Amin et al. present telomere-to-telomere assemblies of nine Borrelia burgdorferi strains from Canada, uncovering the diversity at chromosome ends and plasmid profiles. They identify an lp28-1a plasmid subtype and detect plasmid-chromosome recombination, offering insights into genomic plasticity and potential mechanisms of adaptation in Borrelia.
Researchers at Stanford University engineered a modified version of the immune protein interleukin-10 (IL-10) that retains only its anti-inflammatory properties while eliminating its pro-inflammatory ones. When injected into aged mice, this modified protein stimulated the growth of new neurons and improved performance on memory and learning tasks, such as maze navigation and object recognition. The study, published in Immunity, suggests that age-related cognitive decline is linked to the accumulation of exhausted T-lymphocytes in the brain, chronic inflammation, and impaired microglial function — all of which reduce neurogenesis. The findings indicate that selectively modulating immune signaling could open new avenues for treating neurodegenerative diseases. The team plans to further investigate the protein’s mechanisms and explore ways to target specific cell types more precisely to minimize potential side effects.
A modified immune protein developed by Stanford researchers points to a novel strategy for combating age-related cognitive decline.
Fifteen years ago, I wrote something that annoyed many techno-optimists.
Ten years ago, I filmed it as a podcast.
Today it feels less controversial — and more urgent.
Technology is NOT Enough.
We have the science to feed everyone. We have the tech to provide clean water. We understand climate change. We know how to reduce suffering.
And yet we don’t act.
Bill Faloon presents about thymosin’s potential in 4-minute video excerpt from recent super-longevity presentation. Click the video below to view the presentation.
Ted Brown has been involved in cryonics since the 1960s.
The controversial diet truth backed by 155 dietary surveys across 90 years that food scientists don’t want you to know.
Dan Buettner exposes why meta-analyses prove most nutritional debates wrong and reveals what centenarians actually ate as children to live past 100.
The peasant food formula that’s cheaper than a hamburger, 50 times more nutrient dense, and leaves you completely satisfied.
Plus why the 15 countries with the highest life expectancy all eat white rice daily.
Dan Buettner is a New York Times bestselling author, National Geographic Fellow, and co-producer of the Emmy Award winning Netflix series Live to 100: Secrets of the Blue Zones.
Cellular senescence is generally an irreversible proliferative arrest in damaged normal cells that have exited the cell cycle. These cells display high metabolic activities [1], remain viable, and actively suppress apoptosis [2, 3]. Senescent cells present unique morphological and molecular characteristics and functions that distinguish them from other nondividing cell populations, such as quiescent cells and terminally differentiated cells [4, 5, 6]. The hallmarks of cellular senescence include: prolonged cell cycle arrest, transcriptional changes, acquisition of a bioactive secretome, known as the senescence-associated secretory phenotype (SASP), macromolecular damage, and deregulated metabolism [7].
Replicative senescence was the first cellular senescence subtype to be described [8]. It is induced after serial propagation of normal human cells in culture and is caused by telomere erosion and the consequent increase in DNA lesions [9, 10,11,12]. The limited lifespan of most (perhaps all) cultured primary cells is influenced by the species and tissue type from which they were derived. Senescence can also be triggered by many other intrinsic and extrinsic factors, particularly, replicative stress, oxidative damage, metabolism dysfunctions, cytokines, oncogene activation, and chemotherapy agents. All these factors can induce DNA damage and senescence in normal and cancer cells (in some contexts) [6]. Cellular senescence occurs not only in vitro (i.e., cell culture models), but also in various tissues in vivo [13,14,15,16].
Senescence is an important contributor to cancer and aging, two processes characterized by a time-dependent accumulation of cell damage and dysfunction. Senescence markers are detected in premalignant tumor lesions but not at later stages of tumor development [17,18,19]. The proliferative arrest imposed by cellular senescence represents an early barrier against cancer initiation by preventing the propagation of damaged DNA to the next generation of cells [18,20]. Therefore, it has been proposed that senescence escape is required for tumor progression to overt malignancy [18,21]. On the other hand, senescent fibroblasts can influence their local environment by turning into proinflammatory cells that can promote the growth of transformed or preneoplastic neighboring epithelial cells in culture and in vivo [22,23,24].
Affordable Options Cryopreservation is far more affordable than you might think. There are many ways to fund your cryopreservation. MEMBERSHIP FEES MEMBERSHIP INITIATION HUMAN CRYOPRESERVATION LIFETIME $1,250 once none $28,000 once YEARLY $120 per year $200 once $35,000 once (Human cryopreservation prices do not include “Local Help” cost for a […]
