Aging Reversed / ABC News

Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.

In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.

The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.

Additional information published by Harvard can be found in the following articles.

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.

Stem Cell Secret’s of 115 Year Old Woman

New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.

There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.

Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!

In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.

Blood from world’s oldest woman suggests life limit

Time Magazine: Long-Life Secrets From The 115-Year-Old Woman

Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis

The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.

New Study Reveals Unexpected Sleep Functions

For many years, the prevailing theory was that sleep helped the brain eliminate harmful molecules. However, recent preliminary research on mice suggests this might not be the case. A new study aims to delve deeper into the reasons we need sleep, potentially challenging our initial assumptions. Findings now indicate that physical activity could be more effective than sleep in aiding the brain’s detoxification process.

The scientific community has long emphasized the notion that sleep aids in clearing toxins as a primary reason for sleep, so it was quite surprising to observe contrary results. The research team mentioned that their findings, which were published in the journal Nature Neuroscience, require validation in human studies to confirm these unexpected results.

Previously, it was believed that the brain’s glymphatic system played a crucial role in waste removal during sleep. Yet, a study involving the tracking of fluid movement in mouse brains with a fluorescent dye revealed surprising results. Their findings showed a diminished capacity for toxin removal during sleep and under anesthesia. Specifically, sleeping mice were 30% less efficient at clearing the dye compared to their awake counterparts, and the clearance rate for anesthetized mice dropped by 50%.

The researchers noted that the molecule size might influence the speed at which toxins are transported through the brain, with some substances being eliminated via alternate systems. Currently, it remains unclear why states such as sleep or anesthesia slow down the brain’s molecular clearance. The next phase of their research will focus on understanding the reasons behind this phenomenon. Additionally, the team plans to investigate whether these findings are consistent in human subjects.

Disrupted sleep frequently affects those with dementia, yet it remains uncertain whether this is a result of the disease or a contributing factor to its progression. It is possible that quality sleep plays a role in reducing the risk of dementia for reasons beyond toxin clearance.

Another aspect of the study demonstrates that toxin clearance in the brain is highly efficient during wakefulness. Generally, being awake, active, and engaging in exercise may enhance the brain’s ability to rid itself of toxins more effectively.

To view the original scientific study click below:
Brain clearance is reduced during sleep and anesthesia

Aligning Eating Schedules with Your Body Clock for Longevity

A recent study on mice has revealed that circadian rhythms, which regulate daily physiological processes, are not solely governed by a central clock in the brain. Instead, they involve a more intricate system where molecular clocks in both the brain and muscle tissue work together to maintain muscle health and function. The research further indicates that adjusting these clocks through changes in meal timing could potentially preserve muscle function in the elderly.

In the study researchers employed a mouse model called Bmal1 knockout (KO), which inhibits the expression of the Bmal1 clock gene in the suprachiasmatic nucleus. This is the region in the brain responsible for regulating circadian rhythms. In this model, however, they were able to restore Bmal1 expression in various tissues, including skeletal muscle. The KO mice exhibited unusual patterns of activity and inactivity, oxygen consumption, energy expenditure, and glucose and lipid oxidation compared to wild-type mice, demonstrating disrupted circadian rhythms due to the absence of the Bmal1 gene.

By 26 weeks, the knockout (KO) mice had experienced a decrease in both weight and muscle mass compared to their condition at 10 weeks, along with evidence of mitochondrial damage in their muscles. However, when the expression of the gene was reinstated in both the muscle and brain of certain mice, their muscle mass and strength were maintained. This led researchers to conclude that interaction between the clocks in the brain and muscle is essential to stave off early muscle aging.

As individuals grow older, their sleep-wake cycles undergo changes, and they also experience a loss of muscle mass. This study proposes that these phenomena are closely linked. Typically, aging leads to an adjustment in sleep patterns, with older adults tending to wake up earlier in the morning and go to bed earlier in the evening. However, for some elderly individuals, especially those suffering from neurodegenerative diseases like Alzheimer’s, sleep patterns may become highly erratic and fragmented.

This research has discovered a potential method to restore the functioning of circadian clocks in both the brain and muscles. By adopting a time-restricted feeding regimen for older adult mice, the scientists were able to revive rhythmic gene expression in the muscle tissue, effectively preventing the decline in muscle function.

These results shed light on potential physiological shifts that occur with aging and how time-restricted eating could potentially counteract these changes. However, confirmation through human trials is necessary before drawing extensive conclusions about the effects of the circadian clock on human aging. It remains unclear whether such dietary strategies could help prevent muscle aging in people. The observation that limiting food intake to the active phase of mice partially reinstated the function of the central clock and bolstered the skeletal clock underscores the significant role that timing of eating plays in supporting circadian rhythms.

To view the original scientific study click below:
Brain-muscle communication prevents muscle aging by maintaining daily physiology

Stem Cells Enhance Memory and Combat Inflammation in Mice

Typically, when discussing potential treatments for Alzheimer’s Disease, the focus tends to be on amyloid proteins and the plaques that form in the brain. Yet, recent studies suggest that the disease is influenced by a broader range of factors, such as neuroinflammation and metabolic imbalances. In a significant breakthrough, a team from Michigan Medicine has demonstrated that transplanting human neural stem cells into a mouse model of Alzheimer’s not only enhances memory but also diminishes neuroinflammation. This research highlights a promising new direction for therapeutic approaches.

The transplantation of human neural stem cells into the brains of mice with Alzheimer’s Disease yielded positive results, even though amyloid plaque levels did not change. This supports the idea that targeting neuroinflammation could be an effective therapeutic approach, separate from strategies focusing on amyloid plaques. Furthermore, the treatment normalized inflammation in the microglia, the brain’s primary immune cells, which become hyperactive in Alzheimer’s Disease. As the disease advances, the inflammatory activity of microglia is believed to play a role in the loss of neurons.

The researchers implanted neural stem cells into the memory-related regions of genetically modified mice that carried mutations linked to familial Alzheimer’s Disease. Eight weeks after the transplantation, both the test group and the control group of mice were subjected to the Morris water maze, a test used to evaluate spatial memory and learning abilities.

Researchers discovered that mice with Alzheimer’s Disease, after receiving stem cell transplants, showed restored learning capabilities that matched those of control mice with normal memory functions. Further analysis using spatial transcriptomics, a technique for mapping gene expression across different brain regions, indicated that over 1,000 genes had their expression normalized in the memory centers of the Alzheimer’s mice post-transplantation.

When examining changes in gene expression within microglia, researchers found that genetic markers associated with Alzheimer’s Disease progression had returned to levels nearly identical to those in control mice. This indicates a decrease in neuroinflammation and a potential slowing of the disease.

The scientists emphasized that the positive results observed following the stem cell transplantation need further exploration in mouse models before progressing to studies in larger animals and, ultimately, human trials. This research is crucial and further reinforces the potential of stem cell therapies in treating neurodegenerative diseases. These preliminary studies are essential initial steps toward developing stem cell treatments.

To view the original scientific study click below:
Human neural stem cells restore spatial memory in a transgenic Alzheimer’s disease mouse model by an immunomodulating mechanism

The Role of Mitochondria Transplants in Muscle Function

Mitochondria, often described as the powerhouses of cells, are crucial for converting nutrients into adenosine triphosphate (ATP), the energy currency of cells. Their existence is fundamental to the survival of complex organisms, including humans. However, as we age, mitochondria sustain damage and become less effective.

The process of energy production inherently generates harmful byproducts known as free radicals. These free radicals can wreak havoc within cells, especially harming mitochondrial DNA. Mitochondria lack the robust DNA repair mechanisms found in the nuclear DNA of cells. Over time, mutations accumulate in mitochondrial DNA, leading to a progressive decline in their ability to function effectively and produce energy. This triggers a downward spiral, further impairing mitochondrial performance. In response, several researchers are exploring therapeutic strategies to address this issue. If these efforts prove successful, they could potentially slow or reverse cellular aging.

It is well-established that mitochondria have the ability to move among cells and be taken up by surrounding cells. This knowledge has led to the idea that transplanting healthy mitochondria into older individuals could be an effective method to rejuvenate them. This concept was put into practice in a recent study, where researchers transferred mitochondria to aged subjects. Interestingly, the mitochondria used in the study were sourced from mice that were the same age, rather than from younger mice.

The mitochondria were isolated from donor tissue and then directly administered to the mice in the test group. This was done through injections into the muscle tissue of the hind legs, which provided a straightforward method of delivery. In comparison to the control group, the mice that received mitochondrial transplants exhibited enhanced mitochondrial and muscle function, as well as increased endurance.

The study revealed notable rises in basal levels of cytochrome c oxidase and citrate synthase activities, along with ATP levels in the transplanted mice compared to those given a placebo. Additionally, there was a significant increase, approximately doubled, in the protein expression of mitochondrial indicators in both oxidative and glycolytic muscle types. These improvements in muscle functionality led to marked gains in exercise endurance for the treated mice.

A significant aspect of this study is that despite the mitochondria being sourced from mice that were the same age, there was still observable improvement. This suggests that the introduction of additional mitochondria might dilute the effects of the damaged ones already present in the recipient. Essentially, the inflow of new mitochondria could be mitigating the impact of the mutated ones. Given these findings, it seems logical to hypothesize that using mitochondria from younger donors could yield even better results. Conducting a follow up research with mitochondria obtained from younger mice would be an excellent next step to test this theory.

To view the original scientific study click below:
Mitochondrial Transplantation as a Novel Therapeutic Strategy for Mitochondrial Diseases

How Bright Light Enhances Cognitive Performance

When you find yourself more alert and focused after basking in bright daylight, science offers an explanation. Recent studies reveal that exposure to increased levels of light can directly influence activity in a vital brain region, the hypothalamus, boosting cognitive performance and promoting wakefulness.

This new study represents a substantial leap forward in understanding the biological effects of light on cognition and neurological well-being. While previous research has shown that light exposure increases alertness, this is one of the first studies to pinpoint how it influences the human brain at the neural level.

The research team selected 26 young adults to undertake cognitive tasks within an MRI scanner while experiencing different degrees of light, ranging from total darkness to exceptionally bright illumination. The auditory tasks assessed executive functions such as working memory and emotional processing. Employing a 7 Tesla functional MRI with high resolution, a method offering improved brain imaging, the researchers investigated the impact of light level alterations on activity within distinct regions of the hypothalamus during the tasks. Their discoveries unveiled a noteworthy pattern.

The researchers observed that as light levels heightened, activity in the posterior part of the hypothalamus intensified. Conversely, activity in the inferior and anterior hypothalamus decreased with greater exposure to light. In essence, various segments of this compact brain area, no larger than an almond, responded differently based on the brightness level.

Upon analyzing the participants’ scores on the executive functioning task, the researchers uncovered a distinct correlation: heightened light levels correlated with enhanced performance on cognitive tasks. Interestingly, this improvement was associated with reduced activity in the posterior hypothalamus. The researchers suggest that this indicates the activity in the posterior hypothalamus is not directly linked to light’s beneficial impact on cognitive performance. Instead, it suggests the involvement of other brain regions.

Under conditions of high light levels, specific brain cells might be enlisted to enhance performance on certain cognitive tasks. The authors underscore the need for further research to examine how light affects entire brain networks and their interaction with the cortex, the outer layer of the brain responsible for higher cognition, in order to comprehensively understand these effects.

The present discoveries offer promising prospects. By illuminating the neurological pathways connecting light exposure to cognitive function, this research unveils opportunities for the development of light therapy interventions. Such treatments could offer assistance to individuals grappling with sleep disturbances and alertness issues, while potentially enhancing mood and cognitive performance throughout the day.

To view the original scientific study click below:
Regional response to light illuminance across the human hypothalamus

Young Extracellular Vesicles’ Role in Extending Life

For centuries, the mythic qualities of young blood as a source of rejuvenation captivated human imagination. These beliefs, though rooted in delusion and cruelty, contain a kernel of scientific truth. Studies in heterochronic parabiosis, where the blood systems of young and old animals are connected, have demonstrated that this process can rejuvenate the older participant and accelerate aging in the younger. The exact mechanisms remain unclear. However, recent research has identified extracellular vesicles in the blood as key agents driving many rejuvenating effects.

Extracellular vesicles are small vesicles composed of a lipid bilayer similar to that of cell membranes. Secreted by cells, these vesicles carry diverse molecular cargoes, such as proteins and microRNAs, facilitating intercellular communication. Research has demonstrated that EVs sourced from young blood can confer benefits to older organisms, but the complexity of the molecular interactions involved means that research into the precise mechanisms is still actively underway.

Researchers concentrated on small EVs measuring 200 nanometers or less. To assess their rejuvenating effects, older male mice were given weekly injections of these small EVs sourced from either humans or young mice. The treatment began when the mice were 20 months old and continued until their death. For comparison, control groups of both young and the old mice received equivalent doses of phosphate-buffered saline. The results were notable: the treated mice experienced an increase in median lifespan of 34.4 vs 30.6 months, a significant extension considering the age at which treatment commenced. Additionally, the treatment enhanced various indicators of health span, including reduced frailty and better hair retention.

Further exploration into the treatment’s impact revealed that even a short, two-week regimen significantly reduced the presence of senescent cells and lowered levels of reactive oxygen species across various tissues, aligning them with those found in young control subjects. Similar decreases were noted in the levels of advanced glycation end products and lipofuscin, of which both are deleterious compounds linked to aging characteristics. Proteomic analysis across multiple tissues showed that the small extracellular vesicles had a broad impact, primarily addressing issues like epigenetic changes, mitochondrial dysfunction, and genomic instability, which are recognized as key aging markers. Notably, in muscle tissues and the hippocampus, the treatment effectively rejuvenated markers of mitochondrial health, such as DNA content, ATP production, and mitochondrial structure and quantity.

According to the researchers, since the biological activity of small EVs shows minimal species specificity, they experimented with injecting old mice with small EVs taken from the blood of young humans. This approach replicated many of the positive outcomes seen in earlier experiments. If benefits are reciprocal, this could potentially address the issue of sourcing sufficient quantities of EVs for human therapies.

To view the original scientific study click below:
Small extracellular vesicles from young plasma reverse age-related functional declines by improving mitochondrial energy metabolism

New Study Suggests Acetaminophen May Influence Heart Function

New research conducted on mice indicates that acetaminophen, a common pain relief medication and the active ingredient in Tylenol, may interfere with heart pathways involved in energy production, antioxidants, and protein breakdown. The study reveals that even standard adult dosages of acetaminophen, previously deemed safe, could lead to detrimental changes in heart tissue. These findings contribute to the increasing scrutiny regarding the broad spectrum of potential side effects associated with this widely used drug.

In the study with mice, researchers supplied water containing acetaminophen at a dosage corresponding to 500 mgs daily for a typical adult. Within a week, notable alterations were detected in the protein levels linked to key biochemical pathways essential for cardiac function. These pathways are involved in energy generation, antioxidant processes, and the degradation of impaired proteins.

The findings indicate that acetaminophen, even at doses generally deemed safe for humans, can interfere with multiple signaling pathways in the heart. While researchers anticipated alterations in two to three pathways, the study revealed that more than 20 different pathways were impacted. Previously, acetaminophen was considered to have a low risk of adverse side effects when used according to guidelines.

The extended use of acetaminophen at medium to high doses may cause cardiac problems due to oxidative stress or toxin buildup from the drug’s breakdown, potentially overloading the body’s detox systems. The observed alterations in the study suggest increased stress and mitochondrial dysfunction in the hearts of mice treated with acetaminophen.

This research contributes to our knowledge of acetaminophen’s effects, which are known to include risks of gastrointestinal issues, elevated blood pressure, and liver toxicity with high dosages. The study emphasizes the significance of monitoring both the dosage and duration of use, as long-term consumption at medium to high levels could present more severe risks compared to occasional or low-dose use.

To view the original scientific study click below:
Acetaminophen May Be Less Heart-safe than Previously Thought

Health Concerns Linked to Plant-Based Vegan Meats

Recent research has shown that numerous plant-based meat products, often included in vegan diets, are heavily processed and contain high levels of salt, additives, and saturated fats. According to a recent peer-reviewed study, these plant-based meat alternatives, such as vegan sausages and burgers designed to replicate the taste and texture of meat, do not offer any significant cardiometabolic health advantages over diets that incorporate animal meats. The study specifically examined the impact of these plant-based meat analogues (PBMA) on aspects of cardiometabolic health.

The study consisted of dividing 82 participants into two groups. One group replaced their usual protein sources with six commonly used plant-based meat alternatives (PBMAs), while the other group continued with animal-based protein foods. The study assessed various cardiometabolic health indicators of the participants both before and after the trial period. These indicators included cholesterol levels and the body’s capacity to manage blood pressure and blood sugar levels.

The study determined that over an 8-week period, a diet consisting of plant-based meats did not demonstrate significant cardiometabolic health benefits when compared to a mixed diet that includes both plant and animal foods. The available plant-based meat alternatives on the market today do not provide the same health benefits as a traditional plant-based diet, which typically features whole foods like whole grains, fruits, legumes, and vegetables.

Currently, the manufacture of plant-based meat alternatives (PBMAs) typically requires significant processing, and the final products often contain high levels of saturated fats, salts and additives to replicate the taste and texture and other qualities of actual meat. Despite the meticulous selection of ingredients, recipes, and improvements in processing methods aimed at achieving meat-like textures and flavors, there are still notable differences in the nutritional profiles between PBMAs and traditional animal-based meats. It was noted that the high levels of phytates can interfere with the body’s ability to absorb minerals.

Simply being plant-based does not guarantee a healthier product. Therefore, it is crucial to keep an eye on how frequently these products are consumed by the population and to track the health impacts associated with plant-based meat alternatives.

To view the original scientific study click below:
Plant-Based Meat Analogs and Their Effects on Cardiometabolic Health: An 8-Week Randomized Controlled Trial Comparing Plant-Based Meat Analogs With Their Corresponding Animal-Based Foods