Singularity HUB

We have no good reason to believe that aliens have ever contacted Earth. Sure, there are conspiracy theories, and some rather strange reports about harm to cattle, but nothing credible. Physicist Enrico Fermi found this odd. His formulation of the puzzle, proposed in the 1950s and now known as the Fermi Paradox, is still key to the search for extraterrestrial life (SETI) and messaging by sending signals into space (METI).

The Earth is about 4.5 billion years old, and life is at least 3.5 billion years old. The paradox states that, given the scale of the universe, favorable conditions for life are likely to have occurred many, many times. So where is everyone? We have good reasons to believe that there must be life out there, but nobody has come to call.

This is an issue that the character Ye Wenjie wrestles with in the first episode of Netflix’s 3 Body Problem. Working at a radio observatory, she does finally receive a message from a member of an alien civilization—telling her they are a pacifist and urging her not to respond to the message or Earth will be attacked.

The series will ultimately offer a detailed, elegant solution to the Fermi Paradox, but we will have to wait until the second season.

Or you can read the second book in Cixin Liu’s series, The Dark Forest. Without spoilers, the explanation set out in the books runs as follows: “The universe is a dark forest. Every civilization is an armed hunter stalking through the trees like a ghost, gently pushing aside branches that block the path and trying to tread without sound.”

Ultimately, everybody is hiding from everyone else. Differential rates of technological progress make an ongoing balance of power impossible, leaving the most rapidly progressing civilizations in a position to wipe out anyone else.

In this ever-threatening environment, those who play the survival game best are the ones who survive longest. We have joined a game which has been going on before our arrival, and the strategy that everyone has learned is to hide. Nobody who knows the game will be foolish enough to contact anyone—or to respond to a message.

Liu has depicted what he calls “the worst of all possible universes,” continuing a trend within Chinese science fiction. He is not saying that our universe is an actual dark forest, with one survival strategy of silence and predation prevailing everywhere, but that such a universe is possible and interesting.

Liu’s dark forest theory is also sufficiently plausible to have reinforced a trend in the scientific discussion in the west—away from worries about mutual incomprehensibility, and towards concerns about direct threat.

We can see its potential influence in the protocol for what to do on first contact that was proposed in 2020 by the prominent astrobiologists Kelly Smith and John Traphagan. “First, do nothing,” they conclude, because doing something could lead to disaster.

In the case of alien contact, Earth should be notified using pre-established signaling rather than anything improvised, they argue. And we should avoid doing anything that might disclose information about who we are. Defensive behavior would show our familiarity with conflict, so that would not be a good idea. Returning messages would give away the location of Earth—also a bad idea.

Again, the Smith and Traphagan thought is not that the dark forest theory is correct. Benevolent aliens really could be out there. The thought is simply that first contact would involve a high civilization-level risk.

This is different from assumptions from a great deal of Russian literature about space of the Soviet era, which suggested that advanced civilizations would necessarily have progressed beyond conflict, and would therefore share a comradely attitude. This no longer seems to be regarded as a plausible guide to protocols for contact.

Misinterpreting Darwin

The interesting thing is that the dark forest theory is almost certainly wrong. Or at least, it is wrong in our universe. It sets up a scenario in which there is a Darwinian process of natural selection, a competition for survival.

Charles Darwin’s account of competition for survival is evidence-based. By contrast, we have absolutely no evidence about alien behavior, or about competition within or between other civilizations. This makes for entertaining guesswork rather than good science, even if we accept the idea that natural selection could operate at group level, at the level of civilizations.

Even if you were to assume the universe did operate in accordance with Darwinian evolution, the argument is questionable. No actual forest is like the dark one. They are noisy places where co-evolution occurs.

Creatures evolve together, in mutual interdependence, and not alone. Parasites depend upon hosts, flowers depend upon birds for pollination. Every creature in a forest depends upon insects. Mutual connection does lead to encounters which are nasty, brutish and short, but it also takes other forms. That is how forests in our world work.

Interestingly, Liu acknowledges this interdependence as a counterpoint to the dark forest theory. The viewer, and the reader, are told repeatedly that “in nature, nothing exists alone”—a quote from Rachel Carson’s Silent Spring (1962). This is a text which tells us that bugs can be our friends and not our enemies.

There are many galaxies out there, and potentially plenty of life. Image Credit: X-ray: NASA/CXC/SAO

In Liu’s story, this is used to explain why some humans immediately go over to the side of the aliens, and why the urge to make contact is so strong, in spite of all the risks. Ye Wenjie ultimately replies to the alien warning.

The Carson allusions do not reinstate the old Russian idea that aliens will be advanced and therefore comradely. But they do help to paint a more varied and realistic picture than the dark forest theory.

For this reason, the dark forest solution to the Fermi Paradox is unconvincing. The fact that we do not hear anyone is just as likely to indicate that they are too far off, or we are listening in all the wrong ways, or else that there is no forest and nothing else to be heard.

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

Image Credit: ESO/A. Ghizzi Panizza (www.albertoghizzipanizza.com)

Some memories last a lifetime. The awe of seeing a full solar eclipse. The first smile you shared with your partner. The glimpse of a beloved pet who just passed away in their sleep.

Other memories, not so much. Few of us remember what we had for lunch a week ago. Why do some memories last, while others fade away?

Surprisingly, the answer may be broken DNA and inflammation in the brain. On the surface, these processes sound utterly detrimental to brain function. Broken DNA strands are usually associated with cancer, and inflammation is linked to aging.

But a new study in mice suggests that breaking and repairing DNA in neurons paves the way for long-lasting memories.

We form memories when electrical signals zap through neurons in the hippocampus, a seahorse-shaped region deep inside the brain. The electrical pulses wire groups of neurons together into networks that encode memories. The signals only capture brief snippets of a treasured experience, yet some can be replayed over and over for decades (although they do gradually decay like a broken record).

Like artificial neural networks, which power most of today’s AI, scientists have long thought that rewiring the brain’s connections happens fast and is prone to changes. But the new study found a subset of neurons that alter their connections to encode long-lasting memories.

To do this, strangely, the neurons recruit proteins that normally fend off bacteria and cause inflammation.

“Inflammation of brain neurons is usually considered to be a bad thing, since it can lead to neurological problems such as Alzheimer’s and Parkinson’s disease,” said study author Dr. Jelena Radulovic at Albert Einstein College of Medicine in a press release. “But our findings suggest that inflammation in certain neurons in the brain’s hippocampal region is essential for making long-lasting memories.”

Should I Stay or Should I Go?

We all have a mental scrapbook for our lives. When playing a memory—the whens, wheres, whos, and whats—our minds transport us through time to relive the experience.

The hippocampus is at the heart of this ability. In the 1950s, a man known as H.M. had his hippocampus removed to treat epilepsy. After the surgery, he retained old memories, but could no longer form new ones, suggesting that the brain region is a hotspot for encoding memories.

But what does DNA have to do with the hippocampus or memory?

It comes down to how brain cells are wired. Neurons connect with each other through little bumps called synapses. Like docks between two opposing shores, synapses pump out chemicals to transmit messages from one neuron to another. Depending on the signals, synapses can form a strong connection to their neighboring neurons, or they can dial down communications.

This ability to rewire the brain is called synaptic plasticity. Scientists have long thought it’s the basis of memory. When learning something new, electrical signals flow through neurons triggering a cascade of molecules. These stimulate genes that restructure the synapse to either bump up or decrease their connection with neighbors. In the hippocampus, this “dial” can rapidly change overall neural network wiring to record new memories.

Synaptic plasticity comes at a cost. Synapses are made up of a collection of proteins produced from DNA inside cells. With new learning, electrical signals from neurons cause temporary snips to DNA inside neurons.

DNA damage isn’t always detrimental. It’s been associated with memory formation since 2021. One study found breakage of our genetic material is widespread in the brain and was surprisingly linked to better memory in mice. After learning a task, mice had more DNA breaks in multiple types of brain cells, hinting that the temporary damage may be part of the brain’s learning and memory process.

But the results were only for brief memories. Do similar mechanisms also drive long-term ones?

“What enables brief experiences, encoded over just seconds, to be replayed again and again during a lifetime remains a mystery,” Drs.  Benjamin Kelvington and Ted Abel at the Iowa Neuroscience Institute, who were not involved in the work, wrote in Nature.

The Memory Omelet

To find an answer, the team used a standard method for assessing memory. They hosted mice in different chambers: Some were comfortable; others gave the critters a tiny electrical zap to the paws, just enough that they disliked the habitat. The mice rapidly learned to prefer the comfortable room.

The team then compared gene expression from mice with a recent memory—roughly four days after the test—to those nearly a month after the stay.

Surprisingly, genes involved in inflammation flared up in addition to those normally associated with synaptic plasticity. Digging deeper, the team found a protein called TLR9. Usually known as part of the body’s first line of defense against dangerous bacteria, TLR9 boosts the body’s immune response against DNA fragments from invading bacteria. Here, however, the gene became highly active in neurons inside the hippocampus—especially those with persistent DNA breaks that last for days.

What does it do? In one test, the team deleted the gene encoding TLR9 in the hippocampus. When challenged with the chamber test, these mice struggled to remember the “dangerous” chamber in a long-term memory test compared to peers with the gene intact.

Interestingly, the team found that TLR9 could sense DNA breakage. Deleting the gene prevented mouse cells from recognizing DNA breaks, causing not just loss of long-term memory, but also overall genomic instability in their neurons.

“One of the most important contributions of this study is the insight into the connection between DNA damage…and the persistent cellular changes associated with long-term memory,” wrote Kelvington and Abel.

Memory Mystery

How long-term memories persist remains a mystery. Immune responses are likely just one aspect.

In 2021, the same team found that net-like structures around neurons are crucial for long-term memory. The new study pinpointed TLR9 as a protein that helps form these structures, providing a molecular mechanism between different brain components that support lasting memories.

The results suggest “we are using our own DNA as a signaling system,” Radulovic told Nature, so that we can “retain information over a long time.”

Lots of questions remain. Does DNA damage predispose certain neurons to the formation of memory-encoding networks? And perhaps more pressing, inflammation is often associated with neurodegenerative disorders, such as Alzheimer’s disease. TLR9, which helped the mice remember dangerous chambers in this study, was previously involved in triggering dementia when expressed in microglia, the brain’s immune cells.

“How is it that, in neurons, activation of TLR9 is crucial for memory formation, whereas, in microglia, it produces neurodegeneration—the antithesis of memory?” asked Kelvington and Abel. “What separates detrimental DNA damage and inflammation from that which is essential for memory?”

Image Credit: geralt / Pixabay