Aging in bacteria

 The evolutionary Demography research group at Freie Universitat Berlin studied the differences in the aging process in different samples of E. coli across more than 100 generations, with genetically identical bacteria and identical environment. They discovered a difference in the aging process of these bacteria and found that the aging process from mother to daughter cell. The study found a specific pole at the end of the rod shaped bacteria that got darker as the bacteria aged, meaning that the organism produced less proteins over time, but this behavior did not necessarily take place in the daughter cells, or the cells surrounding it in the same environment, meaning that these E. coli groups have different individualistic aging processes.

An article for the American Society for Microbiology pivots this topic in a different direction, showing that E. coli age in a different way by losing symmetry during multiple instances of binary fission. Showing that parent cells have a tendency to perform the essential reproductive functions over many different generations in comparison to the daughter cells. Eventually, leading for different kinds of mutations that make them die off, but also increasing population fitness.

I think that understanding the process of aging in bacteria is tremendously important when we attempt to understand the way that microbial communities and bacterial communities exist and distribute themselves throughout different periods of time. Do communities that exist in semiaquatic systems age and disappear because of the way they function? Just some thoughts that come into my head. I don’t know if understanding bacterial aging is as helpful to understanding human aging since they are functionally different, understanding stress factors and the way that both kinds of organisms are affected by it is a different kind of question. Overall nice findings and it is very interesting to know that there are scientists studying and reproducing these groundbreaking experiments with simple set ups but objective observations.

https://asm.org/articles/2024/september/do-bacteria-age

https://phys.org/news/2024-11-unexpected-differences-genetically-identical-bacteria.html

The Key to Immortality...Jellyfish!!!

    Turritopsis dohrnii, also known as The Immortal Jellyfish, is exactly the magical creature it sounds like. This little jelly is often found in temperate and tropical water such as the Mediterranean Sea. Like many other animals it has developed specialized survival techniques, in this case, immortality. When threatened, The Immortal Jellyfish is capable of reverting into its polyp form (literally reversing its age/physical development).  To be clear, there are other jellyfish with similar abilities. Multiple jellyfish species are capable of "rewinding" themselves. The Immortal Jellyfish, however, is the only one capable of doing so repeatedly and after entering the medusae phase of development.

    In Comparative Genomics of Mortal and Immortal Cnidarians Unveils Novel Keys Behind Rejuvenation, a research team attempts to uncover what specific genes give The Immortal Jellyfish its rejuvenation ability. This was done by comparing the Immortal Jellyfish's genome to Turritopsis rubra, its non-immortal cousin. Overall, their finding suggest that gene amplification, replication efficiency, DNA repair, and telomere activity are primary differences and potential contributors to increasing rejuvenation abilities. With further study, this research has the potential change the way we think of human aging. Maybe one day in the future the information we learn from The Immortal Jellyfish can be used to extend human life!

The Length of Genes Are Related to Aging

 As people age it was shown that their longer genes are no longer expressed. This research looked at worms, mice, humans, and in particular humans with neurodegenerative diseases. Most research prior has tried to find specific genes or patterns that cause aging, however it was truly about the lengths of the genes. The longer genes are more chance of being damaged. The study focused on aging and neurodegenerative diseases because neural cells are known to be long and slow at dividing. Many of the genes that are associated with diseases like Alzheimers are very long so they are more susceptible of being damaged which could cause these neurodegenerative diseases. Future studies still need to be done in order to find the cause of this phenomenon.  

In my opinion, I think this is a great find in research and I believe with further studies this could help a lot of people with neurodegenerative diseases. Neurodegenerative diseases affect many people as they age and there is still not much known about why and I believe this step of figuring out that aging is related to the length of genes rather than specific genes is a start.

Article Link: https://www.sciencedaily.com/releases/2024/03/240321155352.htm

Additional Link: https://www.news-medical.net/news/20240322/Aging-linked-to-length-of-genes-study-suggests.aspx

Is the Absence of the Y Chromosome Accelerating Cancer Progression in Males?

A new study from Cedars-Sinai Medical Center is showing the loss of the Y chromosome assists cancer cells in avoiding detection by the body's immune system. Aging men can lose the Y chromosome during cell division. In some older men, more than 4 out of 5 white blood cells lack a Y chromosome. Loss of the Y chromosome is shown to be heavily associated with several diseases and cancers in aging men. 

The Ceders-Sinai Medical Center concluded that tumors that lack the Y chromosome grow at a much faster rate and are more aggressive, but are also more vulnerable to immune checkpoint inhibitors. This knowledge could provide an explanation as to certain cancers are worse in men than women. It can also help physicians with treatment pathways and help with the research for alternative tumor treatment.  

For example, T-cell exhaustion is a condition in which T cells lose their ability to kill certain cells, weakening the immune system's fight against cancers and other diseases. If we understood the genetic connection between losing the Y chromosome and T-cell exhaustion, we could potentially find a way to prevent it from occurring altogether. 

Studies found that chemical compound promotes healthy aging

    

    A recently discovered chemical compound helped elderly mice with obesity lose fat and weight, add muscle and strength, reduce age-related inflammation and increase physical activity.

    BAM15, a mitochondrial uncoupler, helps to prevent obesity, or age-related muscle loss accompanied by an increase in fat tissue. As people change, muscle mass becomes more of a concern. They become less active, which increases the chances of falls, strokes, heart disease, poor quality of life, and premature death. It is not so much of a concern in young kids because they are still active when they are young, which helps to maintain the muscle mass.

    In this study, mice were tested with the BAM15 supplement, and they were found to have a decrease in weight, yet still an increase in muscle mass and strength. BAM15 works by making the mitochondria less efficient, resulting the mitochondria to burn more energy. This can be useful in helping the aging age better and healthier, for long-lasting lives. 

Related Article

Role of 'Junk DNA' In Aging and Cancer

Researchers at Washington State University have recently identified a region of DNA known as VNTR2-1 that controls the activity of the telomerase gene. The telomerase gene controls the activity of an enzyme that is responsible for producing telomeres. In normal cells, the length of the telomeres get shorter after each division leading to aging and cell death. In certain cell types, such as reproductive cells and cancer cells, the telomerase gene ensures that the length of the telomere is not shortened. Jiyue Zhu and his team's latest finding of the VNTR2-1 region is notable because it is found in the region of DNA considered as 'junk DNA'. This DNA is usually considered as DNA with little purpose. Their findings support that this region is responsible for aging and cancer. The researchers deleted the DNA sequence in cancer cells causing the telomeres to shorten which led the cells to age and die. These findings show that the reason why we get cancer is more complicated than a mutation of an oncogene. The region of the DNA we used to believed served no purpose is a lot more complicated than we used to think.

Live long and prosper: Study examines genetic gems in Galápagos giant tortoise genomes

Giant tortoises found in the Galápagos have been often known to live over a 100 years. These particular tortoise have evolved to now have extra copies of the genes that fight against the issues associated with aging like cancer. A series of experiments determined that these turtles have cells which are overly sensitive and are able to go through apoptosis (self-destruct) as soon as they are exposed to stresses related to damaged protein. This mechanism allows for destruction of glitchy cells before they turn into tumors which is a way these animals avoid cancer. 

These results were very interesting as it would be expected that animals that are bigger and tend to live longer would have higher cancer rates. Some scientists believe that studying the way some species have evolved to gain traits like this, can be translated to help in human health and disease. This also shows the importance of conserving biodiversity to study species like these turtles to learn how their special mechanisms can help us deal with our health challenges. 

Genomic Analysis of Rockfish Species Gives Insight into the Biology of Longevity

Even within closely related species, fish can have a wide variety in lifespan. One such example is the rockfishes, a genus (Sebastes) that is found along Northern-Pacific coasts. The species, Sebastes minor, has a lifespan of around 11 years while the rockfish species, Sebastes aleutianus, can live more than 200 years. An article explains how a group of researchers examined the genomes of 88 species of rockfishes to see how some species in the genus can live to such long lifespans. They found that the group of rockfishes that can live for over a 105 years have 16 genes that are involved in the enrichment of DNA replication, repair, and maintenance with 5 of those genes exhibited selective signatures in more than one species of rockfish. These genes include WRAP53 and DCLRE1B which are involved in telomere maintenance, and FEN1 which is involved in base excision repair. These group of fish also have more copies of genes that are involved in dialing back the immune system suggesting they are more protected against the effects of 'inflammaging,' an increase in inflammation throughout the body that occurs in most vertebrates including humans.

New Study Shows That Embryos "Reset" Their Age After Taking to The Uterus

Fertilized Human Zygote

When an egg is released into the ovary, it becomes susceptible to fertilization via sperm. When this happens, the egg and sperm become a zygote, which then becomes the developing fetus. 

A new study has shown that, once an egg is fertilized and becomes a zygote, attaching itself to the uterus, all genetic signs of aging appear to "reset". In this study, mice were used. After the egg was fertilized and attached to the uterus, around 4.5-10.5 days after fertilization, biological and genetic signs of aging seemed to pause, and even reverse, for a few days. This data has been consistent with mice and humans.

This "reverse aging" of zygote development could vastly help advance the study and cure of age-related diseases such as cancer, Type 2 Diabetes, Parkinson's Disease, Dementia, and so many others. With enough time, the process of this "reverse aging" could even be used to artificially stop aging in humans later in life.

The mechanism of this reverse aging is still unknown, which opens doors to so many possibilities for further research in the future.

old dogs and aging

 

Dogs go through stages of life just as humans do. In this article, Scientists have come across similarities between the two species. They are useful in studying human aging because dogs are similar to humans in many important ways, such as how they act at a young and old age, and what happens within their DNA as they get older. A study in Vienna was done with border collies and they show the dogs took part in a touchscreen experiment at the University of Veterinary Medicine, which found that older dogs benefit from mind games and other brain exercises. Lab tests can tell how old a human is by the pattern of methylation, the same for dogs. The dog aging project is collecting genetic and other information from a vast number of pet dogs. They suffer a lot of similar ailments such as obesity, arthritis, hypothyroidism, and diabetes. 

https://www.nytimes.com/2020/11/09/science/dogs-aging-behavior.html?searchResultPosition=1

https://www.nih.gov/news-events/news-releases/nih-researchers-reframe-dog-human-aging-comparisons

How the African Turquoise Killifish Can Pause Aging

 

    The African turquoise killifish is able to put its life on hold during embryonic development. This stage, called diapause, suspends all of the fish's activity, and puts the fish into a dormant state. The embryos put their cell growth and development on hold for up to two years, which is a long time compared to the normal killifish adult life span of four months. In a recent study, geneticists compared killifish embryos that had went through diapause with embryos who did not. They analyzed the genetic blueprint of the embryos and found that genes for cell proliferation and organ development were turned off during diapause, as well as other genes being turned on even more for the purpose of turning other genes on and off. A gene that especially stood out was the chromobox 7 gene, or CBX7 gene. They found that CBX7 repressed genes responsible for metabolism, but also turned on genes responsible for maintaining muscle and staying in the diapause state. The coordination of these genes is very complex, but extremely useful for the killifish who lives in such an arid climate. In my opinion, the discovery of the killifish genes that allow the fish to go into diapause and live in a dormant state could change the way humans look at aging. Understanding the genes that allow the fish to do this could help geneticists prolong the lifespan of humans, but could also possibly give insight into treatment for ageing-related diseases. I think that scientists should definitely expand on the African turquoise killifish's genome and genes involved in diapause, and see what else we can do with these genes to benefit humanity.

https://www.sciencenews.org/article/how-african-turquoise-killifish-press-pause-button-aging

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5946070/

Does a Flies' Y Chromosome Contribute to a Shorter Life Span?

 

    In a study recently done by Doris Bachtrog, it was confirmed that the male Y chromosome in flies contributes to a shorter life span. She and her team compared the amount of heterochromatin in young and old male and female flies, and discovered that in males, the amount of heterochromatin (densely packed DNA), was far less than it was in females. The amount of heterochromatin was especially lower in the male's Y chromosome. To further test their hypothesis, they looked at the amount of heterochromatin in XXY females, XYY males, and XO males. They discovered that in the females with a Y chromosome and the males with an extra Y chromosome, the amount of heterochromatin was less, and consequently, life span was reduced. To further confirm the hypothesis that heterochromatin loss shortens life span, the XO males in the experiment lived longer than XY males. After reading this article, it makes sense that a loss of heterochromatin would contribute to aging and early death because a change or loss of heterochromatin is ultimately damaging DNA. A question I would ask would be, does this also take place in humans? Does the loss of heterochromatin, especially in the Y chromosome, shorten the lifespan of human males, like it does in male Drosophila? Women do tend to live longer than men... is this because of the men's Y chromosome? Overall, I thought the article was very informative and I especially appreciated how Bachtrog and her team did multiple studies to test their hypothesis, especially on flies with abnormal numbers of Y chromosomes. 

https://www.the-scientist.com/the-literature/male-flies-y-chromosome-may-contribute-to-earlier-deaths-67683

https://www.nature.com/articles/s12276-020-00497-4

https://www.sciencedirect.com/topics/neuroscience/heterochromatin

Brain Activity’s effects on Human Longevity

https://www.medicalnewstoday.com/articles/326745.php#1

Related Article:
https://www.sciencedaily.com/releases/2019/10/191016131224.htm


Researchers from the Blavatnik Institute at Harvard Medical School discovered how the brain’s neural activity plays a role in human aging and life span. There have been previous studies that had suggested that parts of the nervous system influence aging in animals, but there was not much evidence to show how neural activity affected the lifespan of humans. New findings reveal that neural excitation influences longevity down the insulin and insulin-like growth factor (IGF) signaling pathway. Insulin and IGF are known for molecular influencers of longevity. So, scientists, found that REST, a transcription factor (proteins that control gene expression), suppresses genes that have a role in neural excitation in animals ranging from worms to mammals.

The researchers ran tests in which they blocked REST (or an equivalent transcription factor) in various animal models. The results showed high neural activity and a shortened life span of the animals. In contrast, boosting levels of REST showed lower neural activity and longer life spans. Also, postmortem human brain tissue cell research also showed that individuals whose life span reached 100 years had significantly higher levels of REST in their nuclei relative to those whose life span was 20-30 years shorter.

I thought that this article was really cool because it made me think about how I am going to live my life: do I want to think more or less? Also, it makes me think of what researchers will now do with this knowledge. Will they try to slow down human aging with the REST protein? If the discovery of slowing down aging is a thing while I’m still alive, I would not participate in it.

Drosophila Research Working to Combat Aging

As if Drosophila have not contributed enough to the field of genetics, they are once again being used as a model organism for genetic research. In a recent study, these flies are being analyzed for transcriptome changes that are associated with increased longevity and lower odds of premature aging. As organisms age, their organs begin to malfunction and they are susceptible to conditions such as Sarcopenia, which a condition where skeletal muscle begins to lose its mass and function. This is commonly seen in humans, other mammals, and even flies. The research with Drosophila has revealed that this deteriorating muscle undergoes many changes in gene expression during the aging process. To test their hypothesis, researchers over-expressed a gene in Drosophila that coded for a resistance against glutathione, an antioxidant that causes the muscular deterioration associated with aging. The researchers found that this indeed led to an increased lifespan.

The fact that Drosophila are still being used as model organisms over 100 years after heir first use really amazes me. This research is amazingly useful as well. In the short term, being able to expand the lifespan of fruit flies and other experimental organisms would allow for maximum data collection in terms of scientific experiments. However, the findings of this experiment may also open the door for the next billion dollar industry if this anti-aging process is made possible in humans. The promise of being younger for longer is something that many people would pay absurd amounts to achieve, and whoever is the first to make this possible will have quite the retirement fund.

Life Expectancy Runs In Families, But Not By Genes

Calico Life Sciences is a development company that continues to research to learn much more about the biology of aging as their goal.  For this particular research, they used an open pedigree data from Ancestry.com, the website for Ancestry, the online genealogy resource.  Ancestry has the largest data set that they can use for their studies of longevity.  It is used to measure life span heritability.  Heritability gives us a quantitative value of a trait variation, such as life span, that are due to differences in genes.

It was thought that the estimated life span heritability was between 15 to 30 percent.  The Calico research team studied life span similarities from numerous pedigrees that involved a total of over 400 million people, connected by a parent-child or spouse-spouse relationship.  Initially, siblings and first cousins had heritability estimates no different from what was previously predicted.  However, spouses’ life spans were even more strongly correlated, likely not due to genetic factors but more so having a shared environment.  Even more unexpected was that remote relationship types, as far as a spouse’s sibling’s spouse, still had a similar life span, without being blood relatives or a shared environment.  What the researchers concluded was that assortative mating took place, meaning people tend to select partners with traits like their own.  For instance, wealthy people tend to marry other wealthy people, or tall people choose tall spouses.  This leads to the belief that life span is mainly controlled by genetics, when in actuality, life span heritability was calculated to not even surpass seven percent.

I previously hoped that scientists can discover so much more about the biology of aging through studying genetics.  But if genetics barely has anything to influence an individual’s life span, then alternative directions and paths need to be taken in order to find out the true answers on aging.

For additional information, refer to the original article.

For additional information, click the link of the journal of heritability estimates of human longevity.

Chromosomes Activate Genes Differently as we Age

        Researchers from UConn Health and the Jackson Laboratory for Genomic Medicine have recently discovered that human chromosomes age with us. When we are young, chromosomes are loosely coiled, allowing for thousands of sites to be open and ready to activate genes and make proteins. As we age, some sections of the chromosome curl and become more tightly coiled, making it more difficult for DNA that defends our body against disease to be accessed. 

The genomic study utilized blood samples from 75 healthy, young people (ages 22-40), and 26 samples from healthy seniors (age 65 and up). The researchers isolated immune cells from each blood sample, and looked at how the immune cells’ gene activation changed with aging. The scientists found that regions of chromosome that code for genes that develop and differentiate T-cells, which help defend against the flu, viral infections, and some cancers, are more likely to be open in young people than in seniors. They also discovered that the elderly are more likely to have open regions of chromosome that code for genes associated with cell death and inflammation. Previous studies have shown that chromosomes shrink with age, and that gene expression is affected (The Scientist). However, the discovery of differently coiled chromosomes between young people and seniors had never been seen before in genomic analysis, and is now helping researchers conduct studies in overall disease resilience in older people. I find this topic very interesting because it may lead to medical breakthroughs in the care of the elderly. It is amazing to think that by learning about how the chromosomes age we can possibly make seniors more resilient to certain diseases.

Article: Elderly chromosomes activate genes differently than in the young

The Scientist Article: Aging Shrinks Chromosomes

Stem Cells in the Hypothalamus Can Control Aging

In a recent study, researchers at Albert Einstein College of Medicine, found that as soon as the mice reached 10 month, there was a decline of stem cells in the hypothalamus. The scientists noticed that when they disrupted the stem cells, they had also accelerated the aging of mice because of their premature death as opposed to the mice that aged naturally. Scientists wanted to find out if by increasing the number of stem cells, whether it would reverse the effects of aging in mice. MicroRNAs (miRNAs) are molecules that are release by the stem cells when they begin to act on slowing the aging process. Dongsheng Cai, M.D., PhD.,  a professor of molecular pharmacology at Einstein College of Medicine, withdrew exosomes that contain miRNA from the hypothalamus and injected them into two groups of middle-aged mice. One group had their stem cells plummet and the other were considered "normal." The aging process for both sets of groups had decelerated was noticed through behavioral testing. This study could be an advancement in treating diseases that are age- associated (i.e. Alzheimer's Disease). 

The Genetics of Muscle Growth

An article detailing research from the Institute for Aging Research (IFAR) at Hebrew SeniorLife (HSL) provides us with a better understanding about the genetics behind muscle growth. They focused on the genetics of "lean body mass" which is made up of mostly muscle (which is what gives one that massive but chiseled look that body builders have). Unfortunately, heredity plays a big part in growing muscle. This is why one person can work out for years and not achieve the results that another person (who has better genetics) can accomplish within a month of working out. A related article called The Truth About Body Building Genetics delves more into the specific genes that allow for some to gain muscle more easily than others. This research may help us better understand the process of aging and a condition called sarcopenia which results in decreased muscle mass at older age. Isolating the genes responsible for building lean muscle mass may help those affected with this condition so its possible to develop a treatment plan - or even help out the local scrawny gym rat who's frustrated at not being able to make gains like the big guys.

Brain-aging gene discovered

A new discovery has been found in adults around age 65 that greatly affects their aging of their brain. Columbia University Medical Center found that the gene TMEM106B has different variants that causes this abnormal aging in older adults. After studying data from various autopsied brain samples, researchers came up with a measure called differential aging. Differential aging is the difference between an individuals apparent age (biological) and their true age (chronological). This gene TMEM106B begins to take effect once people reach the age of 65 but researchers found a second variant inside the proganulin gene that affects brain aging as well. These two genes are found on separate chromosomes but are in the same signaling pathway.

It seems like if you have these genetic variants then brain aging is accelerated and causes you to be more vulnerable to brain diseases like Alzheimer's. These discoveries could help researchers to look into potential new targets for preventing and treating certain brain aging diseases.

Link to article

More Info

Reversing the Aging Process?!

 In more recent times, researchers have began reseting the clock in mice.

http://www.domyownpestcontrol.com/images/content/mouse.jpg

 This deals with erasing the epigenomic marks by activating genes responsible for the health of embryonic cells. Scientists have rejuvenated the organs of mice and discovered that they can lengthen their lifespan by 30%! This technique cannot be applied to humans but scientists are well on their way to gaining a better understanding of muscle and organ regeneration. I believe this is an incredible finding! Whether we are either slowing down or reversing aging we are moving forward scientifically and I find that amazing. This is all stemming from work completed ten years ago and I cannot wait to see how this has advanced in ten years to come.

https://www.nytimes.com/2016/12/15/science/scientists-say-they-can-reset-clock-of-aging-for-mice-at-least.htmlrref=collection%2Ftimestopic%2FGenetic%20Engineering&action=click&contentCollection=science&region=stream&module=stream_unit&version=latest&contentPlacement=4&pgtype=collection 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/