BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: aging

The Fountain of Youth for Muscles: Targeting 15-PGDH to Halt Age-Related Weakness

Eventually, everybody ages. While some good things come with age, aspects of aging, such as muscle weakness, can now potentially be stopped. For a long time, scientists have wondered why muscles start to weaken as humans age, but now, due to a recent ScienceNews article, we may be able to answer and solve muscle weakness!

Muscle Tissue: Cross Section Whole Skeletal Muscle

In the article, scientists discovered that inhibition of an an enzyme called 15-hydroxyprostaglandin dehydrogenase, or 15-PGDH for short, can help with strength and more muscle mass in older humans. 15-PGDH breaks down a signaling compound called prostaglandin E2, which activates the production of muscle cells that regenerate damaged muscles. Though it may seem confusing why 15-PGDH breaks down prostaglandin, the enzyme is a tumor suppressor. The enzyme inhibits proliferation so that cancer and other cells can be differentiated. In younger muscle tissue, 15-PGDH was found at reduced and relatively little abundance, but in older muscle fibers, it was found in great abundance, which caused relatively minor muscle repair. In the study, 15-PGDH was inhibited by gene knockout. However, studies show that the enzyme has potential effectors that cause an induced closure of the enzyme’s active site, which inhibits 15-PGDH. This would be an allosteric interaction in which the effector works by binding to the enzyme and changing the shape of the active site so that it can no longer work.

Silence of the Genes

Eventually, everybody ages, so this discovery is important to me. Being able to have optimal strength and energy while being old may be possible, according to the findings made by scientists. Hopefully, by the time I age, these findings can help allow older humans to continue to have peak performance. If you guys have any other studies relating to human muscle deterioration, I would love it if you shared them in the comments!

 

Does Lifestyle and Diet Affect Immune System Aging?

Have you ever heard of the thymus? If not, most people could probably say the same, despite the enormous role it plays in our overall health. The thymus is a small gland in the upper part of the chest that is crucial to the immune systems of children. After puberty, the gland was previously thought to become smaller, gradually turn to fat through a process called fatty regeneration, and lose its function. Through the use of CT scans, a recent study shows that contrary to prior belief, this organ can be significant in adults as well, and the state of it can be influenced by lifestyle, age, and sex.

Diagram showing the position of the thymus gland CRUK 362

The main function of the thymus is to develop all the body’s immune cells before puberty. In order to carry out this function, the gland produces the hormone thymosin. Cells called lymphocytes pass through the thymus where they are fully developed into T cells, with the help of the hormone. Once they are fully developed, they are transferred to the lymph nodes where they help the body fight off infections and prevent autoimmune diseases. Autoimmune diseases occur when an immune system attacks cells from its own body. Have you ever touched your neck when sick and felt a small swollen part? Those are your lymph nodes! When you have an upper respiratory infection, more T cells rush to your lymph nodes to help your body fight off the illness. This is just one example of your immune system in action.

When you think of proteins, what is the first thing you think of? As presented in the AP Biology curriculum, proteins are not just a food group we eat everyday, though they are still very important to ingest! They are part of every cell in our bodies and therefore are crucial to the immune system and the thymus. Immune cells have receptor proteins attached to them that bind to foreign and potentially harmful substances, also called antigens. When the proteins bind to the substance, they trigger the body’s immune system to fight off the antigen. There are two types of immune systems: the innate immune system and the adaptive immune system. The innate immune system fights antigens mostly using killer cells and phagocytes (“eater cells”). The adaptive immune system makes antibodies that are made to fight off specific germs that the cell recognizes.

A new study performed in Sweden looked at the CT scans of 1000 people between the ages of 50-64, and examined the state of their thymuses. The people previously participated in the SCAPIS study which inspected their lifestyles and dietary habits. Results found that 6 out of 10 of the participants had a thymus that was completely turned to fat. It was more common in men and obese people. Dietary habits such as low fiber intake caused more fatty regeneration. People whose thymuses endured more fatty regeneration showed evidence of lower T cell regeneration. Ultimately, the CT scans showed the functionality of the thymus and the immune system. More studies must be performed to fully know whether or not the aging of the immune system affects our health, which is why this research will be expanded to the other 4000 participants of the SCAPIS study.

While people cannot change their sex and age, they can change their lifestyles. This study presents new information that can be used to help people improve their health. For example, I get the common cold once every few months and sometimes the grueling symptoms last for weeks. In the future, I will try to increase my fiber intake over a long period of time, which could possibly lower my chances of getting sick, feeling the harsh symptoms, or having them for a long time. I invite any and all comments to tell me whether or not this information could influence your lifestyle, and how.

The Network to Longer Life

 

A recent collaborative study between scientists at the Buck Institute for Research on Aging, the MDI Biological Laboratory, and the Nanjing University in China found an interesting synergetic pathway between the IIS (insulin signaling pathway) and TOR pathway by studying C.elegans: nematodes that share many genes with human beings.

The short lifespan of C.elegans (three to four weeks) allowed the scientists to identify the cellular pathways that regulated aging. The scientists were able to genetically change the IIS and TOR pathways by using a double mutant on the C.elegans. The alterations were expected to yield a 130% increase in the lifespan of the C.elegans, since altering the IIS pathway yields a 100% increase and altering the TOR pathway yields a 30% increase. However, the math didn’t work out, and that’s a good thing! Surprisingly, the lifespan of the C.elegans increased by 500%.

So, even though the scientists discovered the pathways that regulated aging in C.elegans, the nuances of these interactions are still unclear. A paper discussing this topic relates longevity to the mitochondria’s role in maintaining homeostasis.  Jarod A. Rollins, one of the authors of the paper, hopes to further clarify and investigate the role of mitochondria on aging in his future research.

Even still, the discover of these cellular pathways could lead to longer lives for humans. Pathways such as these were passed down to humans by evolution (conserved) so, the 500% increase in longevity that occurred in C.elegans after alteration could also occur in humans. Although the way in which these pathways affect each other is unclear, we now know that multiple genes and cellular pathways contribute to the aging process.

How do you think that the IIS and TOR pathways affect each other? If our lifespans are expanded in the future, what will be the moral and societal implications?

 

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.

Discovery in Worms Could Save Human Lives in the Future

A germline is the ancestry of one generation of cells to the next ones. But, scientists for a long time did not know how this has not been destroyed. Over time cell’s proteins become deformed and clump together, and this damage gets passed down to the next generation. So, in theory the germline should have already been destroyed, but it is still producing new and healthy life to this day. The question is: how?

Scientists have recently found the answer to this through studying a tiny worm called Caenorhabditis elegans. Similar to humans, these worms rely on certain genes to control their cellular division. In fact, they have a gene called daf-2 which has the ability to more than double their lifespan. After seeing this gene, scientists have realized that there are genes that are involved in repairing cells so that they do not become deformed or clumped.

Photo Source

Caenorhabditis elegans are hermaphrodites where once eggs are mature they travel to the sperm. But, the eggs have a lot of damaged proteins, only not the ones near the sperm. This led scientists to hypothesize that the sperm send out a signal to tell the egg to get rid of its damaged proteins. This signal triggers the lysosomes in the egg cells to become acidic and break down the clumps.

Even though this discovery was found on worms it could have seriously beneficial implications for humans. Stem cells also use lysosomes to get rid of damaged proteins. So this discovery could lead into learning how to treat diseases, such as Alzheimer’s Disease, to clean their aging tissue. A discovery found by studying tiny worms could lead to the answer to how to cure diseases that come with old age.

Is There a Limit to How Old Humans Will Get?

In the 1900s, the life expectancy for humans in the United States was approximately 50 years. Since then, the age to which humans can live has only grown. In 1997, a woman by the name of Jeanne Calment died at the age of 122- an astounding increase from the life expectancy less than a hundred years ago. A new study written about in the New York Times explains that Dr. Vijg, an expert on aging at the Albert Einstein College of Medicine, feels that we have now reached our “ceiling. From now on, this is it: Humans will never get older than 115.” Dr. Vijg and his graduate students published their pessimistic study in the journal Nature, presenting the evidence for their claim.

For their study, Dr. Vijg and his colleagues looked at how many people of varying ages were alive in a given year. Then they compared the figures from year to year, in order to calculate how fast the population grew at each age. For a while, it looked as though the fastest-growing group was constantly becoming older; “By the 1990s, the fastest growing group of Frenchwomen was the 102-year-olds. If that trend had continued, the fastest-growing group today might well be the 110-year-olds.” (NY Times Article). Instead, the increases slowed and eventually stopped, leading Dr. Vijg and his colleagues to conclude that humans have finally hit an upper limit to their longevity. Further research into the International Database of Longevity seemed to validate their findings; No one, except in rare cases like Ms. Calment, had lived beyond the age of 115. It appears as though human beings have hit the ceiling of longevity.

There was a varied mix of responses to the study. Some, like Leonard P. Guarente, a biology professor at MIT, praised it, saying “it confirms an intuition he has developed over decades of research on aging.” Others, like James W. Vaupel, the director of the Max-Planck Odense Center on the Biodemography of Aging, called the new study a travesty and said, “It is disheartening how many times the same mistake can be made in science and published in respectable journals.”

This study is by no means conclusive. It is simply one more piece of research in the ongoing debate over whether human beings will continue to live longer, and will continue to be debated by many experts in the field.

However, one must wonder whether living longer should be the goal. After all, as Dr. Vijg pointed out, “aging is the accumulation of damage to DNA and other molecules. Our bodies can slow the process by repairing some of this damage. But in the end, it’s too much to fix. At some point, everything goes wrong, and you collapse.” While morbid, he makes a valid observation: Humans can only go so long until necessary bodily functions begin to break down. Rather than worrying about whether we will live to an extraordinary age such as Ms. Calment, I concur with Dr. Vijg; the focus should be on living the most amount of healthy years and taking care of our bodies. While it may seem like a great idea to live to the age of 125, what good would that do if you aren’t able to continue with the activities you enjoy because your body is breaking down?

 

Other Relevant Articles:

In Depth Explanation of Longevity: https://en.wikipedia.org/wiki/Longevity

A brief summary of Dr. Vijg’s findings (a bit shorter than the NY Times article): http://www.newser.com/story/232121/human-lifespan-has-likely-maxed-out.html

An interesting article about an entrepreneur’s quest to make people live even longer: https://www.theguardian.com/science/2015/jan/11/-sp-live-forever-extend-life-calico-google-longevity

 

Brand New INSANE Trick To Maintain HUGE TELOMERES!!!

Do YOU want to learn the secret to having BIG, LONG telomeres?

OF COURSE YOU DO!

Do you know what Telomeres are?

Umm….

you might not know what they are, but I’m pretty sure you’re gonna want long ones,

and a few scientists lead by Eli Puterman, an assistant professor of kinesiology at the University of British Columbia in Vancouver, just made a huge breakthrough regarding telomeres.

let me explain.

New research done on Data collected in University of Michigan’s Health and Retirement study and reported on by TheScientist, has found that A.) accumulation of stressful events over the course of a lifetime are associated strongly with shorter telomeres later in life and B.) stressful experiences during childhood have a far greater effect on the shortening of Telomeres in adults than those that occur later in life.

First of all back up. What are Telomeres? And when it comes to Telomeres, does length really matter?

I’ll tell you.

(spoiler alert: length always matters)

Telomeres are caps that go on the end of our DNA. You can think of them like aglets on the end of shoelaces. Telomeres work to protect DNA from becoming damaged, and with that preventing the functionality of DNA from becoming compromised. They’re exactly like that little plastic bit on your shoelaces prevents your lace from becoming frayed, and ruining your shoelace, and your day, and your life.

10085714333_5d4f4d06b2

(the pinks parts are the telomeres)

And a moment of thanks, to the great man who invented aglets.

Harvey Kennnedy,

Thank you.

Back to your telomeres. As we know cells are constantly copying themselves, creating new cells, and every time this happens the telomeres on the end of our DNA become shorter and shorter, before eventually they fail to adequately protect the DNA, causing our cells to lose functionality, and on a larger scale, causing you to age faster. Essentially throughout our lives our telomeres get shorter and shorter, like a candle thats burning lower and lower, it’s a marker for our aging process. A constant reminder of our mortality as humans. A literal ticking clock. We’re all gonna die. Life is meaningless.

You know what’s not meaningless though… BIOLOGY! So while we can never escape the grim reality that our lives are nothing more than the blink of an eye on a fleck of dust that’s drifting through an empty abyss of nothingness, why not try to extend that blink of an eye for as long as we can, so that we can read about research findings in the world of biology! speaking of which…

In the study, a group of 4,598 Americans that had an average age of 69 were asked to identify stressful incidents that occurred in both their youth and later adulthood. They then had their telomere lengths measured from cells from saliva samples. In the study, Part of the study’s findings were that “Each additional adverse event during childhood was associated with an 11 percent-increased odd of shorter telomeres”. These results are staggering to be sure, but are not totally out of the blue. One Judith Carroll who researches the links between behavior and health at UCLA said after the study had been completed “The findings are consistent with other reports suggesting that early life is a particularly vulnerable time when the body is rapidly growing and adapting to its surroundings”.

These results were very strong, however some have taken issue with extrapolating stressful incidents to higher mortality. While it is acknowledged that the shortening of telomeres is associated with aging, some wished the study had gone a step further, and examined whether these shorter telomeres really do result in earlier death. As it is said by Iris Hovatta, a scientist at the University of Helsinki (in Finland)(a country I have never been to, so I can’t confirm whether or not it actually exists)(which is neither here nor there)(whether or not ‘there’ really does exist) “this study did not address the effect of stress on health or lifespan and whether individuals with shorter telomeres have an increased mortality” It’s a fair criticism, but as far as we know now, shortening of telomeres causes aging, and this study puts forth strong evidence of an association between stressful events over the course of a lifetime, especially during youth, and shortening of telomeres.

So what does this mean?

if you don’t want to age, avoid stressful events during your youth.

avoid stuff like forgetting when your blog post was due, then staying up until 3 in the morning to finish it.

Then again biology its pretty much all I have to live for.

give and take I guess, we all have to find a balance that works.

 

Does the aging process influence changes on a cellular level or do changes on a cellular level influence the aging process?

wrinkles

How do humans age? While we are “programmed to die,” there doesn’t seem to be one thing that causes our death by “old age.” For example, one way we carry out our own deaths is found on the cellular level, where we accumulate mutations in the DNA repair process and the cells themselves die, or the enter senescence (non-replicating state) as they age. These processes occur at several different times, overlapping and alternating. Therefore, what appears to be the best time to intervene in order to promote healthy aging? No one knows, but they do know what DNA becomes extremely damaged as time goes on and has an incredible impact on our aging process. The cells have sooner suicide dates where they undergo apoptosis more rapidly than normal, and the loss of too many cells can cause tissue atrophy and dysfunction. In addition to creating a lack of cells, the damaged DNA can even shift epigenetic markers.

Typically, epigenetic marks shift in tumor cells, which can lead to cancerous cells. However, in the early 1990s at Johns Hopkins University, Jean-Pierre Issa was studying changes in DNA methylation in colon cancer cells when he observed shifts in epigenetic markers over time, but not only in tumor cells; he found that (to a lesser degree) these shifts were occurring in healthy cells as well. After mapping DNA methylation in human cells, we know that some areas of the genome become hypermethylated with age while others exhibit reduced methylation. These changes typically occur through DNA replication or DNA damage repair because the histone modifications are not always perfectly reproduced and in order to repair damaged DNA, repair proteins must remove the epigenetic marks to access the damaged genetic material to repair it, and once completed, the epigenetic marks can be omitted or misplaced. These epigenetic alterations have been linked to a reduced regenerative capacity of stem cells with age, and bring up a valuable question:

“Is this an epiphenomenon that happens just because we age, or is it actually causing symptoms or diseases of aging and limiting life span?”

Article source: http://www.the-scientist.com/?articles.view/articleNo/42280/title/How-We-Age/

Sit less, Live longer

Many jobs involve sitting all day

Many jobs involve sitting all day

People tend to spend most of their days sitting. Despite maybe an hour or two spent at the gym, people are sedentary for a majority of their day.  Two studies were performed, one showing that sitting less can slow cells from aging. The other found that standing up, even if your not moving, can be beneficial.

Past studies show that sitting for hours makes a person more likely to develop diabetes, have heart disease, and even die prematurely.

Scientists in Sweden wanted to find out why sitting and illness were linked so they created an experiment altering the time people were sitting or exercising and tracked their physiological results. They focused on the people’s telomere changes. They then compared these telomere lengths to the length of obese, sedentary men and women telomeres. These volunteers then were instructed to exercise and sit less. After six months, the researchers found that their telomeres had lengthened; this means that the cells were getting physiologically younger.

In conclusion, the telomeres shortened much more in response to reduction of sedentary time than to exercising. This means that just be sitting less, one can avoid aging, and other illnesses. Another experiment preformed by Dr. Katzmarzyk found that standing, not even moving, dropped mortality rates. This suggests that standing is not inactive or dangerous, but rather beneficial.

I found this article very interesting to me because I am very active in sports, but I also am sitting a lot in school. I want to know whether the amount of sitting I am doing is greater than my exercise, causing me to age more in the long run. I think it is more important that we are active in school, despite the fact that most of us do after school sports.

image source:

http://en.wikipedia.org/wiki/Occupational_stress  

article source:

http://well.blogs.nytimes.com/2014/09/17/sit-less-live-longer/

other sources:

http://www4.utsouthwestern.edu/cellbio/shay-wright/intro/facts/sw_facts.html

http://www.ncbi.nlm.nih.gov/pubmed/24152707

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.

Aging, a side effect of preventing Cancer?

Nobody wants cancer and about 50 years ago scientists found the body’s natural defense against cancerous cells which was either to kill the cells or to turn them into senescent cells. But in a recent study by The Mayo Clinic researchers they found that if you destroy these senescent cells then the health of the mice improves as the mice get older such as longer lasting fat deposits which would cause wrinkles if they had gone and prolonged development of cataracts. The original mice they had tested had shorter life spans than normal mice so they have started to test normal life span mice to try and replicate the results. The only problem is that the method used to destroy the cells in the mice is not applicable to humans because it requires altering the cells so that any cell which turns into a senescent cell destroys itself. The scientists have gotten around this by saying that people could develop drugs to block anything produced from the senescent cells so that they won’t actually affect the rest of the body. The have already been approached by people who are interested in these results and who want to start development on these drugs. The scientists say this does not actually extend life but it does extend the healthy part of life.

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