The team used artificial intelligence techniques to analyze the pH inside cells and determine if they were cancer cells.
Summary: Mimicking a muscular stress system can provide neuroprotection against aging in both the brain and retina. The signal helps prevent the buildup of misfolded protein aggregates.
Source: St. Jude Children’s Research Hospital.
How do different parts of the body communicate? Scientists at St. Jude are studying how signals sent from skeletal muscle affect the brain.
Welcome to 2021! We left 2020 with COVID-19, yet it continues into the new year; on top of it the virus produced a much more contagious asshole!!!
The evolved strain of COVID-19, known as B.1.1.7, has shown itself in the USA as well as other countries.
Two male members of the Colorado National Guard tested positive for the new strain — referred to as B.1.1.7 or VUI-202012/01 — and neither reported international travel. At least one of the two men is in his 20s.
Continue reading “Florida Becomes 3rd U.S. State To Identify New Coronavirus Variant” »
The more diverse your microbiome, the healthier you are. While diet is often presented to be the deciding factor in your microbiome diversity, the story isn’t so simple. Studies show that nutrition can determine 5%-20% of your gut microbiome, which is enough to concern yourself with, but not enough to rely on as the sole determinant of your microbiome’s health.
Does your gut microbiome have an impact on your longevity? And if so, what can you to live longer? It’s complicated.
One wearable emerged victorious over the others in each of the three categories. I’m including the runners-up for context and to provide an alternative if you’re not convinced by my top pick.
Affiliate Disclaimer: Longevity Advice is reader-supported. When you buy something using links on our site, we may earn a few bucks.
I came to the human life extension community not as a spanner (initially), biohacker, or a young person filled with existential dread, but as a person obsessed with quantified self. As a teen, I used pencil and paper to track my sleep and my food intake. As a college student, I wore a pedometer and tracked my daily steps on a spreadsheet. In 2014, Fitbit released the Fitbit Force, and since then I’ve had some version of top wearable on my wrist, continuously tracking what I do.
Continue reading “3 Best Wearables for Life Extension in 2021” »
Stanford University neurobiologist Sergiu Pașca has been making brain organoids for about 10 years, and his team has learned that some of these tissue blobs can thrive in a dish for years. In the new study, they teamed up with neurogeneticist Daniel Geschwind and colleagues at the University of California, Los Angeles (UCLA), to analyze how the blobs changed over their life spans…
…They noticed that when an organoid reached 250 to 300 days old—roughly 9 months—its gene expression shifted to more closely resemble that of cells from human brains soon after birth. The cells’ patterns of methylation—chemical tags that can affix to DNA and influence gene activity—also corresponded to increasingly mature human brain cells as the organoids aged, the team reports today in Nature Neuroscience.
Organoids develop genetic signatures of postnatal brains, possibly broadening their use as disease models.
Sleep deprivation causes an inflammatory response that results in negative health outcomes.
Summary: Study sheds light on DNA methylation related to sleep deprivation in those with shift-work disorder.
Source: University of Helsinki
Continue reading “A Sleep Disorder Associated With Shift Work May Affect Gene Function” »
Researchers can now control the order in which CAS9 makes edits to cell DNA instead of performing all edits at once.
Researchers from the University of Illinois Chicago have discovered a new gene-editing technique that allows for the programming of sequential cuts—or edits—over time.
CRISPR is a gene-editing tool that allows scientists to change the DNA sequences in cells and sometimes add a desired sequence or genes. CRISPR uses an enzyme called Cas9 that acts like scissors to make a cut precisely at a desired location in the DNA. Once a cut is made, the ways in which cells repair the DNA break can be influenced to result in different changes or edits to the DNA sequence.
Continue reading “Researchers invent new gene-editing tool” »
Cellular senescence is a hallmark of aging, whose onset is linked to a series of both cell and non-cell autonomous processes, leading to several consequences for the organism. To date, several senescence routes have been identified, which play a fundamental role in development, tumor suppression and aging, among other processes. The positive and/or negative effects of senescent cells are directly related to the time that they remain in the organism. Short-term (acute) senescent cells are associated with positive effects; once they have executed their actions, immune cells are recruited to remove them. In contrast, long-term (chronic) senescent cells are associated with disease; they secrete pro-inflammatory and pro-tumorigenic factors in a state known as senescence-associated secretory phenotype (SASP). In recent years, cellular senescence has become the center of attention for the treatment of aging-related diseases. Current therapies are focused on elimination of senescent cell functions in three main ways: i) use of senolytics; ii) inhibition of SASP; and iii) improvement of immune system functions against senescent cells (immunosurveillance). In addition, some anti-cancer therapies are based on the induction of senescence in tumor cells. However, these senescent-like cancer cells must be subsequently cleared to avoid a chronic pro-tumorigenic state. Here is a summary of different scenarios, depending on the therapy used, with a discussion of the pros and cons of each scenario.
Keywords: cellular senescence, senolytics, senomorphics, immunosurveillance, anti-aging therapies.
Cellular senescence is a stress response mechanism induced by different types of insults such as telomere attrition, DNA damage, and oncogenic mutations, among others [1]. First described in cultured human diploid fibroblasts after successive rounds of division [2], its main hallmarks are irreversible growth arrest, alterations of cell size and morphology, increased lysosomal activity, expression of anti-proliferative proteins, resistance to apoptosis, activation of damage-sensing signaling routes. Another important characteristic is the regulated secretion of interleukins (ILs), inflammatory factors, chemokines, proteases and growth factors, termed the senescence-associated secretory phenotype (SASP) [3].
The genome editing technology CRISPR has emerged as a powerful new tool that can change the way we treat disease. The challenge when altering the genetics of our cells, however, is how to do it safely, effectively, and specifically targeted to the gene, tissue and organ that needs treatment. Scientists at Tufts University and the Broad Institute of Harvard and MIT have developed unique nanoparticles comprised of lipids—fat molecules—that can package and deliver gene editing machinery specifically to the liver. In a study published today in the Proceedings of the National Academy of Sciences, they have shown that they can use the lipid nanoparticles (LNPs) to efficiently deliver the CRISPR machinery into the liver of mice, resulting in specific genome editing and the reduction of blood cholesterol levels by as much as 57%—a reduction that can last for at least several months with just one shot.
The problem of high cholesterol plagues more than 29 million Americans, according to the Centers for Disease Control and Prevention. The condition is complex and can originate from multiple genes as well as nutritional and lifestyle choices, so it is not easy to treat. The Tufts and Broad researchers, however, have modified one gene that could provide a protective effect against elevated cholesterol if it can be shut down by gene editing.
The gene that the researchers focused on codes for the angiopoietin-like 3 enzyme (Angptl3). That enzyme tamps down the activity of other enzymes—lipases—that help break down cholesterol. If researchers can knock out the Angptl3 gene, they can let the lipases do their work and reduce levels of cholesterol in the blood. It turns out that some lucky people have a natural mutation in their Angptl3 gene, leading to consistently low levels of triglycerides and low-density lipoprotein (LDL) cholesterol, commonly called “bad” cholesterol, in their bloodstream without any known clinical downsides.
