TEHRAN (Iran News)  Researchers found that during sleep, the brain consolidates memories by repeating patterns of neuronal activity in the hippocampus, which are stored in the cortex.

The study, titled “A Hippocampal Circuit Mechanism to Balance Memory Reactivation During Sleep,” demonstrates that certain parts of the hippocampus go silent at specific times during deep sleep, allowing neurons to reset.

“This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day,” explained Azahara Oliva, assistant professor of neurobiology and behavior and the study’s corresponding author.

The hippocampus, divided into three regions—CA1, CA2, and CA3—has been well studied in areas CA1 and CA3, which are involved in encoding memories related to time and space. However, the study highlights the less understood CA2 region, which appears to generate the silencing and resetting of the hippocampus during sleep.

Using implanted electrodes in the hippocampi of mice, researchers observed neuronal activity during learning and sleep. They found that during sleep, neurons in the CA1 and CA3 regions reproduced the same patterns developed during learning. However, the researchers also noted periods when these regions became silent, allowing for memory reset.

“We realized there are other hippocampal states that happen during sleep where everything is silenced,” said Oliva. “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.”

The study also uncovered that the brain has parallel circuits regulated by two types of interneurons—one responsible for memory regulation and the other for memory resetting.

Researchers believe this understanding could lead to ways to enhance memory or even erase traumatic memories, which could benefit conditions like Alzheimer’s disease and post-traumatic stress disorder.

The findings provide insight into why sleep is essential for maintaining cognitive function and memory, with Oliva noting, “We show that memory is a dynamic process.”

The study was funded by the National Institutes of Health, a Sloan Fellowship, a Whitehall Research Grant, a Klingenstein-Simons Fellowship, and a New Frontiers Grant.

It has been more than 10 years in the making, but scientists are preparing to implant a ‘bionic eye’ in a human subject.

Researchers at Monash University have developed wireless implants that sit on the surface of the brain, which are said to restore vision to the blind, the Daily Mail reported.

Called Gennaris bionic vision system, it includes a custom headgear fitted with a camera and wireless transmitter, a vision processor unit and software and a set of 9×9 millimeter tiles that are implanted into the brain.

Studies of the device, used in sheep, were found to be successful and did not produce any adverse health effects.

The team is currently seeking funding to ramp up manufacturing and distribution of the implant, which they say could soon be used to cure other ailments including paralysis.

The Australian scientists are just one of many working towards connecting the brain to a computer, as Elon Musk has also been designing a chip that he demonstrated in pigs recently.

Monash University began designing its ‘Gennaris bionic vision system’ more than a decade ago, which is a ‘world’s first’ brain implant aimed at restoring site – and it is being prepared for human trials.

The Gennaris bionic vision system is capable of bypassing damaged optic nerves, which are blocking signals being sent from the retina to the ‘vision center’ of the brain.

The design includes a custom headgear fitted with a camera and wireless transmitter, a vision processor unit and software, and a set of 9×9 millimeter tiles that are implanted into the brain.

The attached camera captures the user’s surrounding scene and sends it to the vision processor where the technology extracts data from the transmission.

This then flows to the complex circuitry in each of the implants and is converted into a pattern of electrical pulses that stimulates the brain using microelectrodes.

Professor Lowery, also from the University’s Department of Electrical and Computer Systems Engineering, said: ‘Cortical vision prostheses aim to restore visual perception to those who have lost vision by delivering electrical stimulation to the visual cortex – the region of the brain that receives, integrates and processes visual information.’

‘Our design creates a visual pattern from combinations of up to 172 spots of light (phosphenes) which provides information for the individual to navigate indoor and outdoor environments, and recognize the presence of people and objects around them.’

The team received $1 million in funding last year and is raising another round that is due to occur later this year.

‘If successful, the MVG team will look to create a new commercial enterprise focused on providing vision to people with untreatable blindness and movement to the arms of people paralyzed by quadriplegia, transforming their health care,’ Dr Lewis said.

With the bionic vision system moving into commercial stages, the team is hopefully it could evolve to cure other aliments other than blindness.

Dr. Yan Wong from the Monash Biomedicine Discovery Institute said: ‘The commercialization of the bionic vision technology also ties in nicely to our plans for exploring further applications beyond vision and spinal cord injury, such as the moderation of epilepsy and depression, brain-controlled prosthetics, and the restoration of other vital senses.

‘It aligns with our capabilities in neurobionics at Monash University, and having an engaged industry partner to work alongside will be of enormous value.’

In preclinical studies, the team implanted 10 devices in sheep using a purpose-built insertion system.

Stimulation was delivered through the seven active devices for up to nine months and more than 2,700 hours of stimulation was performed without any observable adverse health effects.

SpaceX and Tesla CEO Elon Musk has been working tirelessly on a similar device through his brain chip startup Neuralink, which he demonstrated in August.

The three little pig’s demo, as he called it, showed an animal named Gertrude with the brain implant. While she snuffed around in a pen, viewers saw her brain activity on a large screen.

When plans to develop the brain-computer interface were first revealed, the firm positioned it as a way to enable people with quadriplegia to control technologies, like a computer or smartphone, with their mind.

However, as many of Musk’s ventures evolve the system developed into much more.

He touched on the idea of ‘conceptual telepathy,’ which allows two individuals to communicate through thoughts with the help of technology.

Forgetfulness and age-related memory lapses are a common complaint for many older adults, but what is still not understood is what causes these changes.

Recent research published by scientists at Baycrest’s Rotman Research Institute (RRI) brings us a step closer to uncovering the answer, which could help with distinguishing signs of dementia earlier.

The study, published in the journal Neuropsychologia, found that among older adults, there is a much weaker relationship between what their eyes see and their brain activity.

“Eye movements are important for gathering information from the world and the memory centre of the brain—the hippocampus—is important for binding this data together to form a memory of what our eyes see,” says Dr. Jennifer Ryan, RRI senior scientist and Reva James Leeds Chair in Neuroscience and Research Leadership. “But we found that older adults are not building up the memory in the same way as younger adults. Something is falling apart somewhere along the path of taking in visual information through the eyes and storing what is seen into a memory.”

Previously, Baycrest researchers had identified a connection between what we see and how we remember—when the eyes view and process more details of an object in front of them, there is more brain activity in the memory centre of the brain. When the object is seen multiple times, there is a progressive drop in hippocampus activity, indicating that what is seen is no longer new information. But this doesn’t happen with older adults.

In the latest study, researchers found that older adults exhibited greater eye movements, but there isn’t a corresponding pattern in brain activity.

“These findings demonstrate that the eyes and brain are taking in information from their surroundings, but the linkage aspect of creating a memory appears to be broken,” adds Dr. Ryan, who is also a psychology professor at the University of Toronto. “When the memory isn’t being created, the object continues to remain unfamiliar to a person, even when they have seen it multiple times.”

The study was conducted with 21 older adults (between the ages of 64 and 79) and 20 younger adults (between the ages of 19 and 28). Research participants were briefly shown faces on a screen where some of the images were displayed multiple times. Researchers analyzed the eye movements and brain scans of individuals as they looked at and analyzed the pictures.

As next steps, researchers will continue exploring the triggers of eye movements and related activity in the brain, which could be used to help predict earlier cognitive decline in Alzheimer’s disease or other related dementias.

A recent study by the University of Bonn at least points in this direction. If the sensor fails, chronic inflammation may result — probably the beginning of a dangerous vicious circle. The publication appears in the journal Frontiers in Molecular Neuroscience.

The activity of the so-called microglial cells plays an important role in brain aging. These cells are part of the brain’s immune defense: For example, they detect and digest bacteria, but also eliminate diseased or defective nerve cells. They also use messenger substances to alert other defense cells and thus initiate a concerted campaign to protect the brain: an inflammation.

This protective mechanism has undesirable side effects; it can also cause damage to healthy brain tissue. Inflammations are therefore usually strictly controlled, Science Daily reported.

“We know that so-called endocannabinoids play an important role in this,” explains Dr. Andras Bilkei-Gorzo from the Institute of Molecular Psychiatry at the University of Bonn. “These are messenger substances produced by the body that act as a kind of brake signal: They prevent the inflammatory activity of the glial cells.”

Endocannabinoids develop their effect by binding to special receptors. There are two different types, called CB1 and CB2. “However, microglial cells have virtually no CB1 and very low level of CB2 receptors,” emphasizes Bilkei-Gorzo. “They are therefore deaf on the CB1 ear. And yet they react to the corresponding brake signals — why this is the case, has been puzzling so far.”

Neurons as “middlemen”

The scientists at the University of Bonn have now been able to shed light on this puzzle. Their findings indicate that the brake signals do not communicate directly with the glial cells, but via middlemen — a certain group of neurons, because this group has a large number of CB1 receptors. “We have studied laboratory mice in which the receptor in these neurons was switched off,” explains Bilkei-Gorzo. “The inflammatory activity of the microglial cells was permanently increased in these animals.”

In contrast, in control mice with functional CB1 receptors, the brain’s own defense forces were normally inactive. This only changed in the present of inflammatory stimulus. “Based on our results, we assume that CB1 receptors on neurons control the activity of microglial cells,” said Bilkei-Gorzo. “However, we cannot yet say whether this is also the case in humans.”

This is how it might work in mice: As soon as microglial cells detect a bacterial attack or neuronal damage, they switch to inflammation mode. They produce endocannabinoids, which activate the CB1 receptor of the neurons in their vicinity. This way, they inform the nerve cells about their presence and activity. The neurons may then be able to limit the immune response. The scientists were able to show that neurons similarly regulatory the other major glial cell type, the astroglial cells.

During ageing the production of cannabinoids declines reaching a low level in old individuals. This could lead to a kind of vicious circle, Bilkei-Gorzo suspects: “Since the neuronal CB1 receptors are no longer sufficiently activated, the glial cells are almost constantly in inflammatory mode. More regulatory neurons die as a result, so the immune response is less regulated and may become free-running.”

It may be possible to break this vicious circle with drugs in the future. It is for instance hoped that cannabis will help slow the progression of dementia. Its ingredient, tetrahydrocannabinol (THC), is a powerful CB1 receptor activator — even in low doses free from intoxicating effect. Last year, the researchers from Bonn and colleagues from Israel were able to demonstrate that cannabis can reverse the aging processes in the brains of mice. This result now suggest that an anti-inflammatory effect of THC may play a role in its positive effect on the ageing brain.

“What we’ve discovered is that if we free up that DNA again, now the aging brain can form long-term memories normally,” said senior author Marcelo Wood, UCI’s Francisco J. Ayala Chair in Neurobiology & Behavior, who will present the findings at the American Association for the Advancement of Science’s annual meeting, in Austin, Texas.

“In order to form a long-term memory, you have to turn specific genes on. In most young brains, that happens easily, but as we get older and our brain gets older, we have trouble with that.”

That’s because the 6 feet of DNA spooled tightly into every cell in our bodies has a harder time releasing itself as needed, he explained. Like many body parts, “it’s no longer as flexible as it used to be.”

The stiffness in this case is due to a molecular brake pad called histone deacetylase 3, or HDAC3, that has become “overeager” in the aged brain and is compacting the material too hard, blocking the release of a gene called Period1. Removing HDAC3 restores flexibility and allows internal cell machinery to access Period1 to begin forming new memories.

Researchers had previously theorized that the loss of transcription and encoding functions in older brains was due to deteriorating core circadian clocks. But Wood and his team, notably postdoctoral fellow Janine Kwapis, found that the ability to create lasting memories was linked to a different process — the overly aggressive enzyme blocking the release of Period1 — in the same hippocampus region of the brain, Science Daily reported.

That’s potentially good news for developing treatments. “New drugs targeting HDAC3 could provide an exciting avenue to allow older people to improve memory formation,” Wood said.

A discovery made by Junhwan Kim, PhD, assistant professor at The Feinstein Institute for Medical Research, is challenging science’s longstanding beliefs regarding the cellular makeup of the brain. This breakthrough was outlined in a study recently published in the journal Molecular and Cellular Biochemistry. Having a full understanding of the brain can help identify new therapies as well as develop guidelines to maintain brain health.

It has long been a belief in the scientific field that the building blocks of brain cells, phospholipids, are enriched by polyunsaturated fatty acids. When trying to prove that the brain, like other major organs, are made of polyunsaturated fatty acids, Dr. Kim and his team were surprised by the results.

“We found the opposite of what science has widely believed — phospholipids containing polyunsaturated fatty acids in the brain are lower than other major organs,” said Dr. Kim. “Knowing that there are lower amounts of polyunsaturated fatty acids in the brain, we may need to rethink how this acid impacts brain health and conditions like oxygen deprivation.”

Dr. Kim and his team analyzed brain, heart, liver and kidney tissue from animals and found that only 60 percent of the brain’s phospholipids were made up of polyunsaturated fatty acids. That’s compared to other organs, where the polyunsaturated fatty acid content is about 90 percent. It has also been previously presumed that high polyunsaturated fatty acids levels in the brain were what made it susceptible to oxygen deprivation or brain injury.

Further research is required to find out the reasoning for the difference in acid levels, but it could also challenge beliefs about polyunsaturated fatty acids’ impact on these conditions, Science Daily reported.

“Dr. Kim’s findings challenge basic assumptions about the brain,” said Kevin J. Tracey, MD, president and CEO of the Feinstein Institute. “This paper is an important step to defining a new research path.”