Most cells in the human body each contain about six feet of DNA. Yet the nucleus, where DNA is coiled, is no larger than a single speck of dust. Despite its density, DNA is not a tangled ball of yarn. It is organized into intricate layers of loops that fold and unfold in response to cues from the cell.

Scientists know that the three-dimensional shape of DNA is important. This long helical thread is peppered with genes that are translated into proteins to drive cellular activity. And the structure of the genome —those layers of loops—determines which genes are active at any given time.

How the three-dimensional structure of the genome is maintained, however, is less clear. Structural changes and abnormalities are associated with many diseases, such as cancer and developmental disorders. Identifying what controls genome structure could yield targets for treatment.

Living to 100 may sound like a dream, but thanks to advancements in anti-aging and longevity research, it’s becoming more of a realistic goal than ever before. While genetics play a role, experts say your daily habits have a major impact on how gracefully—and healthfully—you age. From diet and movement to mindset and skincare, there are key lifestyle shifts and science-backed secrets that can help slow the aging process, boost vitality, and support a longer, more vibrant life.

Robert Love, a neuroscientist, shared three anti-aging and longevity secrets you should know about if you want to “slow down aging” and “even help reverse aging.” According to him, prioritizing sleep, avoiding ultra-processed foods, and taking healthy supplements are some of the best options. Read on to learn more.

Prioritizing sleep is one of the most powerful (and underrated) anti-aging tools you have. During deep sleep, your body goes into repair mode—producing growth hormone, regenerating cells, and fixing damage caused by stress and environmental factors. This nightly “reset” helps keep your skin, organs, and even brain functioning optimally.

Human brains make synaptic connections throughout much of childhood, and the brain’s plasticity enables humans to slowly wire them based upon experiences, contrary to how chimpanzees develop. Humans and chimpanzees share 98.8% of the same genes, but scientists have been looking for what drives the unique cognitive and social skills of humans.

A new study, which was published today in Genome Research, that examined brain samples from humans, chimpanzees, and macaques, collected from birth up to the end of their life span, has found some key differences between the expression of genes that control the development and function of synapses, which are the connections between neurons through which information flows.

Lost memories may be a thing of the past as neuroscientists conduct research on mice to test memory recall. By using optogenetics and stimulating the hippocampus, researchers were able to show that memories reside in specific brain cells, which can be activated to recall the entire memory. Our fo

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The Philadelphia (Ph) chromosome, a product of the reciprocal translocation t(9;22)(q34;q11) between chromosomes 9 and 22, encodes the BCR::ABL1 fusion oncoprotein.¹ The constitutively active BCR::ABL1 tyrosine kinase is a hallmark of chronic myeloid leukemia (CML) and drives a subset of acute lymphoblastic leukemia (ALL). The incidence of Ph positive (Ph⁺) ALL correlates with age, from only 3% in pediatric ALL to around 25% in older adults.² Direct targeting of the BCR::ABL1 kinase with tyrosine kinase inhibitors (TKI) has been a breakthrough in targeted cancer therapy. Despite efforts to counteract TKI resistance and improve safety profiles, refractory BCR::ABL1⁺ leukemia, as well as toxicities and long-term side effects of TKI, present particular therapeutic challenges.^3–5

The clinical relevance of cyclins and their associated cyclin-dependent kinases (CDK) has been a major focus of research for several years. Cyclin-CDK complexes do not only drive the cell cycle, but are also important players in various other cellular processes including transcriptional and epigenetic regulation, metabolism or stem cell self-renewal.⁶ In line with their importance in different pathways, cyclin-CDK complex dysregulation is implicated in many different types of cancer.⁷

Scientists from Mass General Brigham and Beth Israel Deaconess Medical Center have developed a novel gene editing tool called STITCHR. Unlike traditional CRISPR, STITCHR inserts entire genes at precise locations, minimizing unintended mutations. This gene editing tool simplifies use and offers potential as a one-time treatment for genetic disorders.

The technology uses retrotransposons, naturally occurring “jumping genes” found in all eukaryotic organisms, which can move and integrate into genomes. Using computational screening, the researchers identified and reprogrammed a specific retrotransposon to work with the nickase enzyme from CRISPR, forming the complete STITCHR system that allows a precise, seamless gene insertion into the genome.

STITCHR offers the potential to replace or supplement entire genes, creating a more universal treatment option for various genetic diseases. The research team is now working to improve its efficiency and move it toward clinical use. Their study, published in Nature, highlights how insights from basic cellular biology can drive innovation in genetic medicine and lead to new therapeutic tools.

A new study has unveiled when chronic myeloid leukaemia, a type of cancer that affects the blood and bone marrow, arises in life and how fast it grows. Researchers reveal explosive growth rates of cancerous cells years before diagnosis and variation in these rates of growth between patients. Such rapid growth rates had previously not been observed in most other cancers.

Researchers used whole genome sequencing to study when BCR::ABL1 – an abnormal fusion of the different genes called BCR and ABL1, which is known to cause chronic myeloid leukaemia. The team investigated when BCR::ABL1 first arises in a blood cell and how quickly these cells with this genetic change then multiply and expand to lead to a diagnosis of a type of leukaemia.

The research, published in Nature, contributes to the scientific understanding of how strong this abnormal fusion gene is in its ability to drive cancer.

A new study from Weill Cornell Medicine provides insights into how cells maintain the tiny end caps of chromosomes as they divide, a key process in keeping cells healthy. Using yeast, the researchers reveal protein interactions that could explain how the enzyme telomerase is tightly regulated to prevent cells from dividing uncontrollably or aging prematurely.

The preclinical study, published April 17 in Nucleic Acids Research, brings us closer to understanding the mechanisms behind aging and cancer.

Before cells divide, they replicate the double-stranded DNA of each chromosome. The replication machinery does a good job of copying the nucleotide sequences until it gets to the telomeres, the end caps of chromosomes that safeguard the genetic material from damage and normally shorten with aging. That’s when telomerase steps in and produces an overhang in which one DNA strand is a little longer than the other.

An international collaboration between four scientists from Mainz, Valencia, Madrid, and Zurich has published new research in the Proceedings of the National Academy of Sciences, shedding light on the most significant increase in complexity in the history of life’s evolution on Earth: the origin of the eukaryotic cell.

While the endosymbiotic theory is widely accepted, the billions of years that have passed since the fusion of an archaea and a bacteria have resulted in a lack of evolutionary intermediates in the phylogenetic tree until the emergence of the eukaryotic cell. It is a gap in our knowledge, referred to as the black hole at the heart of biology.

“The new study is a blend of theoretical and observational approaches that quantitatively understands how the genetic architecture of life was transformed to allow such an increase in complexity,” stated Dr. Enrique M. Muro, representative of Johannes Gutenberg University Mainz (JGU) in this project.