Lifeboat Foundation

Senescent cells, often described as zombie-like, are ones that have stopped dividing but are still alive.

Research led by the lab of Nancy M. Bonini of the School of Arts & Sciences have uncovered new details about the role of zombie-like cells in brain aging, using the fruit fly as a model.

“Testing people early, so early interventions are possible, is key to longevity,” she says. “Technology, data and AI, and what we’re starting to be able to do with it, are propelling us to a time of greater understanding which will foster earlier, more effective treatment. Or perhaps even therapies that can delay neurodegenerative diseases, pushing back dementia to beyond our lifespan.”

Mind Over Matter goes out on 29th and 30th June on BBC News and 30th June on BBC One.

Lara Lewington will be hosting a Fireside Chat on AI drug discovery with Alex Zhavoronkov at next week’s Founders Longevity Forum. Register your interest to discover how AI is accelerating drug discovery, commercialization and licensing models HERE.

Understanding aging and age-related diseases requires analyzing a vast number of factors, including an individual’s genetics, immune system, epigenetics, environment and beyond. While AI has long been touted for its potential to shed light on these complexities of human biology and enable the next generation of healthcare, we’ve yet to see the emergence of tools that truly deliver on this promise.

Leveraging advanced plasma proteomics, US startup Alden Scientific has developed AI models capable of making the connections needed to accurately assess an individual’s state of health and risk of disease. The company’s tool measures more than 200 different conditions, including leading causes of morbidity and mortality such as Alzheimer’s, heart disease, diabetes and stroke. Significantly, its models also enable an individual to understand how an intervention impacts these risks.

With a host of top Silicon Valley investors among its early adopters, Alden is now using its platform to conduct an IRB-approved health study designed to provide a “longitudinal understanding of the interplay between environmental, biological, and medical data.”

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Aging is a natural part of life and yet one most of us hope to delay. At a certain point when you start feeling the effects of age and want the whole process to stop rushing forward. But can aging really be slowed down?

Continue reading “Can you delay aging? A biochemist explains how” »

Though one in two people will develop some form of cancer in their lifetime, there’s still much we don’t know about this disease. But thanks to continued research efforts, we keep learning more about the biology of cancer. One of these recent discoveries could even transform our understanding of how cancers develop.

But before we talk about the new discovery, let’s first discuss the classical theory that attempts to explain why normal cells become cancer cells. This theory posits that DNA mutations are the primary cause of cancers.

It’s well known that ageing, as well as some lifestyle and environmental factors (such as smoking and UV radiation) cause random DNA mutations (also known as genetic alterations) in our cells. Most genetic alterations trigger cell death or have no consequence.

Advanced glycation end products (AGEs) accumulate in the brain, leading to neurodegenerative conditions such as Alzheimer’s disease (AD). The pathophysiology of AD is influenced by receptors for AGEs and toll-like receptor 4 (TLR4). Protein glycation results in irreversible AGEs through a complicated series of reactions involving the formation of Schiff’s base, the Amadori reaction, followed by the Maillard reaction, which causes abnormal brain glucose metabolism, oxidative stress, malfunctioning mitochondria, plaque deposition, and neuronal death. Amyloid plaque and other stimuli activate macrophages, which are crucial immune cells in AD development, triggering the production of inflammatory molecules and contributing to the disease’s pathogenesis. The risk of AD is doubled by risk factors for atherosclerosis, dementia, advanced age, and type 2 diabetic mellitus (DM). As individuals age, the prevalence of neurological illnesses such as AD increases due to a decrease in glyoxalase levels and an increase in AGE accumulation. Insulin’s role in proteostasis influences hallmarks of AD-like tau phosphorylation and amyloid β peptide clearance, affecting lipid metabolism, inflammation, vasoreactivity, and vascular function. The high-mobility group box 1 (HMGB1) protein, a key initiator and activator of a neuroinflammatory response, has been linked to the development of neurodegenerative diseases such as AD. The TLR4 inhibitor was found to improve memory and learning impairment and decrease Aβ build-up. Therapeutic research into anti-glycation agents, receptor for advanced glycation end products (RAGE) inhibitors, and AGE breakers offers hope for intervention strategies. Dietary and lifestyle modifications can also slow AD progression. Newer therapeutic approaches targeting AGE-related pathways are needed.

The father and son exploring global longevity, inspiring healthier lives and investigating scientific breakthroughs on the horizon.

We are excited to announce a high-stakes debate on one of humanity’s oldest enigmas: aging. This event is not just a discussion, but a contest with a grand prize of 10,000 USDT for the winner. The debate aims to tackle the various theories and methodologies related to aging and seeks to uncover actionable insights through rigorous scientific discourse.

More info 👉 https://openlongevity.org/debates.

Continue reading “Debates: How to Defeat Aging — $10K Prize! Aubrey de Grey VS Peter Fedichev” »

People with a rare mutation that causes Laron syndrome, a form of dwarfism, live healthier lives and could be the key to anti-aging drugs.