory, and metabolic factors of aging” – Leng

The hypothalamus is known to be a key mediator in physiological aging. Over time its tissue becomes inflamed, thereby causing an increase in neuroinflammatory signaling. The inflammation then spreads to the brain and the periphery of the nervous system, promoting aging-related degenerative diseases. Leng’s research showed that Menin, a hypothalamic protein, is an inhibitor of hypothalamic neuroinflammation, therefore inferring a negative correlation between the quantity of Menin and aging processes. 

Mice in the laboratory

Leng observed that Menin in the hypothalamus declines with age. Leng and his colleagues devised an experiment using conditional knockout mice, in which Menin activity could be inhibited. They recorded that Menin-deprived younger mice had an increase in hypothalamic neuroinflammation, aging-related phenotypes including reductions in bone mass and skin thickness, cognitive decline, and modestly reduced lifespan. To fully understand the effects Menin has on aging, Leng “flipped” the experiment and delivered the gene for Menin to elderly mice. Thirty days later, they found improved skin thickness and bone mass, along with better learning, cognition, and balance.


3D rendering of Menin

Connection to AP Bio

Menin is a scaffold protein. One of its many functions is to upregulate the expression of cyclin-dependent kinase (CDK) inhibitors, thereby reducing beta-cell proliferation. This inhibition causes the cells to stop developing after G1. This then halts the entire process of cell division, as the cell cannot replicate its DNA and go through mitosis. 

“I Wanna Live Forever Young”

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.

Mitochondrion (standalone version)-en


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.





Meeting Your Great Great Great… Grandchildren

The MDI Biological Lab along with the Buck Institute of Research on Aging have discovered cell pathways that could increase the human lifespan by 400-500%. “The increase in lifespan would be the equivalent of a human living for 400 or 500 years.” The implications this would have are immense along with some potential drawbacks, but let’s get into the science first.

The research was conducted on C. elegans, a nematode, because “it shares many of its genes with humans and because its short lifespan of only three to four weeks.” The short lifespan allows scientists to quickly see the effects of their efforts to extend the healthy lifespan. The keyword here is “healthy” because prolonging life means nothing unless you can extend the quality as well. The scientists used a double mutant in the insulin signaling and TOR pathways. The alteration in the insulin pathway yields a 100% increase in lifespan and the TOR pathway yields a 30% increase. The incredible discovery though was that when combined the new lifespan was amplified by 500%!! The expected yield was 130%.

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Here depicted is a diagram showing the meaning of a double mutant.

Researchers still say “the discovery in C. elegans of cellular pathways that govern aging, it hasn’t been clear how these pathways interact.” This discovery does lead to the mindset that the important methods of anti-aging are in the interactions between cellular pathways rather than singular pathways. This newly found interaction could also explain why scientists have had trouble discovering “the gene” the governs aging. The combinations of these treatments are described as being similar to the “way that combination therapies are used to treat cancer and HIV.”

It’s odd to picture a world where this treatment could be considered “cosmetic” in a way. Eventually, the human lifespan could expand to hundreds of years with some even living to 1000. The implications that this could have are a current problem we have of overpopulation. It is farfetched, but this would help immensely with the mission to expand into space. The ability to survive with hundreds of years on a potential “colony ship” allows humans to expand to other planets where we would be able to expand greatly. I’ll end with a question: If this treatment was 100% safe and affordable, would you get it? Why or why not?

Ending the Age of Aging Skin

“Your epidermis is showing,” my older sister once mischievously teased. What I at first thought was an inappropriate reference turned out to be an anatomical term for skin. This external tissue takes on a lot, from ultraviolet radiation to harmful chemicals and gases. With age, the damage is visible, as my sister had once indirectly implied, but a new study suggests this physical deterioration is fixable.

Nadine Pernodet, a scientist at the Materials Science and Engineering department at Stony Brook University, looked into how skin function changes due to epigenetic changes. She confirmed that skin cells follow a circadian rhythm (they change based on a daily schedule). For example, skin is relatively dry during the day, acting as a barrier to the elements, while it works to repair itself overnight and is more hydrated in the morning. However, when comparing the human skin cells from younger and older subjects, Pernodet found that these rhythms were only present in the young cells.

Perdenot further investigated with her team, studying other cellular processes that the circadian rhythm affects such as cellular recycling processes (found in lysosomes) and protein production. She utilized metabolomics, a method that measures the presence of metabolites (the products of metabolic processes such as carbohydrates, lipids, and amino acids) at any given time. Scientists removed skin metabolites for analysis using special tape and identified hundreds that affected skin appearance. They found that over sixty percent of metabolites cycled rhythmically for Caucasian women 25 and younger, but that less than twenty percent of those same metabolites oscillated strongly or consistently for women 60 and older.

The results showed that metabolites are more active and follow a circadian rhythm in younger skin cells, revealing how oscillation weakens and skin repair efficiency weakens with age. Though, there is much hope for potential solutions. In identifying the issue, certain skin-treatments have incorporated specific peptides which return the skin to a more youthful rhythm by restoring the once-lacked metabolites. This, in turn, can ultimately reduce visible signs of aging. Brands such as Estee Lauder are at the forefront of this terrain.

The study may also open up more research, as the metabolomic test strip can be used for other parts of the body, revealing other health conditions and issues, too. The future (and our skin 😉 ) looks bright. How do you care for your skin? Which products and habits do you use? Let me know in the comments below.


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Human Microbiome and Age: A Complex Balancing Act


Dozens of studies in the past few years have been dedicated into research on the bacterial microbiome that lives inside of every human being. The cultivation of the microorganisms that live symbiotically inside of us begins as soon as a baby comes out of the womb and is exposed to the world outside of its mother’s uterus. These bacteria are imperative to many, many bodily functions throughout our lives. The link between us and our microbiome is so crucial that a faulty microbiome can easily cause death. An example of how these bacteria are so important is the fact that many molecules we use daily are mainly created by symbiotic bacteria such as Vitamin B and Vitamin K, 75% of which is supplied symbiotically.


The Link Between our Gut and Age

There is a lot of research left for scientists to discover the effects of our microbiomes but one of the most hotly studied aspects of the bacteria that inhabit our gut is their relationship to our age. There is much research showing how our specific colony of bacteria changes over time. One study by Alex Zhavoronkov shows that the specific type of bacteria present at various stages of development stays consist across different people. So consistent in fact that he was able to have a computer teach itself how to predict the age of a subject within 4 years of accuracy based on their microbiome. He noted that of the 95 bacteria he studied, 39 were crucial in determining the age of a subject. This research seems to suggest that the bacteria in our stomach could serve as an accurate biological clock which could be used to analyze the effects of various things such as alcohol consumption, diet and disease have on a persons longevity. The main issue with his study though is that his subjects all represent a sliver of the human population and due to bacteria’s great biodiversity, predicting ages across the globe could be impossible. Yet in any case, the link between our microbiome and our age is certainly a huge possibility.

Can Bacteria Reverse Aging?

No. Bacteria cannot reverse the aging process unfortunately. We simply do not have   enough research and understanding of the link between age and the microbiome inside the human body enough to make such a grand statement. However, one study seems to suggest a chance in this strange idea. In this unorthodox study, the microbiome of young Turquoise Kill Fish was added to the microbiomes of older fish of the same species. The results are surprising. The older fish ended up living lives 37% longer than their unaffected counterparts. The reasons are unclear yet the evidence is stark. Could this mean we could put young bacteria into humans and continue to stretch our lifespans to be longer than 100 years? Again, we do not know but only the future will tell what will happen.

You Are What You Eat


Whenever a person consumes healthier meals and therefore less calories, according to a new study on mice at the NYU Langone Medical Center, they could be lengthening their lives.

Using female mice, scientists fed one group of mice a diet of pellets containing a high amount of calories, while feeding another group of mice a diet of pellets containing 30% less calories. The hippocampus and the region surrounding it in the brains of the mice were then examined for expression of aging-genes throughout various stages of maturity. The results of the study, while not entirely applicable to humans, has shown that the mice that ate the lower calorie diets had less expression of aging genes and had less risk of chronic illnesses such as hypertension and stroke.

“The study does not mean calorie restriction is the ‘fountain of youth,’ but that it does add evidence for the role of diet in delaying the effects of aging and age-related disease.” Stated Stephen D. Ginsberg, a researcher involved with the study. The study examined more than 10,000 genes related to aging, which is a much larger amount than that previously studied by researchers. While the study was performed on mice, the results could be similar in humans, and the researched performed by Dr. Ginsberg and others should serve as a warning for our ever-indulgent world of fast food and high caloric intake.


Forever Young

Photo Credit: Flickr user flatworldsedge

How would you feel if you discovered that your doctors may have found a real fountain of youth?  Well thanks to researchers at the University of Pittsburgh that could someday be a reality.

Dr. Laura Niedernhofer and her fellow researchers have discovered a way to slow down aging, for mice at least.  To conduct their experiment the researchers bred a line of mice with progeria, a disease found in chickens that rapidly increases the aging process.  Normally once a mouse contracts this disease they have only a few days left to live.  After the addition of stem cells as well as some progenitor cells (a similar type of cell) the mice survived up to 66 days.

Now don’t worry its not only some rare poultry disease that this study shows help for.  Mice with mild cases of progeria showed geriatric symptoms similar to those that older humans show, weak leg muscles, walking hunched over and trembling and saw a dramatic improvement.  In fact 75% of the symptoms the mice were experiencing were relieved with only two injections of the stem cell mix given over a period of a few weeks.  Imagine if 75% of an aging human’s symptoms could find relief!

These mice also appear to be showing evidence that the new stem cells didn’t replace their aging stem cells but rejuvenated them as they saw improvement in the brain’s of these mice although the stem cell mix was injected into each mouse’s stomach.  It’s too soon to tell if this stem cell therapy will be able to help humans, but if it did we may have found a real fountain of youth.

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