The feathery gilled pink salamanders stop aging early and can regenerate their limbs. Studying them could be the next step in the journey to unlocking effective anti-aging treatments in humans.
Researchers have successfully demonstrated how astroglia—cells that support the functioning of the brain—can be reprogrammed into cells resembling interneurons.
CRISPR is a way off being using in human treatment – but a new discovery could unlock its potential. Here’s what’s new.
Life Biosciences is a company co-founded by the celebrity geroscientist David Sinclair and is based on his Harvard team’s research into partial cellular reprogramming. In the heated race to translate this promising technology to the clinic, Life has emerged as one of the favorites, inching closer towards clinical trials in humans. Life is counting on its proprietary reprogramming technology that uses only three out of four classic reprogramming factors and on its strong team of scientists and managers. We talked to Dr. Sharon Rosenzweig-Lipson, Life’s Chief Scientific Officer, about the company’s journey, delving deep into the technology and its future.
I’ll start by saying that Life Biosciences is one of the most exciting companies in the longevity field. You might actually become the first company to have a partial reprogramming-based therapy approved.
At Life Biosciences, we’re focused on something that matters to everyone: helping people stay healthier as they age. We’re working on what we call cellular rejuvenation technologies, basically finding ways to turn back the clock in cells and make them more youthful. I came on board as Chief Scientific Officer about a year and a half ago, but I actually got to know the company pretty well before that. I consulted for them for a year, which gave me a chance to look under the hood, see the science they were doing, and I got really excited about what I saw.
Accumulation of senescent cells drives aging and age-related diseases. Senolytics, which selectively kill senescent cells, offer a promising approach for treating many age-related diseases. Using a senescent cell-based phenotypic drug discovery approach that combines drug screening and drug design, we developed two novel flavonoid senolytics, SR29384 and SR31133, derived from the senolytic fisetin. These compounds demonstrated enhanced senolytic activities, effectively eliminating multiple senescent cell types, reducing tissue senescence in vivo, and extending healthspan in a mouse model of accelerated aging. Mechanistic studies utilizing RNA-Seq, machine learning, network pharmacology, and computational simulation suggest that these novel flavonoid senolytics target PARP1, BCL-xL, and CDK2 to induce selective senescent cell death. This phenotype-based discovery of novel flavonoid senolytics, coupled with mechanistic insights, represents a key advancement in developing next-generation senolyticss with potential clinical applications in treating aging and age-related diseases.
LJN and PDR are cofounders of Itasca Therapeutics, developing senotherapeutics for aging and age-related diseases. LJZ, LJN, PDR and the University of Minnesota have filed a provisional patent on the application of flavonoid analogs, including SR29384 and SR31133, as a strategy to treat age-related diseases.
The future of therapeutic apheresis & transfusion medicine — dr. tina ipe, MD, MPH — CEO, regen med clinic.
Dr. Tina Ipe, MD, MPH is Chief Executive Officer at Regen Med Clinic (https://www.regenmed.vip/), a medical practice which provides multi-specialty infusions, cutting-edge treatments such as therapeutic apheresis (plasmapheresis and collections), as well as novel aesthetic treatments, for patients with a variety chronic illnesses.
Actin, a family of proteins that help give cells their shape, are abundant throughout the body.
Humans aren’t the only ones who grow forgetful as they age—fruit flies do, too. But because fruit flies have a lifespan of only about two months, they can be a useful model for understanding the cognitive decline that comes with aging.
A new study published in Nature Communications shows that when a common cell structural protein called filamentous actin, or F-actin, builds up in the brain, it inhibits a key process that removes unnecessary or dysfunctional components within cells, including DNA, lipids, proteins and organelles.
At 81, however, Scott maintains that he does not have time to wait for the FDA to approve the age-reversal treatments needed to achieve his goal of immorality.
“My concern is me, not the regulations which have been created,” he said.
Kenneth Scott travels internationally for experimental treatments, doesn’t use soap, and spends hundreds of thousands of dollars on his quest for immortality.
ASTRONAUTS aboard the International Space Station (ISS) have been told to prepare for an urgent evacuation.
The ISS is aging, and is due to be retired by the end of the decade.
One prevailing hypothesis is that physical fitness mitigates structural brain changes that contribute to cognitive decline. Recent evidence points to a potential role involving myelin —the insulating sheath surrounding neurons that is crucial for efficient neural signaling and overall cognitive health. Myelination facilitates rapid signal transmission and supports neural network integrity.
The degeneration of myelin in the brain is increasingly recognized as a critical factor contributing to disruptions in neural communication, which may play a significant role in the cognitive decline observed in Alzheimer’s disease and other neurodegenerative disorders. Emerging research suggests that myelin breakdown may even precede the formation of amyloid-beta plaques and neurofibrillary tangles—the hallmark pathological features of Alzheimer’s disease. Advanced imaging studies have detected early myelin degeneration in individuals who later develop Alzheimer’s, indicating that myelin damage could be an initial event in the disease’s progression.
Age-related deterioration of myelin is closely associated with cognitive decline. Reduced white matter integrity—often resulting from myelin damage—is correlated with declines in memory, executive function, and processing speed in older adults. As myelin degradation leads to the slowing of cognitive processes and disrupts the synchronization of neural networks, preserving myelin integrity is essential for sustaining cognitive health across the lifespan.
Accumulation of senescent cells drives aging and age-related diseases. Senolytics, which selectively kill senescent cells, offer a promising approach for treating many age-related diseases. Using a senescent cell-based phenotypic drug discovery approach that combines drug screening and drug design, we developed two novel flavonoid senolytics, SR29384 and SR31133, derived from the senolytic fisetin. These compounds demonstrated enhanced senolytic activities, effectively eliminating multiple senescent cell types, reducing tissue senescence in vivo, and extending healthspan in a mouse model of accelerated aging. Mechanistic studies utilizing RNA-Seq, machine learning, network pharmacology, and computational simulation suggest that these novel flavonoid senolytics target PARP1, BCL-xL, and CDK2 to induce selective senescent cell death. This phenotype-based discovery of novel flavonoid senolytics, coupled with mechanistic insights, represents a key advancement in developing next-generation senolyticss with potential clinical applications in treating aging and age-related diseases.
