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Researchers from Cleveland Clinic’s Genome Center have outlined the pathway human herpes simplex virus-1 (HSV1) can use to contribute to Alzheimer’s disease in aging brains. In a report published in Alzheimer’s & Dementia, investigators also share two FDA-approved, commercially available drugs that reverse this pathway in a laboratory setting.
The findings are the first concrete evidence to support the previously controversial link between human herpesviruses (HHVs) and Alzheimer’s disease. Illustrating the potential for herpes to trigger dementia aids continued efforts to prevent and cure neurodegenerative disease, says senior author and Genome Center director Feixiong Cheng, Ph.D…
For most people, contracting a herpes infection is just an inconvenient or harmless fact of life. Many herpesviruses are individually present in a large percentage of people worldwide, meaning virtually every human being on earth is expected to contract at least three types of herpesviruses by adulthood. Some of these viruses don’t cause symptoms, while others only cause minor illnesses like mono or chickenpox. However, even after these illnesses subside, an infected individual still carries herpesviruses for the rest of their life, with only minor symptoms like occasional cold sores.
Scientists are uncovering the powerful role hormones play in skin aging, revealing new potential treatments for wrinkles, hair graying, and overall skin health.
While traditional anti-aging hormones like retinoids and estrogen have been widely used, new research highlights a broader range of hormones that influence skin structure, pigment, and resilience.
Hormones and Anti-Aging Potential.
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A biomaterial that can mimic certain behaviors within biological tissues could advance regenerative medicine, disease modeling, soft robotics and more, according to researche(rs at Penn State.
Materials created up to this point to mimic tissues and extracellular matrices (ECMs) — the body’s biological scaffolding of proteins and molecules that surrounds and supports tissues and cells — have all had limitations that hamper their practical applications, according to the team. To overcome some of those limitations, the researchers developed a bio-based, “living” material that encompasses self-healing properties and mimics the biological response of ECMs to mechanical stress.
They published their results in Materials Horizons, where the research was also featured on the cover of the journal.
Stacy Andersen has studied people who are 100 and over for two decades. The importance of sleep for healthy aging is one of the biggest lessons she’s learned.
Exosomes are small vesicles with diameters ranging from 30 to 150 nm. They originate from cellular endocytic systems. These vesicles contain a rich payload of biomolecules, including proteins, nucleic acids, lipids, and metabolic products. Exosomes mediate intercellular communication and are key regulators of a diverse array of biological processes, such as oxidative stress and chronic inflammation. Furthermore, exosomes have been implicated in the pathogenesis of infectious diseases, autoimmune disorders, and cancer. Aging is closely associated with the onset and progression of numerous diseases and is significantly influenced by exosomes. Recent studies have consistently highlighted the important functions of exosomes in the regulation of cellular senescence.
What if we could live forever?Imagine a world where death is no longer inevitable and humanity unlocks the secrets to eternal life. In this video, we explore…
Many aspects of inflammation increase with aging in mice and humans. Transcriptomic analysis revealed that many murine anti-aging interventions produce lower levels of pro-inflammatory proteins. Here, we explore the hypothesis that different longevity interventions diminish NF-κB levels, potentially mediating some of the anti-inflammatory benefits of lifespan-extending interventions. We found that the NF-κB protein p65 is significantly downregulated in the liver of several kinds of slow-aging mice. These included both sexes of GHRKO and Snell Dwarf mutant mice, and in females only of PAPPA KO mice. P65 is also lower in both sexes of mice treated with rapamycin, canagliflozin, meclizine, or acarbose, and in mice undergoing caloric restriction. Two drugs that extend lifespan of male mice, i.e. 17α-estradiol and astaxanthin, however, did not produce lower levels of p65.