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This Protein Slows the Aging Brain, and We Know How to Counter It

Aging is particularly harsh on the hippocampus, the brain region responsible for learning and memory.

Now, researchers at UC San Francisco have identified a protein that’s at the center of this decline.

They looked at how the genes and proteins in the hippocampus changed over time in mice and found just one protein that differed between old and young animals. It’s called FTL1. Old mice had more FTL1, as well as fewer connections between brain cells in the hippocampus and diminished cognitive abilities.


Scientists discover a protein that gets concentrated in the brain during aging, leading brain connections to wither and cognitive decline to accelerate — and a way to counter its effects.

How Dr. Bill Andrews Plans to Cure Aging in 3 Years

Anybody got a spare $130 million?


Dr. Bill Andrews, a trailblazing scientist, is on a mission to cure aging. From a childhood dream sparked at age 10 to his pioneering telomerase research, he reveals how Sierra Sciences could reverse aging in just three years with $130 million in funding. Yet, investor demands for quick returns stand in his way.
He believes that a Biotech Freedom Zone through Immortalis—a revolutionary approach to bypass funding and regulatory hurdles—is the catalyst to transform longevity research, making health affordable and aging a thing of the past.

Join the community behind the first ever Biotech Freedom City:
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Longevity expert explains whether we can reduce plaque build-up in our arteries and decrease the risk of a heart attack

It is a very common belief that once plaque builds up in the arteries, it is there to stay, a slow, irreversible path towards heart disease. Doctors generally prescribed lifelong medication, stents, or even surgery as the only way forward. But as longevity expert Dr Vass, trained at Cornell, points out, that it might not all be true. Science now shows that arterial plaque can indeed be managed, reduced, and even stabilised if the root causes are targeted. So, can plaque really be reversed, and can this lower the risk of heart attacks? Here’s all we need to know about it.

Why do some people age faster than others? Study identifies genes at play

It’s a fact of life: Some people age better than others. Some ease into their 90s with mind and body intact, while others battle diabetes, Alzheimer’s or mobility issues decades earlier. Some can withstand a bad fall or bout of the flu with ease, while others never leave the hospital again.

New University of Colorado Boulder-led research, published in Nature Genetics, sheds light on why that is.

In it, an international team of co-authors identifies more than 400 genes associated with accelerated aging across seven different sub-types. The study reveals that different groups of genes underlie different kinds of disordered aging, a.k.a. frailty, ranging from cognitive decline to mobility issues to social isolation.

Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases

With the intensification of global aging, the incidence of age-related diseases (including cardiovascular, neurodegenerative, and musculoskeletal disorders) has been on the rise, and cellular senescence is identified as the core driving mechanism. Cellular senescence is characterized by irreversible cell cycle arrest, which is caused by telomere shortening, imbalance in DNA damage repair, and mitochondrial dysfunction, accompanied by the activation of the senescence-associated secretory phenotype (SASP). In this situation, proinflammatory factors and matrix-degrading enzymes can be released, thereby disrupting tissue homeostasis. This disruption of tissue homeostasis induced by cellular senescence manifests as characteristic pathogenic mechanisms in distinct disease contexts. In cardiovascular diseases, senescence of cardiomyocytes and endothelial cells can exacerbate cardiac remodeling.

Scientists just found a protein that reverses brain aging

Scientists at UCSF have uncovered a surprising culprit behind brain aging: a protein called FTL1. In mice, too much FTL1 caused memory loss, weaker brain connections, and sluggish cells. But when researchers blocked it, the animals regained youthful brain function and sharp memory. The discovery suggests that one protein could be the master switch for aging in the brain — and targeting it may one day allow us to actually reverse cognitive decline, not just slow it down.

An energy metabolism-engaged nanomedicine maintains mitochondrial homeostasis to alleviate cellular ageing

Through binding mitochondrial ATP synthase, engineered nanomedicines rejuvenate aged bone stem cells and restore osteogenesis, reversing osteoporosis in mice and offering a potential senolytic therapy for skeletal ageing.

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