Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: genetics – Page 21

Genetic test predicts obesity in childhood

What if we could prevent people from developing obesity? The World Obesity Federation expects more than half the global population to develop overweight or obesity by 2035. However, treatment strategies such as lifestyle change, surgery and medications are not universally available or effective.

By drawing on genetic data from over five million people, an international team of researchers has created a genetic test called a (PGS) that predicts adulthood obesity already in early childhood. This finding could help to identify children and adolescents at higher genetic risk of developing obesity, who could benefit from targeted preventative strategies, such as lifestyle interventions, at a younger age.

“What makes the score so powerful is its ability to predict, before the age of five, whether a child is likely to develop obesity in adulthood, well before other risk factors start to shape their weight later in childhood. Intervening at this point can have a huge impact,” says Assistant Professor Roelof Smit from the NNF Center for Basic Metabolic Research (CBMR) at the University of Copenhagen and lead author of the research published in Nature Medicine.

Genetically modified gut bacteria show promise for combating kidney stones in clinical trial

The human gut microbiome has been shown to impact health in a myriad of ways. The type and abundance of different bacteria can impact everything from the immune system to the nervous system. Now, researchers at Stanford University are taking advantage of the microbiome’s potential for fighting disease by genetically modifying certain bacteria to reduce a substance that causes kidney stones. If scientists are successful at modifying gut bacteria, this can lead to therapeutic treatments for a wide range of diseases.

However, the study, published in Science, shows that this is not a simple task. The researchers used the bacterium Phocaeicola vulgatus, which is already found in the microbiome of humans, and modified it to break down and also to consume porphyran, a nutrient derived from seaweed. The porphyran was used as a way to control the population of Phocaeicola vulgatus by either adding more porphyran or reducing the amount, which should kill off the bacteria due to a lack of food.

The study was made up of three parts: one testing the modified bacteria on rats, one trial with healthy humans and one trial on people with enteric hyperoxaluria (EH). EH is a condition in which the body absorbs too much oxalate from food, leading to and other kidney issues, if not treated.

Inhibitory neurons catch up during brain development

In the study, the researchers also explored how the accelerated maturation of later-born inhibitory neurons is regulated. They identified specific genes involved in this process and uncovered how they control when and to what extent a cell reads and uses different parts of its genetic code. They found that the faster development of later-born inhibitory neurons turns out to be linked to changes in the developmental potential of the precursor cells that generate them—changes which are, in turn, triggered by a reorganization of the so-called ‘chromatin landscape.’

In simple terms, this means that cells adjust the accessibility of certain regions of DNA in the cell nucleus, making key instructions on how and when to develop more readable.

The human brain is made up of billions of nerve cells, or neurons, that communicate with each other in vast, interconnected networks. For the brain to function reliably, there needs to be a fine balance between two types of signals: Excitatory neurons that pass on information and increase activity, and inhibitory neurons that limit activity and prevent other neurons from becoming too active or firing out of control. This balance between excitation and inhibition is essential for a healthy, stable brain.

Inhibitory neurons are generated during brain development through the division of progenitor cells – immature cells not yet specialized but already on the path to becoming neurons. The new study uncovered a surprising feature of brain development based on findings in mice: During this essential process, cells born later in development mature much more quickly than those produced earlier.

“This faster growth helps later-born neurons catch up to those produced earlier, so that by the time all these neurons are incorporated into neural networks, they are at a similar stage of development,” said a research group leader. “This is important, as otherwise, earlier-born neurons—having had more time to form connections—could end up with far more synaptic links than those created later. Without this adjustment, the network could be thrown off balance, and individual cells would have too many or too few connections.”

From telomeres and senescence to integrated longevity medicine: redefining the path to extended healthspan

Despite significant advances in aging research, translating these findings into clinical practice remains a challenge. Aging is a complex, multifactorial process shaped by many factors including genetic, metabolic, and environmental factors. While medical advancements have extended lifespan, healthspan remains constrained by cellular senescence, telomere attrition, and systemic inflammation—core hallmarks of biological aging. However, emerging evidence suggests that telomere dynamic is not inevitable but can be influenced by oxidative stress, lifestyle choices, and metabolic regulation. This review examines how telomere-based biomarkers and metabolic interventions can drive personalized longevity medicine, enabling targeted strategies to delay aging.

Protein aggregation is linked to altered RNA processing

Neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, are devastating and incurable diseases. Although many neurodegenerative diseases are characterized by abnormal protein aggregation in the brain, a limited understanding of whether and how aggregated proteins cause brain cell dysfunction and death represents a major barrier to developing effective treatments.

Inspired by similar approaches in cardiovascular disease and cancer, the researchers focused on rare genetic forms of neurodegeneration as a powerful way to uncover fundamental mechanisms tying protein aggregation to brain disease. Thier work unexpectedly linked protein aggregation in genetic forms of neurodegeneration to disrupted processing of transfer RNAs (tRNAs), revealing an important mechanism that might be therapeutically targeted in these disorders.

The authors were interested in genetic forms of neurodegeneration caused by GGC trinucleotide repeat expansions (DNA sequence mutations caused by copying this 3-letter sequence too many times in a row). These mutations produce aggregation-prone proteins with long stretches of a single repeated amino acid (glycine).

Reversing The Age-Related DHEA-S Decline: Cholesterol, Gut Bacteria

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD

Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.

At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
Use Code: CONQUERAGING At Checkout.

Clearly Filtered Water Filter: https://get.aspr.app/SHoPY

Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ6…M0&irgwc=1
Use Code: CONQUERAGING

NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/

Continue reading “Reversing The Age-Related DHEA-S Decline: Cholesterol, Gut Bacteria” | >

Study reveals hidden regulatory roles of ‘junk’ DNA

A new international study suggests that ancient viral DNA embedded in our genome, which were long dismissed as genetic “junk,” may actually play powerful roles in regulating gene expression. Focusing on a family of sequences called MER11, researchers from Japan, China, Canada, and the US have shown that these elements have evolved to influence how genes turn on and off, particularly in early human development.

The findings are published in the journal Science Advances.

Transposable elements (TEs) are repetitive DNA sequences in the genome that originated from ancient viruses. Over millions of years, they spread throughout the genome via copy-and-paste mechanisms.

A common food additive solves a sticky neuroscience problem

An interdisciplinary team working on balls of human neurons called organoids wanted to scale up their efforts and take on important new questions. The solution was all around them.

For close to a decade now, the Stanford Brain Organogenesis Program has spearheaded a revolutionary approach to studying the brain: Rather than probe intact brain tissues in humans and other animals, they grow three-dimensional brain-like tissues in the lab from , creating models called human neural organoids and assembloids.

Beginning in 2018 as a Big Ideas in Neuroscience project of Stanford’s Wu Tsai Neurosciences Institute, the program has brought together neuroscientists, chemists, engineers, and others to tackle the neural circuits involved in pain, genes that drive neurodevelopmental disorders, new ways to study brain circuits, and more.

Different Bacterial Genes Have Different Turn-Ons

Not all genes respond in the same way to regulation by the same molecule—a property that might enable cells to produce complex genetic responses.

Genes in living cells may become active or may be suppressed in response to environmental stimuli such as heat or the availability of nutrients. For bacteria, this gene regulation often appears to be a simple “on-off switch” controlled by regulatory proteins called transcription factors (TFs). But researchers have now found that different genes might respond differently to the same stimulus even if they are regulated by the same TF [1]. The team activated genes involved in DNA repair and observed gene-to-gene variations in their protein production patterns. Such differences might have been exploited by evolution to achieve complex responses with relatively few molecular components, the researchers suggest.

In the typical scenario, a TF binds to a region of a so-called promoter, a DNA sequence next to a gene. If the TF is the type that blocks gene expression, it prevents the enzyme RNA polymerase from binding and thus from beginning the process of producing the protein that the gene encodes. Because of thermal fluctuations (noise), the TF may spontaneously unbind, allowing gene expression to proceed until it rebinds. The rate of TF binding depends on its concentration, so fluctuations in concentration will cause changes in gene expression.

/* */