Lifeboat Foundation

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.”

Through the looking glass: Researchers now have a way to conduct experiments on biological neurons in vitro. These human brain organoids – there are 16 in total – are aimed at developing the world’s first living processor and can be accessed remotely through an online platform for $500 a month if you are a university or educational institution.

The platform was developed by FinalSpark, a Swiss biocomputing startup, which reports that three dozen universities have expressed interest in using their platform. FinalSpark highlights the significant energy savings it could offer in the training and operation of large artificial neural networks, such as those used in large language models. However, this achievement is still a ways off: the project is just in its beginning phases, and co-founder Fred Jordan states that such an ambitious goal can only be achieved through international collaboration.

The biological component uses forebrain organoids derived from human induced pluripotent stem cells. These organoids can survive for years and contain neurons, oligodendrocytes, and astrocytes characteristic of the forebrain region, according to a paper published in the scientific journal Frontiers.

For decades, the study of genetic disease was focused on genes that code for protein. But scientists have now identified a novel neurodevelopmental disorder that is caused by mutations in a gene that does not code for protein, called RNU4-2. These mutations lead to neurological symptoms that cause cognitive dysfunction, but have not previously been linked together as one disease. These findings have been reported in Nature Medicine.

In this work, the investigators analyzed whole-genome sequencing data from over 5,000 cases of intellectual disability and over 46,000 unaffected individuals. The research focused on unusual variations in the sequences of 41,132 genes that do not code for protein. The research revealed a gene that is apparently a common cause of neurodevleopmental problems. The scientists also determined that these mutations often arise spontaneously, and are not usually inherited from a parent.

Researchers at NCI and Memorial Sloan Kettering Cancer Center have developed an artificial intelligence (AI) tool that uses routine clinical data to predict whether someone’s cancer will respond to immune checkpoint inhibitors, a type of immunotherapy drug that helps immune cells kill cancer cells.

AI tool uses routine clinical data to predict whether someone’s cancer will respond to immune checkpoint inhibitors.

Advances in gene editing technology have led to the first successful transplant of a pig kidney into a human.

Joint research led by Yutaro Shuto, Ryoya Nakagawa, and Osamu Nureki of the University of Tokyo determined the spatial structure of various processes of a novel gene-editing tool called “prime editor.” Functional analysis based on these structures also revealed how a “prime editor” could achieve reverse transcription, synthesizing DNA from RNA, without “cutting” both strands of the double helix. Clarifying these molecular mechanisms contributes greatly to designing gene-editing tools accurate enough for gene therapy treatments. The findings were published in the journal Nature.

The 2020 Nobel Prize in Chemistry was awarded to Jennifer Doudna and Emmanuelle Charpentier for developing a groundbreaking yet simple way to edit DNA, the “blueprint” of living organisms. While their discovery opened new avenues for research, the accuracy of the method and safety concerns about “cutting” both strands of DNA limited its use for gene therapy treatments. As such, research has been underway to develop tools that do not have these drawbacks.

The prime editing system is one such tool, a molecule complex consisting of two components. One component is the prime editor, which combines a SpCas9 protein, used in the first CRISPR-Cas gene editing technology, and a reverse transcriptase, an enzyme that transcribes RNA into DNA. The second component is the prime editing guide RNA (pegRNA), a modified guide RNA that identifies the target sequence within the DNA and encodes the desired edit. In this complex, the prime editor works like a “word processor,” accurately replacing genomic information. The tool has already been successfully implemented in living cells of organisms such as plants, zebrafish, and mice. However, precisely how this molecule complex executes each step of the editing process has not been clear, mostly due to a lack of information on its spatial structure.

A small, seemingly unremarkable fern that only grows on a remote Pacific island was on Friday crowned the Guinness World Record holder for having the largest genome of any organism on Earth.

The New Caledonian fern, Tmesipteris oblanceolata, has more than 50 times more DNA packed into the nucleus of its cells than humans do.

If the DNA from one of the fern’s cells – which are just a fraction of a millimetre wide – were unravelled, it would stretch out to 106 metres (350 feet), scientists said in a new study.

Directed with clinical precision by Academy Award winner Robert Wise, this compelling account of the earth’s first biological crisis is perhaps the most chillingly realistic science fiction thriller ever made. After an errant satellite crashes on Earth near a remote New Mexico village, the recovery team discovers that almost everyone in the town are victims of a horrible death, with the mysterious exception of an infant and an old homeless man. The survivors are brought to a state-of-the-art laboratory descending five stories beneath the ground where the puzzled scientists race against time to determine the nature of the deadly microbe before it wreaks worldwide havoc. A trailblazer in the areas of special effects and inventive sets, The Andromeda Strain is based on Michael Crichton’s best-selling novel that created national paranoia for its topical relevance to the first moon landing.

It’s estimated that almost half of the world’s population — about 3.7 billion people under the age of 50 — are infected with (HSV-1), which can cause oral herpes. About half a billion people between the ages of 15 and 49 are infected with herpes simplex virus-2 (HSV-2), the cause of genital herpes. There are therapeutics that can eliminate some symptoms of herpes, like blisters, but there is no cure for the infection, and those who are infected can spread the virus to others. Studies have suggested that HSV-1 may increase the risk of dementia, and HSV-2 raises the risk of HIV infection.

Scientists have now developed a gene therapy that can eliminate as much as 90 percent of oral herpes and 97 percent of genital herpes infections in pre-clinical mouse models. The gene therapy also reduced the level of virus that was released from an individual in a mouse model of the infection. These reductions took about one month to be completed, and more of the virus seemed to be eliminated over time. The work has been reported in Nature Communications.