Lifeboat Foundation: Safeguarding Humanity
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Category: genetics – Page 89

When We’re Overly Optimistic about the Pace of Life Extension Research

I have a new essay out via the wonderful site Merion West. The article is based on some of my experimental writings at Oxford. I hope you’ll read and consider it. I’m highly worried life extension science isn’t moving forward fast enough!

“Sadly, biological humans are likely to be mortal for centuries more, unless a dramatic increase of both resources and life extension scientists are marshaled.”

Certain well-known gerontologists and longevity experts around the world believe that sometime in this century—probably in the next 15–50 years—medicine will likely overcome and cure most forms of disease, and even death itself. Billionaires such as Meta’s Mark Zuckerberg, Amazon’s Jeff Bezos, Alphabet’s Larry Page, and Oracle’s Larry Ellison have jumped on board, pledging billions of dollars to “conquering all disease by this century” and mortality altogether.

These business titans hope age reversal techniques via genetic editing therapies, stem cell rejuvenation, 3D bioprinting of organs, and the widespread creation of synthetic organs like artificial hearts could keep people indefinitely young and healthy. If biological human death from disease and aging are overcome, then only catastrophic accidental death—such as an airplane crash or incineration—can kill people. (Accidental death in this vein accounts for about seven percent of all deaths in the United States.)

Transhumanists believe that the human being is like a machine—an entity that can be fixed and made to overcome nearly all biological death. The question is how fast can this be done? If the human being is indeed a machine-like entity as nearly all credible scientists propose, then the answer almost certainly rests not in the limits of biology but, rather, in the amount of work and resources put into the life extension field.

Regular aspirin use may help lower risk of colorectal cancer, study finds, especially for those with unhealthy lifestyles

(CNN) — Regular aspirin use may keep the oncologist away, at least when it comes to colorectal cancer, according to a new study, and people with unhealthy lifestyles seemed to see the greatest benefit.

Colorectal cancer is the second most common cause of cancer death worldwide, predicted to cause more than 52,500 deaths in the US alone in 2023. About 153,020 people in the US were diagnosed with the condition in 2023, and it’s become much more prevalent among people under 55, with numbers more than doubling in this group from a decade ago, studies show.

The causes of colorectal cancer can be genetic, but certain lifestyle factors also seem to raise risk, including eating an unhealthy diet, not getting enough exercise, drinking alcohol, smoking and having a high body mass index.

Seventh patient ‘cured’ of HIV: why scientists are excited

Yay face_with_colon_three

A 60-year-old man in Germany has become at least the seventh person with HIV to be announced free of the virus after receiving a stem-cell transplant1. But the man, who has been virus-free for close to six years, is only the second person to receive stem cells that are not resistant to the virus.

“I am quite surprised that it worked,” says Ravindra Gupta, a microbiologist at the University of Cambridge, UK, who led a team that treated one of the other people who is now free of HIV2,3. “It’s a big deal.”

The first person found to be HIV-free after a bone-marrow transplant to treat blood cancer4 was Timothy Ray Brown, who is known as the Berlin patient. Brown and a handful of others received special donor stem cells2,3. These carried a mutation in the gene that encodes a receptor called CCR5, which is used by most HIV virus strains to enter immune cells. To many scientists, these cases suggested that CCR5 was the best target for an HIV cure.

Scientists ‘Mind Controlled’ Mice Remotely in Extraordinary World First

At the mere flick of a magnetic field, mice engineered with nanoparticle-activated ‘switches’ inside their brains were driven to feed, socialize, and act like clucky new mothers in an experiment designed to test an innovative research tool.

While ’mind control’ animal experiments are far from new, they have generally relied on cumbersome electrodes tethering the subject to an external system, which not only requires invasive surgery but also sets limits on how freely the test subject can move about.

In what is claimed to be a breakthrough in neurology, researchers from the Institute for Basic Science (IBS) in Korea have developed a method for targeting pathways in the brain using a combination of genetics, nanoparticles, and magnetic fields.

Mapping the Mechanisms of Aging

Aging is a universal experience, evident through changes like wrinkles and graying hair. However, aging goes beyond the surface; it begins within our cells. Over time, our cells gradually lose their ability to perform essential functions, leading to a decline that affects every part of our bodies, from our cognitive abilities to our immune health.

To understand how cellular changes lead to age-related disorders, Calico scientists are using advanced RNA sequencing to map molecular changes in individual cells over time in the roundworm, C. elegans. Much like mapping networks of roads and landscapes, we’re charting the complexities of our biology. These atlases uncover cell characteristics, functions, and interactions, providing deeper insights into how our bodies age.

In the early 1990s, Cynthia Kenyon, Vice President of Aging Research at Calico, and her former team at UCSF discovered genes in C. elegans that control lifespan; these genes, which influence IGF1 signaling, function similarly to extend lifespan in many other organisms, including mammals. The genetic similarities between this tiny worm and more complex animals make it a useful model for studying the aging process. In work published in Cell Reports last year, our researchers created a detailed map of gene activity in every cell of the body of C. elegans throughout its development, providing a comprehensive blueprint of its cellular diversity and functions. They found that aging is an organized process, not merely random deterioration. Each cell type follows its own aging path, with many activating cell-specific protective gene expression pathways, and with some cell types aging faster than others. Even within the same cell type, the rate of aging can vary.

Epigenetics Unlocks Secrets of Memory Formation

Summary: A new study reveals that the epigenetic state of neurons determines their role in memory formation. Neurons with open chromatin states are more likely to be recruited into memory traces, showing higher electrical activity during learning.

Researchers demonstrated that manipulating these epigenetic states in mice can enhance or impair learning. This discovery shifts the focus from synaptic plasticity to nuclear processes, offering potential new avenues for treating cognitive disorders.

Chromatin plasticity predetermines neuronal eligibility for memory trace formation

It is clear that specific memories are not stored in individual specific neurons.

But the epigenetic state of neurons influences whether they become part of memory…

Memories are encoded by sparse populations of neurons but how such sparsity arises remains largely unknown. We found that a neuron’s eligibility to be recruited into the memory trace depends on its epigenetic state prior to encoding. Principal neurons in the mouse lateral amygdala display intrinsic chromatin plasticity, which when experimentally elevated favors neuronal allocation into the encoding ensemble. Such chromatin plasticity occurred at genomic regions underlying synaptic plasticity and was accompanied by increased neuronal excitability in single neurons in real time. Lastly, optogenetic silencing of the epigenetically altered neurons prevented memory expression, revealing a cell-autonomous relationship between chromatin plasticity and memory trace formation. These results identify the epigenetic state of a neuron as a key factor enabling information encoding.

Unlock Gene Networks Using Limited Data with AI Model Geneformer

Geneformer is a recently introduced and powerful AI model that learns gene network dynamics and interactions using transfer learning from vast single-cell transcriptome data. This tool enables researchers to make accurate predictions about gene behavior and disease mechanisms even with limited data, accelerating drug target discovery and advancing understanding of complex genetic networks in various biological contexts.

Developed by researchers at the Broad Institute of MIT and Harvard and their collaborators, the AI model Geneformer uses the highest-expressed genes in sc-RNA expression data to generate a dense representation of each cell, which can be used as features for various downstream predictive tasks. What makes Geneformer unique, however, are the capabilities its architecture enables, even when trained on very little data.

Geneformer has a BERT-like transformer architecture and was pre-trained on data from about 30M single-cell transcriptomes across various human tissues. Its attention mechanism enables it to focus on the most relevant parts of the input data. With this context-aware approach, the model can make predictions by considering ‌relationships and dependencies between genes.