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Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 10:04am

Turns out that DdrC scans for breaks along the DNA and when it detects one it snaps shut—like a mousetrap. This trapping action has two key functions.

It neutralizes it (the DNA damage), and prevents the break from getting damaged further. And it acts like a little molecular beacon. It tells the cell 'Hey, over here. There's damage. Come fix it.

Typically proteins form complicated networks that enable them to carry out a function. DdrC appears to be something of an outlier, in that it performs its function all on its own, without the need for other proteins. The team was curious whether the protein might function as a "plug-in" for other DNA repair systems.

They tested this by adding it to a different bacterium: E. coli. It actually made the bacterium over 40 times more resistant to UV radiation damage. This seems to be a rare example where you have one protein and it really is like a standalone machine.

In theory, this gene could be introduced into any organism—plants, animals, humans—and it should increase the DNA repair efficiency of that organism's cells.

DdrC is just one out of hundreds of potentially useful proteins in this bacterium. The next step is to prod further, look at what else this cell uses to fix its own genome—because  scientists are sure to find many more tools where they have no idea how they work or how they're going to be useful until they look. And they are looking for them now.

Robert Szabla et al, DdrC, a unique DNA repair factor from D. radiodurans, senses and stabilizes DNA breaks through a novel lesion-recognition mechanism, Nucleic Acids Research (2024). DOI: 10.1093/nar/gkae635

Part 2

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 10:00am

Newly discovered protein stops DNA damage

Researchers have discovered a protein that has the never-before-seen ability to stop DNA damage in its tracks. The finding could provide the foundation for developing everything from vaccines against cancer, to crops that can withstand the increasingly harsh growing conditions brought on by climate change.

The researchers found the protein—called DdrC (for DNA Damage Repair Protein C)—in a fairly common bacterium called Deinococcus radiodurans (D. radiodurans), which has the decidedly uncommon ability to survive conditions that damage DNA—for example, 5,000 to 10,000 times the radiation that would kill a regular human cell.  Deinococcus also excels in repairing DNA that has already been damaged.

Newly discovered protein stops DNA damage: Could lead to cancer vaccines and drought-resistant crops

Part 1

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 9:32am

Why do plants wiggle?

Sunflower plants wiggling ( known as  "circumnutations")

Plants don't usually shift around like animals but, instead, move by growing in different directions over time.

Plants naturally and consistently arranged themselves into a zig-zag pattern, almost like the teeth of a zipper. The arrangement likely helps the plants maximize their access to sunlight as a group.

In greenhouse experiments and computer simulations, researchers showed that sunflowers take advantage of circumnutations to search the environment around them for patches of sunlight.

For climbing plants, it's obvious that it's about searching for supports to twine on.

 If they moved with just the right amount of randomness, however, the sunflowers formed that tell-tale zig-zag, which, in real life plants, provides a lot of access to sunlight.

 Chantal Nguyen et al, Noisy Circumnutations Facilitate Self-Organized Shade Avoidance in Sunflowers, Physical Review X (2024). DOI: 10.1103/PhysRevX.14.031027

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 9:08am

Sleep resets neurons for new memories the next day, study finds

While everyone knows that a good night's sleep restores energy, a new  study finds it resets another vital function: memory.

Learning or experiencing new things activates neurons in the hippocampus, a region of the brain vital for memory. Later, while we sleep, those same neurons repeat the same pattern of activity, which is how the brain consolidates those memories that are then stored in a large area called the cortex. But how is it that we can keep learning new things for a lifetime without using up all of our neurons?

A study, "A Hippocampal Circuit Mechanism to Balance Memory Reactivation During Sleep,"  published in Science, finds at certain times during deep sleep, certain parts of the hippocampus go silent, allowing those neurons to reset.

This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day.

The hippocampus is divided into three regions: CA1, CA2 and CA3. CA1 and CA3 are involved in encoding memories related to time and space and are well-studied; less is known about CA2, which the current study found generates this silencing and resetting of the hippocampus during sleep.

The researchers now realized that there are other hippocampal states that happen during sleep where everything is silenced. The CA1 and CA3 regions that had been very active were suddenly quiet. It's a reset of memory, and this state is generated by the middle region, CA2.

Cells called pyramidal neurons are thought to be the active neurons that matter for functional purposes, such as learning. Another type of cell, called interneurons, has different subtypes. The researchers discovered that the brain has parallel circuits regulated by these two types of interneurons—one that regulates memory, the other that allows for resetting of memories.

The researchers think they now have the tools to boost memory, by tinkering with the mechanisms of memory consolidation, which could be applied when memory function falters, such as in Alzheimer's disease. Importantly, they also have evidence for exploring ways to erase negative or traumatic memories, which may then help treat conditions such as post-traumatic stress disorder.

The result helps explain why all animals require sleep, not only to fix memories, but also to reset the brain and keep it working during waking hours. 

 Lindsay A. Karaba et al, A hippocampal circuit mechanism to balance memory reactivation during sleep, Science (2024). DOI: 10.1126/science.ado5708. www.science.org/doi/10.1126/science.ado5708

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 8:59am

The new study focuses on the MEC, but not on the stored information needed for spatial navigation or an animal's current location. Instead, the experiments performed now concentrate on how this brain region creates maps of future positions, which are continuously updated as animals move.

While rats traversed an open square field in search of freely available water that was moved around to different locations, the researchers recorded all movements, which included hundreds of trajectories. At the same time, they recorded the activity of individual brain cells in the MEC.

Afterward, they checked how well the  brain activity over time matched the rats' changing positions.

They found that the activity of some brain cells in the MEC created an internal grid that mapped future positions within the field. For example, an MEC cell might encode a certain location in the field, but only when a rat reached a spot 30 cm to 40 cm earlier in a route that eventually crossed that location—regardless of which direction the rat was coming from.

This is very different from the grid cells that helped win the Nobel Prize, which become active only when an animal is currently in a particular location. The authors call the newly discovered neurons "predictive grid cells," and conducted several follow-up experiments to get a better idea of what exactly they encode.

First, they tested whether the newly discovered grid cells predicted the future location in terms of distance or time from the present. They found that both were encoded, although the "gridness" of the cells was higher when considering distance.

They also found that future positions were faithfully encoded in different situations, whether the rats were trying to go to specific targets or if they were randomly foraging for food. This means that the function of the predictive grid cells is not limited to goal-directed behavior.

This study provides important insights into the mechanisms of spatial navigation and episodic memory formation in hippocampal and entorhinal cortical circuits.

Ayako Ouchi et al, Predictive grid coding in the medial entorhinal cortex, Science (2024). DOI: 10.1126/science.ado4166. www.science.org/doi/10.1126/science.ado4166

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 8:54am

Navigating the future: Brain cells that plan where to go

Researchers  have discovered a region of the brain that encodes where an animal is planning to be in the near future. Linked to internal maps of spatial locations and past movements, activity in the newly discovered grid cells accurately predicts future locations as an animal travels around its environment.

Published in Science on August 15, the study helps explain how planned spatial navigation is possible.

It might seem effortless, but navigating the world requires quite a bit of under-the-hood brain activity. For example, simply walking around a supermarket picking up groceries requires internalized maps of the outside world, information about one's own changing position and speed, and memories about where one has been and what one is trying to buy.

Much of this kind of information is contained in cells within two connected parts of the brain—the hippocampus and the medial entorhinal cortex, or MEC for short—which are extremely similar in all mammals, from rats to humans. In particular, the MEC contains maps of an animal's current location in space, a discovery that won the Nobel Prize for Physiology or Medicine in 2014.

Prediction grid cells in the medial entorhinal cortex became active before rats entered the region of space that they encode. In this video, activity of two neurons is represented by the flashing of red and blue squares. for convenience, the squares are placed in the location of the grid that the neurons encode. Credit: RIKEN

Part 1

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 8:31am

Cleaning up the aging brain: Scientists restore brain's waste removal system

Alzheimer's, Parkinson's, and other neurological disorders can be seen as "dirty brain" diseases, where the brain struggles to clear out harmful waste. Aging is a key risk factor because, as we grow older, our brain's ability to remove toxic buildup slows down. However, new research in mice demonstrates that it's possible to reverse age-related effects and restore the brain's waste-clearing process.

This research work shows that restoring cervical lymph vessel function can substantially rescue the slower removal of waste from the brain associated with age. Moreover, this was accomplished with a drug already being used clinically, offering a potential treatment strategy.

First described by Nedergaard and her colleagues in 2012, the glymphatic system is the brain's unique waste removal process that uses cerebrospinal fluid (CSF) to wash away excess proteins generated by energy hungry neurons and other cells in the brain during normal activity. This discovery pointed the way for potential new approaches to treat diseases commonly associated with the accumulation of protein waste in the brain, such as Alzheimer's (beta amyloid and tau) and Parkinson's (alpha-synuclein).

In healthy and young brains, the glymphatic system does a good job of flushing away these toxic proteins. However, as we age, this system slows, setting the stage for these diseases.

Once laden with protein waste, CSF in the skull needs to make its way to the lymphatic system and ultimately the kidneys, where it is processed along with the body's other waste. The new research combines advanced imaging and particle tracking techniques to describe for the first time in detail the route via the cervical lymph vessels in the neck through which half of dirty CSF exits the brain.

In addition to measuring the flow of CSF, the researchers were able to observe and record the pulsing of lymph vessels in the neck that helps draw CSF out of the brain.

Unlike the cardiovascular system which has one big pump, the heart, fluid in the lymphatic system is instead transported by a network of tiny pumps. These microscopic pumps, called lymphangions, have valves to prevent backflow and are strung together, one after another, to form lymph vessels.

The researchers found that as the mice aged, the frequency of contractions decreased, and the valves failed. As a result, the speed of dirty CSF flowing out of the brains of older mice was 63 percent slower compared to younger animals.

The team then set out to see if they could revive the lymphangions and identified a drug called prostaglandin F2α, a hormone-like compound commonly used medically to induce labor and known to aid smooth muscle contraction. The lymphangions are lined with smooth muscle cells, and when the researchers applied the drug to the cervical lymph vessels in older mice, the frequency of contractions and the flow of dirty CSF from the brain both increased, returning to a level of efficiency found in younger mice.

These vessels are conveniently located near the surface of the skin, scientists know they are important, and they now know how to accelerate function. They can see how this approach, perhaps combined with other interventions, could be the basis for future therapies for these diseases.

Restoration of cervical lymphatic vessel function in aging rescues cerebrospinal fluid drainage, Nature Aging (2024). DOI: 10.1038/s43587-024-00691-3

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 8:19am

By mapping out the evolving roles of various cell types involved in regeneration, Mokalled and her colleagues found that the flexibility of the surviving injured neurons and their capacity to immediately reprogram after injury lead the chain of events that are required for spinal cord regeneration.

If these injury-surviving neurons are disabled, zebrafish do not regain their normal swim capacity, even though regenerative stem cells remain present.

When the long wiring of the spinal cord is crushed or severed in people and other mammals, it sets off a chain of toxicity events that kills the neurons and makes the spinal cord environment hostile against repair mechanisms.

This neuronal toxicity could provide some explanation for the failure of attempts to harness stem cells to treat spinal cord injuries in people. Rather than focus on regeneration with stem cells, the new study suggests that any successful method to heal spinal cord injuries in people must start with saving the injured neurons from death.

Neurons by themselves, without connections to other cells, do not survive.

In zebrafish, researchers think severed neurons can overcome the stress of injury because their flexibility helps them establish new local connections immediately after injury. This research work suggests this is a temporary mechanism that buys time, protecting neurons from death and allowing the system to preserve neuronal circuitry while building and regenerating the main spinal cord.

There is some evidence that this capacity is present but dormant in mammalian neurons, so this may be a route to new therapies, according to the researchers.

They  are hopeful that identifying the genes that orchestrate this protective process in zebrafish—versions of which also are present in the human genome —will help us find ways to protect neurons in people from the waves of cell death that we see following spinal cord injuries.

Zebrafish use surprising strategy to regrow spinal cord, Nature Communications (2024). DOI: 10.1038/s41467-024-50628-y

Part 2

Comment by Dr. Krishna Kumari Challa on August 16, 2024 at 8:16am

Zebrafish use surprising strategy to regrow spinal cord: Findings could help identify ways to heal spinal cord damage

Zebrafish are members of a rarefied group of vertebrates capable of fully healing a severed spinal cord. A clear understanding of how this regeneration takes place could provide clues toward strategies for healing spinal cord injuries in people. Such injuries can be devastating, causing permanent loss of sensation and movement.

A new study maps out a detailed atlas of all the cells involved—and how they work together—in regenerating the zebrafish spinal cord.

In an unexpected finding, the researchers showed that survival and adaptability of the severed neurons themselves is required for full spinal cord regeneration. Surprisingly, the study showed that stem cells capable of forming new neurons—and typically thought of as central to regeneration—play a complementary role but don't lead the process.

Unlike humans' and other mammals' spinal cord injuries, in which damaged neurons always die, the damaged neurons of zebrafish dramatically alter their cellular functions in response to injury, first to survive and then to take on new and central roles in orchestrating the precise events that govern healing, the researchers found. Scientists knew that zebrafish neurons survive spinal cord injury, and this new study reveals how they do it.

The surprising observation the researchers made is that there are strong neuronal protection and repair mechanisms happening right after injury. They think these protective mechanisms allow neurons to survive the injury and then adopt a kind of spontaneous plasticity—or flexibility in their functions—that gives the fish time to regenerate new neurons to achieve full recovery.

This study has identified genetic targets that will help researchers promote this type of plasticity in the cells of people and other mammals.

Part 1

Comment by Dr. Krishna Kumari Challa on August 15, 2024 at 11:04am

WHO declares mpox outbreaks in Africa a global health emergency as a new form of the virus spreads

The World Health Organization declared the mpox outbreaks in Congo and elsewhere in Africa a global emergency on Wednesday, with cases confirmed among children and adults in more than a dozen countries and a new form of the virus spreading. Few vaccine doses are available on the continent.

Earlier this week, the Africa Centers for Disease Control and Prevention announced that the mpox outbreaks were a public health emergency, with more than 500 deaths, and called for international help to stop the virus' spread.

The Africa CDC previously said mpox, also known as monkeypox, has been detected in 13 countries this year, and more than 96% of all cases and deaths are in Congo. Cases are up 160% and deaths are up 19% compared with the same period last year. So far, there have been more than 14,000 cases and 524 people have died.

Source: various news agencies

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