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‘We just discovered the impossible’: how giant baby galaxies are shaking up our understanding of the early Universe
“Look at this,” says Erica’s message. She is poring over the very first images from the brand new James Webb Space Telescope (JWST).

It is July 2022, barely a week after those first images from the revolutionary super telescope were released. Twenty-five years in the making, a hundred to a thousand times more powerful than any previous telescope, one of the biggest and most ambitious scientific experiments in human history: it is hard to not speak in superlatives, and it is all true.

The telescope took decades to build, because it had to be made foldable to fit on top of a rocket and be sent into the coldness of space, 1.5 million kms from Earth. Here, far from the heat glow of the Earth, JWST can detect the faintest infrared light from the distant universe.

Little did I know that among the pictures is a small red dot that will shake up our understanding of how the first galaxies formed after the Big Bang. After months of analysis, my colleagues and I just published our results in Nature.

Hunting new kinds of galaxies

Erica and I are on the hunt to discover new types of galaxies. Galaxies that the venerable Hubble Space Telescope had missed, even after decades of surveying the sky.

She and I go back 15 years. We met when she was a first-year student at a Californian liberal arts college and I was a freshly minted PhD straight out of university, just starting my first gig as a researcher in Los Angeles. JWST was only a distant rumor.

Somehow, many years later, our paths crossed again, and now Assistant Professor Erica Nelson of the University of Colorado and I are finding ourselves at the tip of the spear attacking the first data of a very real JWST.

“UFOs”, she calls the new galaxies, and I can read a giant grin between the lines: “Ultra-red Flattened Objects”, because they all look like flying saucers. In the color images they appear very red because all the light is coming out in the infrared, while the galaxies are invisible at wavelengths humans can see.

Infrared is JWST’s superpower, allowing it to spy the most distant galaxies. Ultraviolet and visible light from the first stars and galaxies that formed after the Big Bang is stretched out by the expansion of the universe as it travels towards us, so by the time the light reaches us we see it as infrared light.

Impossibly early, impossibly massive galaxies

All of Erica’s galaxies look like saucers, except one. I stare at the little red dot on the screen. That is no UFO. And then it hits me: this is something very different. Much more important.

I run the analysis software on the little pinprick and it spits out two numbers: distance 13.1 billion light years, mass 100 billion stars, and I nearly spit out my coffee. We just discovered the impossible. Impossibly early, impossibly massive galaxies.

At this distance, the light took 13 billion years to reach us, so we are seeing the galaxies at a time when the universe was only 700 million years old, barely 5% of its current age of 13.8 billion years. If this is true, this galaxy has formed as many stars as our present-day Milky Way. In record time.

And where there is one, there are more. One day later I had found six.

Images of six candidate massive galaxies, seen 500–800 million years after the Big Bang.NASA / ESA / CSA / I. Labbe, Author provided

Astronomy’s missing link?

Could we have discovered astronomy’s missing link? There has been a long-standing puzzle in galaxy formation. As we look out in space and back in time, we see the “corpses” of fully formed, mature galaxies appear seemingly out of nowhere around 1.5 billion years after the Big Bang.

These galaxies have stopped forming stars. Dead galaxies, we call them, and some astronomers are obsessed with them. The stellar ages of these dead galaxies suggest they must have formed much earlier in the Universe, but Hubble has never been able to spot their earlier, living stages.

Early dead galaxies are truly bizarre creatures, packing as many stars as the Milky Way, but in a size 30 times smaller. Imagine an adult, weighing 100 kilos, but standing 6cm tall. Our little red dots are equally bizarre. They look like baby versions of the same galaxies, also weighing in at 100 kilos, with a height of 6cm.

Too many stars, too early

There is a problem, however. These little red dots have too many stars, too early. Stars form out of hydrogen gas, and fundamental cosmological (“Big Bang”) theory makes hard predictions on how much gas is available to form stars.

To produce these galaxies so quickly, you almost need all the gas in the universe to turn into stars at near 100% efficiency. And that is very hard, which is the scientific term for impossible. This discovery could transform our understanding of how the earliest galaxies in the universe formed.

The six galaxies and their surroundings in the sky. NASA / ESA / CSA / I. Labbe, Author provided

The implication is that there is different channel, a fast track, that produces monster galaxies very quickly, very efficiently. A fast track for the top 1%.

In a way, each of these candidates can be considered a “black swan”. The confirmation of even one would rule out our current “all swans are white” model of galaxy formation, in which all early galaxies grow slowly and gradually.

Checking the fingerprints

The first step to solve this mystery is to confirm the distances with spectroscopy, where we put the light of each of these galaxies through a prism, and split it into its rainbow-like fingerprint. This will tell us the distance to 0.1% accuracy.

It will also tell us what is producing the light, whether it is stars or something else more exotic.

By chance, about a month ago, JWST already targeted one of the six candidate massive galaxies and it turned out to be a distant baby quasar. A quasar is a phenomenon that occurs when gas falls into a supermassive black hole at the centre of a galaxy and starts to shine brightly.

This is really exciting on the one hand, because the origin of supermassive black holes in galaxies is not understood either, and finding baby quasars might just hold the key. On the other hand, quasars can outshine their entire host galaxy, so it is impossible to tell how many stars are there and whether the galaxy is really that massive.

Could that be the answer for all of them? Baby quasars everywhere? Probably not, but it will take another year to investigate the remaining galaxies and find out.

One black swan down, five to go.

Ivo Labbe, ARC Future Fellow / Associate Professor, Swinburne University of Technology

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Up to 40% of FTD cases have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, more than a dozen genes have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment.

I am a researcher who studies the development of FTD and related disorders, including the motor neuron disease amyotrophic lateral sclerosis, or ALS. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases.

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Bruce Willis’ family announced his diagnosis of frontotemporal dementia on Feb. 16, 2023.

Genetic causes of FTD

Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic.

How mutated proteins contribute to FTD has been under intense investigation for decades. For instance, one of the key proteins in FTD, called tau, helps stabilize certain structures in neurons and can form clumps in diseased brains. Another key protein, progranulin, regulates cell growth and a part of the cell called the lysosome that breaks down cellular waste products.

Remarkably, the most common genetic mutation in FTD – in a gene called C9orf72 – also causes ALS. In fact, apart from the mutations in genes that encode for tau and progranulin, most genetic mutations that cause FTD also cause ALS. Another protein, TDP-43, forms clumps in the brains of over 95% of ALS cases and almost half of FTD cases. Thus, these disorders share close links in genetics and pathology.

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Frontotemporal dementia typically affects people under 60.

Modifier genes

The same genetic mutation can cause FTD in one patient, ALS in another or symptoms of both FTD and ALS at the same time. Remarkably, some people who carry these genetic mutations may have no obvious symptoms for decades.

One reason the same mutation can cause both FTD and ALS is that, in addition to lifestyle and environmental factors, other genes may also influence whether mutated genes lead to disease. Identifying these modifier genes in FTD, ALS and other neurodegenerative diseases could lead to new treatment approaches by boosting the activity of those that protect against disease or suppressing the activity of those that promote disease.

Modifier genes have long been a focus of research in my laboratory at the University of Massachusetts Chan Medical School. When my laboratory was still in San Francisco, we collaborated with neurologist Bruce Miller and generated the first stem cell lines from FTD patients with mutations in progranulin and C9orf72. These stem cells can be turned into neurons for researchers to study in a petri dish. My team also uses fruit flies to identify modifier genes and then test how they influence disease in neurons from patients with FTD or ALS.

For instance, in close collaboration with cell biologist J. Paul Taylor, my laboratory was among the first to discover a small subset of modifier genes that help transport molecules into or out of the nucleus of a neuron. We also discovered modifier genes that encode for some proteins that help repair damaged DNA. Targeting these modifier genes using gene-silencing techniques developed by Nobel laureate Craig Mello and other researchers at UMass Chan could offer potential treatments.

Treating behavioral changes in FTD

Because the brain is an extremely complex organ, it can be very difficult to understand what causes personality and behavioral changes in FTD patients.

Over the years, my team has used mice to study the causes of these changes. For instance, we found that the reduced social interaction we observed in mice engineered to have FTD is linked to two different disease proteins in the same part of the brain, suggesting that this symptom may be caused by defects in the same neural circuit. These deficits could be reversed by injecting a molecule called microRNA-124 into the prefrontal cortex, the part of the brain that controls social behaviors.

Moreover, with my longtime collaborator neuroscientist Wei-Dong Yao, our labs found that mice with FTD have defects at the synapses in this part of the brain. Synapses are areas where neurons are in contact with each other and play an important role in transporting information in the nervous system. Recently, he found that lack of empathy in another mouse model of FTD could be reversed by increasing activity in the prefrontal cortex.

Further research to understand the molecular mechanisms and brain circuitry behind FTD offer hope that its devastating symptoms, including behavioral and personality changes, will be treatable in the future.

Fen-Biao Gao, Professor of Neurology, Gov. Paul Cellucci Chair in Neuroscience Research, UMass Chan Medical School

This article is republished from The Conversation under a Creative Commons license. Read the original article.

"You know, it's a very good point," Scarborough said. "The president of the United States, the commander in chief, his preeminent responsibility constitutionally, you know, is to protect this country, protect the country as commander in chief. You can do two things at once. As Brit also said, just because officials show up to get their pictures taken doesn't really mean anything. The question is, what policies are being put in place?"

"Now, listen, could Pete Buttigieg and other officials in the Biden administration gone there sooner?" he added. "Yeah, even Pete Buttigieg says he could have gone there sooner. A lot of them should have gone there sooner. It is just idiocy to be attacking a president of the United States for risking his life, going into a war zone to send a strong message, pushing back against Russian tyranny. I mean, hell, do we go back and look at every time Ronald Reagan was going across the world to push back against communism, to see what disaster was going on in America and criticize him? I didn't hear Republicans do that."

Trump, on the other hand, showed up in East Palestine wearing a "Make America Great Again" hat bragging about the branded water he was donating to the town, and the "Morning Joe" host was disgusted.

"The guy is so gross, he really is, talking about Trump water, branded Trump water," Scarborough said. "By the way, he's such a hypocrite, too, talking about attacking Joe Biden while Joe Biden is going, you know, risking his life fighting for western democracy, something he doesn't give a damn about. The guy who talks about suspending the Constitution. It's just absolutely insane. By the way, where was that guy when there were disasters, when there were train disasters when he was president of the United States? I never saw him out, I never saw him out. Where was he? Why did he decide to go here?"

The goal of the legislation, writes Politico, appears to be to "spark a larger legal battle with the goal of eventually overturning New York Times v. Sullivan, the landmark 1964 U.S. Supreme Court ruling that limits public officials’ ability to sue publishers for defamation."

Seth Stern, director of advocacy for the Freedom of the Press Foundation, tells Politico that he believes the legislation is a flagrant violation of the United States Constitution's First Amendment.

“I have never seen anything remotely like this legislation,” he said. “I can’t say I have seen every bill ever introduced, but I’d be quite surprised if any state Legislature had seriously considered such a brazen and blatantly unconstitutional attack on speech and press freedoms.”

DeSantis has been notoriously combative with non-conservative media outlets and typically only gives interviews with friendly outlets such as Fox News. This bill, however, would take DeSantis' war with the mainstream press out of the realm of public jousting and into the realm of courtrooms.
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