Empowerment
Studies We Have Analised
Gene Therapy-Mediated Partial Reprogramming Extends Lifespan and Reverses Age-Related Changes in Aged Mice
A recent study published in Cell demonstrates that gene therapy-mediated partial reprogramming can significantly extend the lifespan and improve the health of aged mice. By using adeno-associated viruses to deliver three of the Yamanaka factors (OCT4, SOX2, and KLF4, collectively known as OSK) to 124-week-old mice, researchers achieved a remarkable 109% increase in median remaining lifespan compared to controls.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10909732/
Effect of rapamycin on aging and age-related diseases-past and future
In 2009, rapamycin was found to extend mouse lifespan when given later in life, showing that drugs can affect aging without early intervention. This highly influential 2020 review, cited by over 300 other published studies, includes results for Everolimus in animal experiments (GeroScience 2021 43 page 1139), where many mice lived 100-440% longer. Rapamycin and related drugs are immunosuppresants and can also prevent, but not cure, cancer. They work by slowing down certain natural responses, which also unfortunately slows wound healing.
https://pubmed.ncbi.nlm.nih.gov/33037985/
Rapamycin: An InhibiTOR of Aging Emerges From the Soil of Easter Island
The study reviews how rapamycin and its analog everolimus can extend lifespan by blocking a pathway called mTOR, which is involved in aging. While rapamycin effectively increases lifespan in animal studies, long-term use can cause side effects by interfering with certain important cellular functions. The authors suggest that adjusting dosage schedules or using similar drugs that target mTOR more selectively could help reduce these side effects, making rapamycin and everolimus safer options for anti-aging treatments.
https://pubmed.ncbi.nlm.nih.gov/27208895/
Intermittent Administration of Rapamycin Extends the Life Span of Female C57BL/6J Mice
This study reviews rapamycin’s role in extending lifespan by inhibiting the mTOR signaling pathway, highlighting its benefits and limitations as a standalone treatment. It emphasizes that combining rapamycin with other therapies may overcome limitations and enhance its effectiveness for lifespan extension and health improvement.
https://pubmed.ncbi.nlm.nih.gov/27091134/
Transcriptional activation of endogenous Oct4 via the CRISPR/dCas9 activator ameliorates Hutchinson-Gilford progeria syndrome in mice
This study demonstrates the potential of CRISPR/dCas9 technology to activate the Oct4 gene, promoting cellular rejuvenation in a mouse model of Hutchinson-Gilford progeria syndrome.This approach reflects innovative methods to address aging and age-related diseases by leveraging gene expression to restore cellular health.
https://pubmed.ncbi.nlm.nih.gov/36964992/
A Safer Path to Cellular Rejuvenation: Endogenous Oct4 Activation via CRISPR/dCas9 in Progeria Mouse Models
The study shows that activating endogenous Oct4 using CRISPR/dCas9 safely rejuvenates cells, reverses aging-related epigenetic changes, reduces progerin expression, and extends lifespan in a progeria mouse model. This approach offers a safer alternative to traditional OSKM reprogramming methods.
https://pubmed.ncbi.nlm.nih.gov/37327373/
Reprogramming to recover youthful epigenetic information and restore vision
The study demonstrates that expressing the reprogramming factors Oct4, Sox2, and Klf4 (OSK) in mouse retinal ganglion cells safely restores youthful DNA methylation patterns, promotes axon regeneration after injury, and reverses vision loss in models of glaucoma and natural aging. These findings highlight that youthful epigenetic information remains stored in mammalian tissues and can be leveraged through controlled epigenetic reprogramming to reverse aging-related functional decline, aligning closely with the rejuvenation concepts described in the provided script.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7752134/
Epigenetic reprogramming to rejuvenate retinal ganglion cells and sustainably reverse glaucoma-induced vision loss
This study demonstrates that long-term epigenetic reprogramming using Oct4, Sox2, and Klf4 (OSK) safely and sustainably restores vision in mice with glaucoma-induced vision loss. Using a doxycycline-inducible dual AAV system, researchers achieved complete visual recovery within two months, maintaining healthy vision levels for nearly a year without adverse effects, aligning closely with rejuvenation concepts.
https://iovs.arvojournals.org/article.aspx?articleid=2791047
Sustained Vision Recovery by OSK Gene Therapy in a Mouse Model of Glaucoma
The year-long study investigated the effects of continuous versus cyclic OSK expression on aging and rejuvenation in mice. Findings suggest that both expression patterns can induce rejuvenation, highlighting potential therapeutic strategies for age-related degeneration.
Loss of epigenetic information as a cause of mammalian aging
According to this theory, the loss of epigenetic information refers to the gradual deterioration shown by the epigenetic markers. This includes changes in DNA methylation, histone modifications, and chromatin structure that occur over time. These changes lead to dysregulated gene expression, causing cells to lose their identity and function, ultimately manifesting as aging. This study supports the concept that there exists a “backup copy” of the youthful epigenetic information that can be accessed to reverse aspects of aging.
https://pubmed.ncbi.nlm.nih.gov/36638792/
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Research Collaboration
Longevity Pink collaborates with researchers and scientists to promote groundbreaking studies in life extension, ensuring that findings are shared widely and contribute to the greater good of society.
