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Category: biotech/medical – Page 9

6 Discoveries From Top Labs Proving Age Reversal Works


In this video, we break down six major scientific breakthroughs from July to September that are pushing us closer to true age reversal — from AI-designed drugs and senolytics to epigenetic reset and real human results.
You’ll see how AI, wet-lab automation, and new biomarkers are accelerating longevity research faster than ever before — and what this means for your future healthspan.

0:51 — Breakthrough #1: AI Becomes the Scientist.
1:30 — Breakthrough #2: Reprogramming at 50× Speed.
2:24 — Breakthrough #3: Human Results Are Finally Here.
2:52 — Breakthrough #4: AI Discovers Drugs From Scratch.
3:38 — Breakthrough #5: Aging Now Has a Dashboard.
4:12 — Breakthrough #6: The Telomere Puzzle (TEN1)
4:38 — The Double-Edged Sword of Rejuvenation.
5:04 — The LEV Cycle.

📌 ABOUT THIS CHANNEL
Easy Insight simplifies the science of longevity — from AI-driven age reversal and gene editing to breakthroughs that could let us outpace aging itself.
No hype. No speculation. Just easy, factual insight into how technology may redefine human healthspan.

🔍 KEY TOPICS
longevity, AI longevity, artificial intelligence, anti-aging, rejuvenation, CRISPR, epigenetic reprogramming, healthspan extension, age reversal, LongevityEscapeVelocity, biotechnology, Easy Insight, biomarkers, senolytics, telomeres.

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Endothelial insulin resistance induced by adrenomedullin mediates obesity-associated diabetes

The hormone adrenomedullin disrupts insulin signaling in blood vessel cells, contributing to systemic insulin resistance in obesity-associated type 2 diabetes, according to a Science study from earlier this year in mice.

The results suggest a potential new target for treating obesity-related metabolic disease.

Insulin resistance is a hallmark of obesity-associated type 2 diabetes. Insulin’s actions go beyond metabolic cells and also involve blood vessels, where insulin increases capillary blood flow and delivery of insulin and nutrients. We show that adrenomedullin, whose plasma levels are increased in obese humans and mice, inhibited insulin signaling in human endothelial cells through protein-tyrosine phosphatase 1B–mediated dephosphorylation of the insulin receptor. In obese mice lacking the endothelial adrenomedullin receptor, insulin-induced endothelial nitric oxide–synthase activation and skeletal muscle perfusion were increased. Treating mice with adrenomedullin mimicked the effect of obesity and induced endothelial and systemic insulin resistance. Endothelial loss or blockade of the adrenomedullin receptor improved obesity-induced insulin resistance.

Tenascin-C from the tissue microenvironment promotes muscle stem cell maintenance and function through Annexin A2

Tenascin-C (TnC) produced by the fibro-adipogenic progenitors (FAPs) is required for MuSC maintenance and function. FAP-secreted TnC signals through Annexin-A2 on the MuSC surface to promote self-renewal and regeneration potential.

Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque prefrontal cortex

The human brain is a fascinating and complex organ that supports numerous sophisticated behaviors and abilities that are observed in no other animal species. For centuries, scientists have been trying to understand what is so unique about the human brain and how it develops over the human lifespan.

Recent technological and experimental advances have opened new avenues for neuroscience research, which in turn has led to the creation of increasingly detailed descriptions of the brain and its underlying processes. Collectively, these efforts are helping to shed new light on the underpinnings of various neuropsychiatric and neurodevelopmental disorders.

Researchers at Beijing Normal University, the Changping Laboratory and other institutes have recently set out to study both the human and macaque brain, comparing their development over time using various genetic and molecular analysis tools. Their paper, published in Nature Neuroscience, highlights some key differences between the two species, with the human pre-frontal cortex (PFC) developing slower than the macaque PFC.

“Unraveling the cellular and molecular characteristics of human prefrontal cortex (PFC) development is crucial for understanding human cognitive abilities and vulnerability to neurological and neuropsychiatric disorders,” wrote Jiyao Zhang, Mayuqing Li, and their colleagues in their paper. “We created a comparative repository for gene expression, chromatin accessibility and spatial transcriptomics of human and macaque postnatal PFC development at single-cell resolution.”

Human-specific molecular and cellular regulatory programs prolong prefrontal cortical maturation by orchestrating postnatal development of neurons and glia, with implications for cognitive function and susceptibility to neurodevelopmental disorders.

Continue reading “Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque prefrontal cortex” | >

Therapeutic VEGFC treatment provides protection against traumatic-brain-injury-driven tauopathy pathogenesis

How traumatic brain injury (TBI) mechanistically contributes to neurodegenerative disease remains poorly understood. Marco et al. find that therapeutic viral vector-based delivery of VEGFC recuperates meningeal lymphatic drainage deficits post-TBI and protects against severe development of tauopathy, neurodegeneration, and cognitive decline in the PS19 mouse model of tauopathy.

Novel ATXN10 Repeat Motif Patterns in Peruvian Families Modify Disease Onset

This study used a novel multiplex 20-gene panel with Cas9-targeted, amplification-free long-read sequencing and optical genome mapping to elucidate ATXN10 repeat motif patterns and investigated genotype-phenotype correlations in index cases of 6 multigenerational spinocerebellar ataxia type 10 kindreds from Peru.

Spinocerebellar ataxia type 10 (SCA10, Online Mendelian Inheritance in Man (OMIM)# 603516) is a rare autosomal-dominant disorder caused by an expanded pentanucleotide repeat in the ATXN10 gene on chromosome 22q13.3.1 Although rare globally, SCA10 accounts for 45% of spinocerebellar ataxia cases in Peru, where the population is approximately 70% Amerindian.2,3

A typical ATXN10 allele has 10–32 ATTCT repeats. Intermediate alleles from 280 to 850 repeats may have reduced penetrance4 while alleles over 850 repeats result in full disease penetrance.5 In our recent study on ATXN10 expansions in healthy Peruvians, we found expanded alleles in 3.7% of Mestizos and 9.9% of Indigenous American nonataxic individuals.6

Conventional methods fail to accurately determine ATXN10 repeat size and structure: Southern blot often overestimates repeats while repeat-primed PCR cannot measure repeats over 1,250 bp or detect alternate repeats without specific repeat primers.7

Why the human brain matures slower than its primate relatives

The human brain is a fascinating and complex organ that supports numerous sophisticated behaviors and abilities that are observed in no other animal species. For centuries, scientists have been trying to understand what is so unique about the human brain and how it develops over the human lifespan.

Recent technological and experimental advances have opened new avenues for neuroscience research, which in turn has led to the creation of increasingly detailed descriptions of the brain and its underlying processes. Collectively, these efforts are helping to shed new light on the underpinnings of various neuropsychiatric and neurodevelopmental disorders.

Researchers at Beijing Normal University, the Changping Laboratory and other institutes have recently set out to study both the human and macaque brain, comparing their development over time using various genetic and molecular analysis tools. Their paper, published in Nature Neuroscience, highlights some key differences between the two species, with the human pre-frontal cortex (PFC) developing slower than the macaque PFC.

Researchers Unveil a 4D Blueprint of the Human Genome

In a major step toward understanding how the physical form of DNA shapes human biology, researchers at Northwestern University working with the 4D Nucleome Project have created the most comprehensive maps yet of the genome’s three-dimensional organization over time and space. The work is described in a new study published in Nature.

The research, based on experiments in human embryonic stem cells and fibroblasts, provides an expansive picture of how genes interact with one another, fold into complex structures, and shift their positions as cells carry out normal functions and divide. The study was co-led by Feng Yue, the Duane and Susan Burnham Professor of Molecular Medicine in the Department of Biochemistry and Molecular Genetics.

“Understanding how the genome folds and reorganizes in three dimensions is essential to understanding how cells function,” said Yue, who is also director of the Center for Advanced Molecular Analysis and founding director of the Center for Cancer Genomics at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. “These maps give us an unprecedented view of how genome structure helps regulate gene activity in space and time.”

Scientists found a way to restore brain blood flow in dementia

A new study suggests that dementia may be driven in part by faulty blood flow in the brain. Researchers found that losing a key lipid causes blood vessels to become overactive, disrupting circulation and starving brain tissue. When the missing molecule was restored, normal blood flow returned. This discovery opens the door to new treatments aimed at fixing vascular problems in dementia.

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