Lifeboat Foundation

Around the world, people are living longer — not just because child mortality is dropping, but also because we’re staying healthy for more years as we age. In the future, regenerative medicine and other new developments may help most people remain youthful much longer than they do today. In this talk, Aubrey de Grey, Chief Science Officer at the SENS Research Foundation, discusses the biology and sociology of what could be a massive shift in the way we live.

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The macrophages resident in the brain and spinal cord appear to be a key element in the progression of Alzheimer’s disease, according to the results of a new mouse study.

Microglial mayhem

As we age, our immune cells become increasingly dysfunctional; once-helpful cells can behave in harmful ways, promoting persistent inflammation, impairing tissue regeneration, and possibly also facilitating the progression of age-related diseases.

In a recent study, a team of researchers has discovered that a naturally occurring protein called Lipocalin-type prostaglandin D synthase (L-PGDS) prevents, and can destroy, the protein aggregates associated with Alzheimer’s disease.

Surprisingly common and with critical functions

L-PGDS is a common protein, second only to albumin, in the human brain. It provides several critical functions, including regulation of processes and protection against further damage from ischemic strokes. It has been shown to be a molecular chaperone, preventing amyloid beta from forming the deadly aggregates associated with Alzheimer’s, and, perhaps most importantly, it has been shown to destroy aggregates that already exist. Not surprisingly, people who suffer from Alzheimer’s disease lack adequate amounts of this critical protein.

The answer to halting triple-negative breast cancer, the deadliest of all breast cancers, may have just been discovered by researchers from Boston Children’s Hospital.

A CRISPR gene-editing system — all encompassed into a nanogel capsule, that is then injected into the affected person’s body — is the potential antidote to stopping the growth of triple-negative breast cancer tumors.

Continue reading “CRISPR Nanogel Pill Could Be the Answer to Stop Triple-Negative Breast Cancer” »

One way that scientists can non-invasively study the human brain is by growing “mini-brains,” clusters of brain cells each about the size of a pea, in the lab. In a fascinating progression of this line of research, a team this week reports that they observed human-like brainwaves from these organoids.

Previous studies of mini-brains have demonstrated movement and nerve tract development, but the new study from researchers at the University of California San Diego, led by biologist Alysson Muotri, is the first to record human-like neural activity. In their paper, published in Cell Stem Cell on Thursday, the researchers write that they observed brain wave patterns resembling those of a developing human. This sophistication in the in vitro model is a step to enable scientists to use mini-brains to study brain development, model diseases, and learn about the evolution of brains, according to Muotri.

Scientists have created miniature brains from stem cells that developed functional neural networks. Despite being a million times smaller than human brains, these lab-grown brains are the first observed to produce brain waves that resemble those of preterm babies. The study, published August 29 in the journal Cell Stem Cell, could help scientists better understand human brain development.

“The level of neural activity we are seeing is unprecedented in vitro,” says Alysson Muotri, a biologist at the University of California, San Diego. “We are one step closer to have a model that can actually generate these early stages of a sophisticated neural network.”

The pea-sized brains, called cerebral organoids, are derived from human pluripotent stem cells. By putting them in culture that mimics the environment of brain development, the stem cells differentiate into different types of brain cells and self-organize into a 3D structure resembling the developing human brain.

As part of continuing efforts to ensure their vehicles are the safest cars on the road, Tesla’s “Bug Bounty” program gives awards to security researchers that uncover vulnerabilities in the company’s various product systems. Perhaps one of the most impressive parts of that program, however, is Tesla’s ability to remedy the flaws quickly. In the most recent example of their dedication to security, a Bug Bounty find from April this year is now being patched via an over-the-air (OTA) update in 2019.32.

Last year, a Tesla Model S key fob was hacked by a team led by Lennert Wouters of Katholieke Universiteit Leuven in Belgium (KU Leuven). The security flaw enabled would-be car thieves to clone a fob in less than two seconds, after which the vehicle could be driven off. Tesla subsequently offered a multi-part fix: PIN to Drive, a software update, and a new fob. Wouters again found a very similar flaw in the new fob, but this time the fix only required an OTA update which patched both the vehicle software and the fob’s configuration via radio waves.