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Category: genetics

We doubled human lifespans in the last 200 years. Can we do it again? | Andrew Steele

“Over the last 10 or 15 years, scientists have really started to understand the fundamental underlying biology of the aging process. And they broke this down into 12 hallmarks of aging.”

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We track age by the number of birthdays we’ve had, but scientists are arguing that our cells tell a different, more truthful story. Our biological age reveals how our bodies are actually aging, from our muscle strength to the condition of our DNA.

The gap between these two numbers may hold the key to treating aging – which could help save 100,000 lives per day and win us $38 trillion dollars.

00:00 Rethinking longevity.
01:27 Understanding aging.
02:58 Biological age and epigenetics.
04:29 New frontiers in longevity science.
08:04 Future possibilities and ethical questions.
10:24 The moral debate around living longer.

AI tool uncovers genetic blueprint of the brain’s largest communication bridge

For the first time, a research team led by the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC has mapped the genetic architecture of a crucial part of the human brain known as the corpus callosum—the thick band of nerve fibers that connects the brain’s left and right hemispheres. The findings open new pathways for discoveries about mental illness, neurological disorders and other diseases related to defects in this part of the brain.

The corpus callosum is critical for nearly everything the brain does, from coordinating the movement of our limbs in sync to integrating sights and sounds, to higher-order thinking and decision-making. Abnormalities in its shape and size have long been linked to disorders such as ADHD, bipolar disorder, and Parkinson’s disease. Until now, the genetic underpinnings of this vital structure had remained largely unknown.

In the new study, published in Nature Communications, the team analyzed and from over 50,000 people, ranging from childhood to late adulthood, with the help of a new tool the team created that leverages artificial intelligence.

Hair-thin fiber can control thousands of brain neurons simultaneously

Fiber-optic technology revolutionized the telecommunications industry and may soon do the same for brain research.

A group of researchers from Washington University in St. Louis in both the McKelvey School of Engineering and WashU Medicine have created a new kind of fiber-optic device to manipulate neural activity deep in the brain. The device, called PRIME (Panoramically Reconfigurable IlluMinativE) fiber, delivers multi-site, reconfigurable optical stimulation through a single, hair-thin implant.

“By combining fiber-based techniques with optogenetics, we can achieve deep-brain stimulation at unprecedented scale,” said Song Hu, a professor of biomedical engineering at McKelvey Engineering, who collaborated with the laboratory of Adam Kepecs, a professor of neuroscience and of psychiatry at WashU Medicine.

Viral Appropriation of Specificity Protein 1 (Sp1): The Role of Sp1 in Human Retro- and DNA Viruses in Promoter Activation and Beyond

Specificity protein 1 (Sp1) is a highly ubiquitous transcription factor and one employed by numerous viruses to complete their life cycles. In this review, we start by summarizing the relationships between Sp1 function, DNA binding, and structural motifs. We then describe the role Sp1 plays in transcriptional activation of seven viral families, composed of human retro- and DNA viruses, with a focus on key promoter regions. Additionally, we discuss pathways in common across multiple viruses, highlighting the importance of the cell regulatory role of Sp1. We also describe Sp1-related epigenetic and protein post-translational modifications during viral infection and how they relate to Sp1 binding. Finally, with these insights in mind, we comment on the potential for Sp1-targeting therapies, such as repurposing drugs currently in use in the anti-cancer realm, and what limitations such agents would have as antivirals.

Automated chloroplast screening platform speeds up crop trait development

Chloroplasts—the “light power plants” of plant cells—are increasingly the focus of synthetic biology. These organelles house the photosynthetic apparatus and host several metabolic pathways that are of great interest for engineering new traits. Gene insertion into chloroplasts is precise and carries a lower risk of transgene escape.

Despite this potential, chloroplast biotechnology remains in its infancy because standardized, scalable methods for rapid testing of diverse genetic parts have been missing. A research team from the Max Planck Institute for Terrestrial Microbiology in Marburg has now presented a micro‑algal platform that allows automated, fast, and large‑scale testing of chloroplast genetic modifications.

The study is published in the journal Nature Plants.

Small brain region linked to schizophrenia risk through unique gene changes

New research published in the American Journal of Psychiatry provides new molecular insights into the role of the habenula, a pea-sized brain region that helps regulate motivation and mood, in contributing to the risk of schizophrenia. A team of researchers at Lieber Institute for Brain Development and Johns Hopkins found that many schizophrenia-related molecular changes appear to be specific to this region, suggesting the habenula could be a potential target for future treatments.

Schizophrenia is a heritable disorder, and a combination of multiple genetic variants contributes to it. This study sought to understand how molecular changes in the habenula region of the brain contribute to the development of . The authors note that they focused on the habenula because of its “emerging role in and functional influence on neurotransmitter systems impacted in schizophrenia.”

The study team, led by Ege A. Yalcinbas, Ph.D., used cutting-edge molecular techniques to analyze postmortem human brains, resulting in the creation of the first cell-by-cell and within-cell gene expression map of the human habenula (Hb). They then compared from 35 individuals with schizophrenia and 33 nonpsychiatric donors.

Functionally dominant hotspot mutations of mitochondrial ribosomal RNA genes in cancer

To study selection for somatic single nucleotide variants (SNVs) in tumor mtDNA, we identified somatic mtDNA variants across primary tumors from the GEL cohort (n = 14,106). The sheer magnitude of the sample size in this dataset, in conjunction with the high coverage depth of mtDNA reads (mean = 15,919×), enabled high-confidence identification of mtDNA variants to tumor heteroplasmies of 5%. In total, we identified 18,104 SNVs and 2,222 indels (Supplementary Table 1), consistent with previously reported estimates of approximately one somatic mutation in every two tumors1,2,3. The identified mutations exhibited a strand-specific mutation signature, with a predominant occurrence of CT mutations on the heavy strand and TC on the light strand in the non-control region that was reversed in the control region2 (Extended Data Fig. 1a, b). These mutations occur largely independently of known nuclear driver mutations, with the exception of a co-occurrence of TP53 mutation and mtDNA mutations in breast cancer (Q = 0.031, odds ratio (OR) = 1.43, chi-squared test) (Extended Data Fig. 2a and Supplementary Table 4).

Although the landscape of hotspot mutations in nuclear-DNA-encoded genes is relatively well described, a lack of statistical power has impeded an analogous, comprehensive analysis in mtDNA16,17. To do so, we applied a hotspot detection algorithm that identified mtDNA loci demonstrating a mutation burden in excess of the expected background mutational processes in mtDNA (Methods). In total, we recovered 138 unique statistically significant SNV hotspots (Q 0.05) across 21 tumor lineages (Fig. 1a, b and Supplementary Table 2) and seven indel hotspots occurring at homopolymeric sites in complex I genes, as previously described by our group (Extended Data Fig. 2b and Supplementary Table 3). SNV hotspots affected diverse genetic elements, including protein-coding genes (n = 96 hotspots, 12 of 13 distinct genes), tRNA genes (n = 8 hotspots, 6 of 22 distinct genes) and rRNA genes (n = 34 hotspots, 2 of 2 genes) (Fig. 1b, c, e).

Holographic optogenetics could enable faster brain mapping for new discoveries

Recent technological advances have opened new possibilities for neuroscience research, allowing researchers to map the brain’s structure and synaptic connectivity (i.e., the junctions via which neurons communicate with each other) with increasing precision.

Despite these developments, most widely employed methods to image synaptic connectivity are slow and fail to precisely record changes in the connections between in vivo, or in other words, while animals are awake and engaging in specific activities.

Two different research groups, one based at Columbia University and UC Berkeley, and the other at the Vision Institute of Sorbonne University in Paris, introduced a promising approach to study synapses in vivo. Their proposed mapping strategies, outlined in two Nature Neuroscience papers, combine holographic optogenetics, a method to selectively and precisely stimulate or silence specific neuron populations, with .

A gene from 100-year-olds could help kids who age too fast

Scientists have uncovered a breakthrough in the fight against a rare genetic condition that causes children to age much faster than normal. The discovery involves “longevity genes” found in people who live exceptionally long lives, often beyond 100 years. Researchers from the University of Bristol and IRCCS MultiMedica found that these genes, which help maintain the health of the heart and blood vessels during aging, could reverse some of the damage caused by this devastating disease.

The study, published in Signal Transduction and Targeted Therapy, is the first to show that a gene from long-lived individuals can slow down heart aging in a model of Progeria. Known scientifically as Hutchinson-Gilford Progeria Syndrome (HGPS), this rare and fatal disorder causes children to exhibit signs of “accelerated aging.”

Progeria stems from a mutation in the LMNA gene, which leads to the creation of a harmful protein called progerin. This protein disrupts normal cell function, particularly in the heart and blood vessels. Most affected children die in their teenage years from heart complications, though some, like Sammy Basso — the oldest known person with Progeria — live longer. Sammy passed away on October 24, 2024, at the age of 28.

HUMAN Stem Cells Have Reversed Age In Monkey’s with ZERO Side Effects

Age Reversal in Primates has been achieved. We have it now.

Anti-aging gene therapy, stem cell rejuvenation, and FOXO3 longevity research take center stage in this episode of Longevity Science News with Emmett Short. This groundbreaking study out of Beijing shows that gene-edited human stem cells—specifically FOXO3-enhanced senescence-resistant mesenchymal progenitor cells (SRCs)—can reverse biological aging in elderly monkeys, restoring youthful brain structure, bone density, immune strength, and even ovarian function. By upgrading the FOXO3 longevity gene, scientists created stem cells that resist cellular senescence, DNA damage, and oxidative stress, effectively making the monkeys younger from the inside out. MRI scans revealed increased cortical thickness and improved memory-related connectivity, while biological age clocks showed a 3–5 year reversal across 54% of tissues—equivalent to 9–15 years of human rejuvenation. Emmett explains how these anti-aging stem cells, epigenetic resets, and exosome-based rejuvenation pathways could revolutionize regenerative medicine, longevity biotech, and future human trials. He also explores the costs, ethics, and long-term implications of turning back time at the cellular level. If you’re passionate about biohacking, gene editing, lifespan extension, or the future of anti-aging science, this is the video for you.

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Watch next: Artificial Blood: The SciFi Anti-Aging Tech That’s Now in Human Trials.
https://www.youtube.com/watch?v=3xz1lcGdQPc.

If you’re into the cutting edge of anti-aging science, subscribe and share with someone who wants to live longer, healthier, and stronger.

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