The science of longevity is an important topic for many researchers: how we might add years to our lifespans, and avoid disease and age-related decline at the same time.
There are a multitude of angles to approach the topic from too, whether it’s the genetics we’re born with or the food we eat along life’s journey.
Now, an international team of researchers is proposing that longevity interventions and research should start at the earliest ages possible – even before birth.
When the engineers used gene editing to suppress the PIEZO1 gene, the cells became “deaf” to the physical tugging. Even when the magnets vigorously exercised the gel, the blood vessels barely sprouted at all. This proved that physical force directly activates this cellular gatekeeper, signaling the vessel that it’s time to grow and branch out.
Engineering organized microvascular networks remains a critical challenge in tissue engineering and regenerative medicine. While biochemical approaches for patterning angiogenesis via growth factor delivery have shown promise, their inability to pattern sustained growth factors with spatiotemporal control limits effectiveness. Here, we demonstrate that dynamically patterned mechanical forces enable precise spatiotemporal control over angiogenic sprouting. We developed a magnetically actuated human vessel-on-a-chip platform that integrates a perfusable endothelialized microchannel within a collagen matrix and allows noninvasive and tunable mechanical stimulation across three spatial dimensions and time (4D). Using an automated 3-axis actuator, we systematically investigated how strain magnitude, frequency, and direction modulate endothelial cell behavior and vessel morphogenesis.
Welcome to functional immortality, folks.
I say functional rather than absolute because no one will ever REALLY live FOREVER. Even if we can reverse aging and become immune to all diseases (which is exactly what is happening right now even as I write this) there will still be accidents, suicides, wars, and murders. — Still…a BILLION years would be enough for me.
What about you?
A new study reveals that mature cells retain the ability to transform into stem cells after injury. The regenerative process, driven by macrophages, may offer new strategies for repairing damaged tissues.
For most women, the body begins to change dramatically in their 40s or 50s. This transition, known as menopause, is defined as 12 consecutive months without a menstrual period, marking the end of the reproductive years. While researchers are aware of the functions the ovaries perform during active reproductive years, what happens to the organ after menopause is largely a mystery.
A recent study in Molecular Human Reproduction investigated what happens to the ovary in mice after it stops producing eggs, a period known as the post-reproductive stage, similar to menopause in humans.
Researchers found that even after the ovary can no longer support reproduction, it doesn’t simply become inactive. Instead, aging ovaries undergo remarkable changes, producing a different set of signaling molecules from those of younger ovaries.
Branchlike structures called dendrites that extend from neurons appear to make their own computations independent of the cell body, helping individual brain cells store memories of the past, respond to the present and anticipate the future, a study led by UT Southwestern Medical Center researchers suggests.
The findings, published in Science, represent a paradigm shift in current models of how learning and memory take place.
“This shifts our entire perspective. Rather than acting as simple switches, neurons behave more like sophisticated processors with internal divisions of labor, dramatically increasing the brain’s computational capacity,” said Attila Losonczy, M.D., Ph.D., professor at the Peter O’Donnell Jr. Brain Institute of Neuroscience and director of the Program in Memory Longevity (PML) at UT Southwestern.
We may age at different rates, but none of us escapes aging. A study in mice and human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increasing inability, with advancing age, to gobble up another immune cell type.
So-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice, including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.
In mice, selectively disabling this receptor exclusively on tissue-resident macrophages prevented chronic inflammation-driven disorders of aging, including frailty, excessive fat accumulation and heart trouble. It also substantially slowed cognitive decline, said Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley professor of neurology and neurological sciences.
While GLP-1 drugs can curb cardiometabolic dysfunction, reducing the risk of life-limiting and life-threatening diseases that would otherwise shorten health and lifespan, mechanistic evidence that they directly influence the biology of aging remains limited.
Can GLP-1 drugs rewind the epigenetic clock?
UCSD researchers conducted a post hoc analysis of a Phase 2b clinical trial evaluating the use of semaglutide in human immunodeficiency virus (HIV)-associated lipohypertrophy (HALS).
