Tag Archives: hippocampus

Mice can develop neural signs of depression when forced to watch other mice experiencing stress

Depression is a global problem, affecting an ever-growing number of individuals. In a bid to better understand its physiological underpinnings, a team from the Tokyo University of Science has explored how neural deterioration in areas of the brain such as the hippocampus, as well as physical and psychological stress, is tied to depression.

Image credits Tibor Janosi Mozes.

There are several theories regarding why and how depression emerges, both from psychological and physiological factors. In regards to the latter, the “neurogenic hypothesis of depression” has garnered a lot of scientific interest. It states that depression can stem from physical degradation in areas of the brain such as the hippocampus, degradation which can be incurred by stress.

While the link between physical stress and depression has been investigated in the past, much less is known about the effects of psychological stress. A new study aims to give us a better understanding of this topic, using mice as a model organism.

A grinding toll

“The number of individuals suffering from depression has been on the rise the world over. However, the detailed pathophysiology of depression still remains to be elucidated. So, we decided to focus on the possible mechanism of psychological stress in adult hippocampal neurogenesis, to understand its role in depressive disorders,” says Prof. Akiyoshi Saitoh from Tokyo University of Science, co-lead author of the study.

“We have found out that chronic mental stress affects the neurogenesis of the hippocampal dentate gyrus. Also, we believe that this animal model will play an important role in elucidating the pathophysiology of depression, and in the development of corresponding novel drug.”

For the study, the team exposed mice to “repeated psychological stress” in order to test how this impacts hippocampus degeneration in their brains. The experiment consisted of making the mice experience chronic social defeat stress (cSDS) via their peers — a source of psychological stress for the animals, as they are a highly social species. Chronic social defeat stress is an experimental tool through which stress is induced in a subject (such as a mouse), the ‘naive mouse’ to ‘aggressor’ mice. As part of this research, the mice were made to witness the naive mice, who were participating in the stressful situation.

After this exposure, the team analyzed their brains to measure the level of degradation it produced in key brain areas, as well as noting changes in behavior.

First off, they report that the mice exposed to this repeated source of stress started exhibiting behavioral issues such as social withdrawal, indicative of depression. In their brains, more specifically the dentate gyrus area of the hippocampus, the team recorded a decreased survival rate of new-born neurons compared to those of controls. This area is heavily involved in memory and sensory perception.

Lower new-born neuron survival rates persisted for up to four weeks after the animals were exposed to the stress-inducing scenarios. Chronic treatment with antidepressant fluoxetine was efficient in restoring neuronal survival rates for these mice. Other characteristics, such as cell growth, differentiation, and maturation rates were not impacted by stress in the experimental mice (as compared to controls), the team adds.

The authors link neural degradation in the hippocampus to the emergence of depression through the fact that avoidance behaviors in the experimental mice was “significantly enhanced” 4 weeks after the last stress-inducing exercise, compared to the first day after it. This behavior, they explain, is likely produced by degradation mounting in neurons of the hippocampus following the experience.

Although these findings have not yet been validated in humans, the authors believe that they can form an important part of understanding how depression emerges in the brain even among us. Further work is needed to validate the results and see whether they translate well to humans, however.

The paper “Chronic vicarious social defeat stress attenuates new-born neuronal cell survival in mouse hippocampus” has been published in the journal Behavioural Brain Research.

Western junk-food diet can slow down your brain and make you eat even more junk

Switching from a healthy diet to a western diet (high fat, high added sugar) for a little as one week can significantly impair cognitive function and encourage people to eat more even when they’re full.

Disruption in the hippocampus, a region that is known to have a major role in learning and memory, seems to be the likely cause.

Credit: Pixabay.

It’s not the first time something like this has been suggested. Research in the past found that when animals are fed a Western-style diet (rich in saturated fat and added sugar), they show impairment in memory and learning tests. There is a growing body of evidence suggesting that the same conclusion applies to humans and that hippocampal lesions can deregulate a person’s appetite.

Psychologists at Macquarie University in Sydney wanted to put this to the test and enlisted 110 young, lean students, aged 20 to 23, who generally ate a healthy diet.

Half of the students were randomly assigned to a junk food diet for an entire week, while the other half carried on with their normal diet.

The participants in the Western-style diet group had to have a breakfast of a toasted sandwich and a milkshake, high in saturated fat and added sugar, or Belgian waffles, as well as one main meal and a dessert from a popular fast-food chain. Bearing these changes aside, the students were asked to otherwise maintain their normal diet and lifestyle.

At the end of the study, the researchers found that those on the Western-style diet had an appetite for palatable food such as snacks and chocolate even when they were full. They also scored worse on memory tests.

“When we see cake, chocolate or crisps, for example, we remember how nice they are to eat.  When we are full the hippocampus normally supresses these memories, reducing our desire to eat.  We found that lean healthy young people exposed to one week of a junk food diet developed impaired hippocampal function and relatively greater desire to eat junk food when full.  Junk food may then act to undermine self-control by increasing desire,” the researchers stated in a press release.

These results seem to indicate that junk food might cause disruption in the hippocampus, impairing memory and making it harder to resist the temptation to eat even more junk food, which in turn generates more damage to the hippocampus and triggers a vicious cycle of overeating. The more people craved for palatable food when full, the more impaired their hippocampal function was, judging from memory tests.

“More broadly, this experiment, alongside those from the other animal and human studies cited here, suggests that a WS-diet causes neurocognitive impairments following short-term exposure,” the authors concluded.

Western-style diets, characterized by foods high in sugar, salt, and fat, as well as protein from red meat (i.e. burgers, processed meat, ready meals, fries, etc), have been previously associated with the development of obesity-related diseases such as type 2 diabetes, cardiovascular disease, and high blood pressure.

The authors of the new study, which was published in Royal Society Open Science, think that there will come a time when authorities will be pressured to impose restrictions on processed food, similarly to how some policies in place today deter smoking and drinking alcohol.

Another study published last month showed how sugar can trigger changes in the brain similarly to an addiction. After just 12 days of being on a high sugar diet, participants suffered major changes in the brain’s dopamine and opioid systems.

Old photographs.

The hippocampus is the curator of our memories, new study suggests

A new study is looking into how our minds ‘auto-complete’ memories. The mastermind behind all that, turns out, is the hippocampus.

Old photographs.

Image credits Karolina Grabowska.

Our brains split memories into a bundle of different types of data: what happened, where it happened, what we were feeling at the time. These disparate elements tie together into a congruent whole as a memory pops back up into our minds. Look at a picture you’ve taken at the beach, for example, and you can almost feel the scent of sea spray and sunscreen. We don’t actively work to recall these bits, but our minds supply it anyway — akin to a memory ‘auto-complete function’.

Needs more context

A new collaborative study between the Universities of Birmingham and Bonn analyzed the mechanisms underpinning this automated recall feature in a bid to help us better understand memory.

For the study, the team worked with 16 patients at the University Clinic of Epileptology in Bonn — one of Europe’s biggest epilepsy centers. The clinic specializes in the treatment of severe forms of temporal lobe epilepsy. As part of this, some patients have electrodes implanted into their brains (so the doctors can identify exactly which areas cause the seizures to have them removed). Of course, people aren’t thrilled to have anything implanted into their brain, so this gave researchers a rare opportunity to tap into our pound of gray matter.

They showed the participants a range of scene images. Each was paired with one of two different objects — either a raspberry or a scorpion. Participants were allowed 3 seconds to memorize each image-object combination. Following a short break, they were shown the images again and asked to recall the objects they were paired within in the initial phase. The control group only had to remember the scene images and not their associated objects. All the while, the team monitored participants’ patterns of brain activity.

“We focused on two brain regions — the hippocampus and the neighbouring entorhinal cortex,” explains Prof. Florian Mormann, who heads the Cognitive and Clinical Neurophysiology group at the University of Bonn Medical Centre.

The hippocampus has been documented to play a role in associative memory (which is what this study focused on) but we still have very little idea of how it fulfills this task. The team was able to find that neurons in the hippocampus activate start firing dramatically during memory recall. The same was observed in the control group. However, this activity persisted much longer for the experimental group than it did for the controls, and the former also showed activation in the entorhinal cortex in parallel to the hippocampus.

Hippocampus.

The hippocampus is highlighted.
Image credits Anatomography / Life Science Databases.

The team further reports that this similarity (between recall and learning) was so striking that a computer algorithm they devised could tell whether a participant was remembering the raspberry or the scorpion.

“The pattern of activation in the entorhinal cortex during successful recall strongly resembled the pattern of activation during the initial learning of the objects,” explains Dr. Bernhard Staresina from the University of Birmingham.

“We call this process reinstatement. The act of remembering put neurons in a state that strongly resembles their activation during initial learning.”

This reinstatement process, the team believes, is governed by neurons in the hippocampus. In effect, they act like hiperlinks in a Wikipedia article, guiding the rest of the brain to wherever a particular memory it wants is stored.

The paper “Recollection in the human hippocampal-entorhinal cell circuitry” has been published in the journal Nature Communications.

Hippocampus.

Researchers identify clump of neurons that block, or allow, frightful memories into our minds

New research is looking into the cells that block, or allow, frightening memories to pop up into our minds.

Hippocampus.

Image credits Henry Gray / Anatomy of the Human Body (1918) via Wikimedia.

Researchers at The University of Texas at Austin have identified the group of neurons that handle scary, recurrent memories. The findings could help us better tailor therapy for the treatment of anxiety, phobias, and post-traumatic stress disorder (PTSD).

Frightful relapse

“There is frequently a relapse of the original fear, but we knew very little about the mechanisms,” said Michael Drew, associate professor of neuroscience and the senior author of the study. “These kinds of studies can help us understand the potential cause of disorders, like anxiety and PTSD, and they can also help us understand potential treatments.”

Drew and his team worked with a group of lab mice, which they trained to associate a distinctive box with fear. Each mouse was repeatedly placed inside the box and given a harmless electrical shock until they started associating this box with feelings of pain. Needless to say, this rendered the mice quite scared of having to go inside said box.

The end result was that the mice would display fear when inside the box. In the second step of the experiment, the same mice were placed inside the box without receiving the shock. They kept displaying fear initially, the team reports. However, as exposure to the box continued without the shock being administered, the association weakened. Eventually, the mice stopped showing signs of fear. The authors explain that repeated exposure without the painful shock created extinction memories in the mice’s minds in place of the earlier, painful and fear-inducing memories.

This is a glimpse of how our brain stores and handles conditioned responses, a process which has been heavily studied and documented ever since Pavlov and his drooling dogs. However, there are still things we don’t understand. Among these, and something the team wanted to understand, is how and why memories or responses we thought were behind us can still pop up in our minds, triggering spontaneous recovery (think of it as a form of traumatic-memory relapse).

In order to find out, they artificially activated fear responses and suppressed extinction trace memories through the use of optogenetics (a technique that uses light to turn neurons on or off).

“Artificially suppressing these so-called extinction neurons causes fear to relapse, whereas stimulating them prevents fear relapse,” Drew said. “These experiments reveal potential avenues for suppressing maladaptive fear and preventing relapse.”

Drew’s team was surprised to find that the brain cells responsible for suppressing or allowing fear memories to surface are nestled in the hippocampus. The traditional view is that fear is born of the amygdala, the primitive ‘lizard’ level of our brains. The hippocampus is actually heavily involved in aspects of memory, but generally in the process of linking memory with spatial navigation. The team’s hypothesis is that the hippocampus’ job is to provide spatial context for memories, i.e. where something happened or how you got there.

Their findings could, therefore, explain why exposure therapy — one of the most common treatment avenues for fear-based disorders — sometimes simply stops working. Exposure therapy works by creating safe (extinction) memories to override the initial, traumatic one. For example, someone who’s scared of spiders after being bitten by one can undertake exposure therapy by letting a harmless spider crawl on his hand.

While the approach is sound, the team reports, it hinges on our hippocampus‘ willingness to play ball.

“Extinction does not erase the original fear memory but instead creates a new memory that inhibits or competes with the original fear,” Drew said.

“Our paper demonstrates that the hippocampus generates memory traces of both fear and extinction, and competition between these hippocampal traces determines whether fear is expressed or suppressed.”

The findings suggest we should revisit how we time exposure therapy, and how frequently patients should undergo exposure sessions, according to the authors.

Paper DOI http://dx.doi.org/10.1038/s41593-019-0361-z

brain

Humans as old as 79 still generate new neurons, stirring new debate

A new study seems to suggest that humans are capable of growing new neurons well into old age, contradicting previous research that found neurogenesis stops altogether after childhood.

brain

Credit: Pixabay.

The team at the Columbia University in New York carefully scrutinized the autopsied brain samples sourced from 28 individuals who had died abruptly at ages 14-79. Researchers zoomed in on the hippocampus, which is the seat of learning and memory formation in the brain, looking for newly formed neurons and the state of blood vessels.

Surprisingly, the researchers found that older people had a similar ability to make thousands of new neurons in the hippocampus, from progenitor cells (stem cells), as younger people had. The idea that both young and old humans alike produce new neurons was reinforced by the fact that the hippocampus had equivalent volumes across all ages.

To identify neurogenesis, the researchers had to look for specific clues like proteins produced by neurons at particular stages of their development. For instance, proteins like GFAP and SOX2 are released by stem cells when these turn into neurons, while proteins like Ki-67 are generated by the development of newborn neurons. Across all ages, the researchers found proteins linked with newborn neurons in the dentate gyrus, which is an area of the hippocampus where neurons are born.

The number of neural stem cells was a bit lower in people in their 70s compared to individuals in their 20s. However, the older brains still possessed thousands of these cells and the number of neurons in an intermediate to an advanced stage of development was found to be the same across all age groups.

In today’s context of an aging populace, the findings are particularly important with the threat of widespread dementia looming. The findings suggest that the elderly may retain more of their cognitive and emotional abilities longer into old age than previously thought possible.

Dots represent new nerve cells. Roughly the same number of dots exist in the hippocampus of both people in their 20s (top) and in their 70s (bottom). Credit: Columbia University.

Dots represent new nerve cells. Roughly the same number of dots exist in the hippocampus of both people in their 20s (top) and in their 70s (bottom). Credit: Columbia University.

Maura Boldrini, associate professor of neurobiology at Columbia University and lead author of the new study, cautions, however, that the newly formed neurons in old age may be less capable of forming new connections, partly due to aging blood vessels.

However, it was only last month that a study performed at the University of California in San Francisco came to the opposite conclusion. After analyzing brain samples from 59 adults and children, the researchers wrote: “we found no evidence of young neurons or the dividing progenitors of new neurons” in the hippocampi of people older than 18. They found some evidence of new neural growth in children younger than one year and some signs of this happening in children aged 7 to 13. This study, which some have called ‘sobering’, suggested that the very vast majority of the human hippocampus is generated during fetal development.

Referring to the new findings, Arturo Alvarez-Buylla, who is a researcher at the University of California in San Francisco, said that “the cells they [scientists at Columbia] call new neurons in the adult hippocampus are very different in shape and appearance from what would be considered a young neuron in other species, or what we have observed in humans in young children.”

Hopefully, more research will shed light on the matter. Neither of the two studies has the last word — but this is a good debate to be had.

Scientific reference: Cell Stem Cell, Boldrini et al.: “Human Hippocampal Neurogenesis Persists Throughout Aging” http://www.cell.com/cell-stem-cell/fulltext/S1934-5909(18)30121-8 , DOI: 10.1016/j.stem.2018.03.015.

 

 

Stress chess.

Stress ruins memory, but you can outrun this effect

Turns out you can simply run from your problems — stress-related memory problems, to be exact.

Stress chess.

Image via PxHere.

New research from the Brigham Young University shows that exercise helps protect your memory from the negative impacts of stress. According to the findings, based on mouse trials in the lab, running could help mitigate the destructive effect of stress on synapses in the hippocampus, a part of the brain which handles learning and memory.

Running at full efficiency

“Exercise is a simple and cost-effective way to eliminate the negative impacts on memory of chronic stress,” said study lead author Jeff Edwards.

The biological systems that underpin memory formation-and-recall, our memory “hardware,” if you will, are synapses between neurons. Each memory (made of congruent bits of information) is initially encoded in a few such connections, but becomes more stable over time, as repeated recalls determine the neurons that store it to create more synapses — a process called long-term potentiation (LTP). Pronounced or chronic stress, however, has been shown to weaken synaptic ties between these memory-storing neurons, decreasing LTP and ultimately affecting our ability to retain memories and their quality.

Edwards’ team set out to find if physical exercise can help insulate LTP processes, and thus overall memory, from the effects of stress. For the paper, the team worked with two groups of mice over a 4-week period. One group, the control sample, was left sedentary, while the other was given running wheels to exercise. The mice in this latter group averaged 5km (3.1mi) of running per day.

Half of the mice in each group were then put through a battery of stress-inducing trials, such as being made to walk on an elevated platform or swimming in cold water. The authors measured the rats’ LTP one hour after each stress-inducing trial.

They report that exercise helps maintain normal levels of LTP even in the face of chronic, or sustained, stress. Stressed mice in the exercise group had significantly greater LTP than those in the control group, and performed just as well as non-stressed mice on a maze experiment designed to test their memory. Additionally, they found mice in the exercise group made “significantly fewer” memory errors in the maze compared to sedentary mice.

All in all, the findings are quite exciting but should be taken with a grain of salt, as the team worked with mice alone, not human subjects. Still, the results suggest exercise might be an effective method to conserve your learning and memory capacity from high levels of stress. Don’t wait until the findings can be replicated in human trials, though, because exercise is an important part of a healthy and happy life.

“The ideal situation for improving learning and memory would be to experience no stress and to exercise,” Edwards said.

“Of course, we can’t always control stress in our lives, but we can control how much we exercise. It’s empowering to know that we can combat the negative impacts of stress on our brains just by getting out and running.”

So go out there and show everyone that you can, in fact, outrun your (memory) problems!

The paper “Running exercise mitigates the negative consequences of chronic stress on dorsal hippocampal long-term potentiation in male mice” has been published in the journal Neurobiology of Learning and Memory.

Playing computer games could help keep your brain in good shape, new study reports

Mario does wonders for your brain, apparently.

When it comes to their neurological and psychological effects, computer games stir a heated debate. Some studies have indicated a connection between violent games and aggression, but studies are often inconsistent, and just as many studies point to the contrary. Even more interestingly, recent research has shown that gaming can lead to an improvement in cognition. Now, a new study by University of Montreal researchers found that participants who played 3D platforming games, like the iconic Super Mario 64, had more grey matter in their hippocampus after playing. The findings carried on for participants of all ages.

Previous studies have shown similar results, but only for young males in their 20s — the key demographic for computer games, but not truly representative for the entire population. Now, they carried out similar studies for seniors. The team recruited 33 people aged 55 to 75 and split them into three groups: one of them had to play Super Mario 64 regularly, take the second took piano lessons for the first time, and the third did nothing.

Playing Super Mario 64 increases hippocampal grey matter in older adults. Differences highlighted here. Image credits: Grey et al / PLoS ONE.

The piano lessons group and the control group had no increase in their grey matter — but the Super Mario 64 group did. Lead researcher Gregory West says that games like the Super Mario force participants to build a cognitive map of the virtual environment, which stimulates the hippocampus. This also helps reverse the atrophy of grey matter which tends to come with old age.

“The good news is that we can reverse those effects and increase volume by learning something new, and games like Super Mario 64, which activate the hippocampus, seem to hold some potential in that respect,” West said in a statement. “It remains to be seen whether it is specifically brain activity associated with spatial memory that affects plasticity, or whether it’s simply a matter of learning something new.”

Grey matter in the hippocampus is vital for the central nervous system, and in the hippocampus particularly, it contributes to the transformation of short-term memories into long-term memories and to spatial orientation. Grey matter in the hippocampus is also a significant biomarker for neurological and psychiatric disorders including Alzheimer’s.

It was also previously shown that London Taxi drivers displayed more grey matter in the posterior hippocampus than a matched control group.

While we should always this type of study with a grain of salt, results are encouraging. It shows that you’re never too old for gaming, and at least for the hippocampus — it’s better for you than taking piano lessons.

Journal Reference: Greg L. West et al. Playing Super Mario 64 increases hippocampal grey matter in older adultshttps://doi.org/10.1371/journal.pone.0187779

Children shoes

Why we can’t remember things before age 3-4

Children shoes

Credit: Pixabay.

Ever tried to pinpoint your very first memory? If you have, then you know how difficult this is. There’s a whole slew of events from your early childhood that seem to stream through your head, but which one was first? If you’re lucky, maybe you can recollect events from as early as age three, but before that, it’s rather well accepted that you can’t. Some people claim they have memories from an even earlier age, but this can’t be proven. With this in mind, one might ask: why can’t I remember anything before age 3-4?

The place where our early childhood disappears

Canadian researchers tackled this very important question in neuroscience and found that what’s commonly referred to as “child amnesia” is due to an overload of the hippocampus — the area of the brain responsible for filing memories from the short-term to the long-term storage.

“The hippocampus matures slowly and probably doesn’t reach any reasonable maturity until we’re 3 or 4,” says Dr. Eric Kandel, Kavli professor and director of the Kavli Institute for Brain Science at Columbia University and senior investigator at the Howard Hughes Medical Institute. “While 2- and 3-year-olds can remember things for a short time, the hippocampus is required for long-term storage of those memories.”

If you’ve ever raised kids, then you might have noticed that they form memories just fine even as toddlers. They’ll remember that trip they had by the seaside a few weeks back, but surprise, surprise they’ll wipe it right off in a mere few months’ time. This can be frustrating for some parents, but the truth of the matter is this is not only natural, but necessary since their brains, and most importantly their hippocampus, is still developing.

[RELATED] Toddlers are a bunch of hypocrites, study finds

To explain why this happens, though, the researchers led by Paul Frankland, a senior scientist at the Hospital for Sick Children in Toronto, hypothesized that the memories themselves actually ended up in the long-term “memory storage room” — it’s just that the hippocampus lost track of where these were put. Imagine a tiny room that rapidly grows into a whole warehouse, but you only have a limited amount of resources to keep track of and successfully store and tag goods for later retrieval — you’ll get a lot of boxes tucked away with no idea what’s inside them, and most likely you’ll leave them like that.

This is what happens to the hippocampus as it matures and huge numbers of new neurons come online and need to be hooked into existing circuits. As growth slows down, the brain is better at keeping pace and can do a better job of tracking where memories get stored, which is why long-term memories become better as youngsters get older.

“They can’t form stable memories of what happens in the first few years,” Frankland says. “I have a daughter who is 4 years old and because we were working on this study, I would always ask her questions about her memories of places we visited 2, 3 months ago. It’s clear that she can form memories with quite some detail. But four years from now she won’t remember anything.”

Think of memory as like orzo, Patricia Bauer, a professor of psychology at Emory who studies early memory.

“It’s not like one big piece of lasagna noodle. Memories are made up of these little tiny bits of information that are coming in literally across the entire cortex. Parts of the brain are taking those little bits of information and knitting them together into something that’s going to endure and be a memory,” she said.

cooked-orzoi

Scientists liken the childhood hippocampus to a rough-meshed colander that lets orzo creep through. Credit: IndustryEats.

Adults have a fine-mesh net to catch the orzo. Babies have a big-holed colander: the orzo slips through.

“What’s happening with the baby is that a lot of the information is escaping even as the baby is trying to get it organized and stabilized.” In early infancy, a lot of experiences never become memories—they slip away before they can be preserved.

To test this theory, the researchers worked with baby mice, which have the same problem as baby humans. Teach a baby mouse to solve a maze and he’ll forget his way around it within a few days.

A few infant mice were genetically engineered to have a slower neuron build-up in their hippocampus. It was found then that these baby mice were more successful at retrieving long-term memories and could solve the maze after a much longer period of time since they first learned to navigate it.

The findings are pretty clear: toddlers face a hippocampus overload issue. Interestingly enough, the researchers might even have a chance at testing their theory out on humans directly. There are many children suffering from brain cancer who are prescribed medication, which, as side effects, slow down the generation of new neurons.

“We can check to see if the treatment preserves memories of things that happened just before the chemotherapy, just as it did in the mice,” Frankland says.

In-game overlaid map from Call of Duty. A new study found such approaches are turning gamers into responsive spatial learners. This is associated with less gray matter in the hippocampus. Credit: Wikia.

Not all video games are equal: some hurt your brain while others improve cognition

Do video games make children aggressive? What about cognition? These are not simple yes or no questions as a recent study performed by researchers at the University of Montreal and McGill University in Canada found out.

Their work suggests first-person shooters can reduce gray matter, particularly in the hippocampus — a critical brain region involved in memory, navigation, and spatial learning. The findings don’t apply to all kinds of action video games, though. Rather, the scientists learned that those video games where no spatial memory strategy is required are responsible for the effect. Those video games that emphasized spatial memory strategies were actually associated with an increase in gray matter in the hippocampus.

In-game overlaid map from Call of Duty. A new study found such approaches are turning gamers into responsive spatial learners. This is associated with less gray matter in the hippocampus. Credit: Wikia.

In-game overlaid map from Call of Duty. A new study found such approaches are turning gamers into responsive spatial learners. This is associated with less gray matter in the hippocampus. Credit: Wikia.

Gray matter bread crumbs

For the first part of the study, the researchers recruited 33 volunteers who either habitually played video games or never did so. Before the experiment, each participant was interviewed about the strategies they use to navigate in order to learn whether or not they were spatial learners or response learners. A spatial learn navigates an environment such as a maze by learning about the relationship between specific landmarks and target objects such as the middle of the maze. Contrary, a response learner uses counting, patterning, and memorizing a series of steps to find their target along the way.

After the participants had their brains scanned, the team found that habitual action video gamers had significantly less gray matter in their hippocampus and used response strategies more.

In the second and third part of the study, 42 and 21 participants, respectively, had to play 90 hours of either an action video game (Call of Duty or Battlefield), a video game platform (Super Mario 64), or an action-role playing game (Dead Island). After the training round, the participants underwent magnetic resonance imaging (MRI) brain scans and had their brain tissue density measured.

Gamers who used non-spatial response strategies had significantly less gray matter in the hippocampus. Those who used hippocampus-dependent spatial strategies, however, saw a marked increase in gray matter.

“These results show that video games can be beneficial or detrimental to the hippocampal system depending on the navigation strategy that a person employs and the genre of the game,” says Greg West, associate professor at the University of Montreal, who led the research.

West and colleagues think that in-game GPS or maps overlayed on the display of most action games are making gamers too spatially responsive. Action games that don’t have overlaid maps prod players to remember relationships between landmarks and thus encourage spatial learning.

“These results show that video games can be beneficial or detrimental to the hippocampal system depending on the navigation strategy that a person employs and the genre of the game,” the authors reported.

Findings appeared in the journal Molecular Psychiatry

Conversation

That urge to complete other people’s sentences? Turns out the brain has its own Auto Correct

The hippocampus might have a much more central role to play in language and speech than we’ve ever suspected, a team of US neuroscientists claims. They examined what happens in people’s brains when they finish someone else’s sentence.

Conversation

Image credits Isa Karakus / Pixabay.

Do you ever get that urge to blurt out the last word of somebody else’s sentence? Happens to me all the time. And it seems scientists do it too because a team led by senior researcher at the Donders Centre for Cognition and Radboud University Medical Centre Vitoria Piai looked into the brains of 12 epileptic patients to make heads and tails of the habit. What they’ve found flies against everything we currently know about how memory and language interact in our brains.

The 12 patients were taking part in a separate study trying to understand their unique patterns of brain activity. Each one of their brains was monitored with a set of electrodes. Piai and her team told the participants a series of six-syllable (but incomplete) sentences, “she came in here with the…” or “he locked the door with the…” for example. After the sentence was read out to them the researchers held up a card with the answer printed on it, all the while monitoring how the patients’ hippocampi — on their non-epileptic side of the brain — responded.

When the missing word was obvious, ten out of the twelve subjects showed bursts of synchronised theta waves in the hippocampus, a process indicative of memory association.

“The hippocampus started building up rhythmic theta activity that is linked to memory access and memory processing,” said Robert Knight from the Department of Psychology, Helen Wills Neuroscience Institute, University of California, Berkeley and co-author of the paper.

But when the answer wasn’t so straightforward, their hippocampi ramped up even more as it tried (without success) to find the correct word — like an engine revving up with the clutched pulled down.

The original auto correct

“[The results] showed that when you record directly from the human hippocampal region, as the sentence becomes more constraining, the hippocampus becomes more active, basically predicting what is going to happen.”

Just like the auto correct feature replaces a more unusual word the first time you use it but adapts over time to not only stop replacing it, but also starts filling it in for you, the findings suggest that our minds try to fill blanks in dialogue drawing from our memory stores of language and the interlocutor’s particularities of speech, linking memory and language.

“Despite the fact that the hippocampal area of the medial part of the temporal lobe is well known to be linked to spatial and verbal memory in humans, the two fields have been like ships running in the fog, unaware that the other ship is there,” Knight added.

This would mean that the hippocampus plays a much more important role in language, previously thought to be the domain of the cortex — though right now, the team doesn’t know exactly how this link works. Because of this, the team hopes to continue their work to better understand the bridge between memory and language, which will hopefully give us a better understanding of the brain itself.

Another implication would be that, because at least part of the act of speaking is handled by the hippocampus and not the cortex, language might not be so human-only as we’d like to believe.

The full paper “Direct brain recordings reveal hippocampal rhythm underpinnings of language processing” has been published in the journal PNAS.

Pictured here is a synapse between an axon (green) and dendrite (yellow) from the reconstructed rat hippocampus. Credit: Salk Institute

Brain’s memory may be 10 times larger than previously thought

A groundbreaking research out of the Salk Institute suggests synapses are 10 times bigger in the hippocampus. Conversely, this means the memory capacity is 10 times larger than previously thought, given synapse size is directly related to memory. Moreover, the team found these synapses adjust in size constantly.

Every 20 minutes, synapses grow bigger or smaller, adjusting themselves for optimal neural connectivity. The clues could prove paramount to developing artificial intelligence or computers that are more akin to the human brain: phenomenal computing power using minimal energy input.

 Pictured here is a synapse between an axon (green) and dendrite (yellow) from the reconstructed rat hippocampus. Credit: Salk Institute

Pictured here is a synapse between an axon (green) and dendrite (yellow) from the reconstructed rat hippocampus. Credit: Salk Institute

What are memories? Neuroscientists reckon memories are microscopic chemical changes at the connection points between neurons in the brain called synapses. These junctions connect the output ‘wire’ (an axon) from one neuron to an input ‘wire’ (a dendrite) of a second neuron. The signal travels across the synapse via neurotransmitters — chemicals that communicate information like glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine etc. — and each neuron can have thousands of these synapses. There are 100 billion neurons in the human brain, each of which connects to up to 10,000 other neurons. By some estimates, there are over 100 trillion synapses in the human brain.

Though information is thought to travel through most of the neural circuits and networks of the brain, the consensus is that memories are coded and structured in the area of the brain called the hippocampus.

Terry Sejnowski, Salk professor, and Kristen Harris, co-senior author and professor of neuroscience at the University of Texas, Austin, reconstructed every dendrite, axon, glial process, and synapse from a volume of hippocampus the size of a single red blood cell. They were baffled by the complexity they discovered.

This 3D reconstruction of rat hippocampus tissue showed that in some cases a single axon from one neuron formed two synapses reaching out to a single dendrite of a second neuron. In other words, the first neuron was sending a duplicate signal. But was this really a duplicate? What about the connection strength? The researchers sought to answer these questions and more by measuring the size of the synapses.

Typically, neuroscientists class synapses size as being small, medium and large with little room left for interpretation in between.

Advanced microscopy and computational algorithms were deployed to reconstruct the rat’s brain in terms of connectivity, shapes, volumes and surface area down to a nanomolecular level.

“We were amazed to find that the difference in the sizes of the pairs of synapses were very small, on average, only about eight percent different in size. No one thought it would be such a small difference. This was a curveball from nature,” says Tom Bartol, a Salk staff scientist.

When the team plugged this seemingly dismissive eight percent difference into their models, they found it mattered a lot. Typically, the difference in size between the smallest and largest synapses vary by a factor of 60. Most synapses are small. Given synapses of all sizes differ by 8%, the researchers determined there could be as many as 26 different categories of synapse size — not just small, medium or large. “Our data suggests there are 10 times more discrete sizes of synapses than previously thought,” says Bartol. “This is roughly an order of magnitude of precision more than anyone has ever imagined,” says Sejnowski.

There’s more to it. Synapses don’t always work. Only 10 to 20% of the time these activate neurons. “We had often wondered how the remarkable precision of the brain can come out of such unreliable synapses,” says Bartol.

We now may have an answer.  The team used their new data and a statistical model to find out how many signals it would take a pair of synapses to get to that eight percent difference. For every 1,500 events, a small synapse will change in size, or every 20 minutes. Bigger synapses need a couple hundred events, or 1 to 2 minutes.

“This means that every 2 or 20 minutes, your synapses are going up or down to the next size. The synapses are adjusting themselves according to the signals they receive,” says Bartol.

“Our prior work had hinted at the possibility that spines and axons that synapse together would be similar in size, but the reality of the precision is truly remarkable and lays the foundation for whole new ways to think about brains and computers,” says Harris. “The work resulting from this collaboration has opened a new chapter in the search for learning and memory mechanisms.” Harris adds that the findings suggest more questions to explore, for example, if similar rules apply for synapses in other regions of the brain and how those rules differ during development and as synapses change during the initial stages of learning.

“The implications of what we found are far-reaching,” adds Sejnowski. “Hidden under the apparent chaos and messiness of the brain is an underlying precision to the size and shapes of synapses that was hidden from us.”

“This is a real bombshell in the field of neuroscience,” says Terry Sejnowski, Salk professor and co-senior author of the paper, which was published in eLife. “We discovered the key to unlocking the design principle for how hippocampal neurons function with low energy but high computation power. Our new measurements of the brain’s memory capacity increase conservative estimates by a factor of 10 to at least a petabyte, in the same ballpark as the World Wide Web.”

The adult brain works on only 20 watts of continuous power. That’s less than a dim light bulb, but a conventional machine that could simulate the entire human brain would need to have an entire river’s course bent just to cool it! Now, computer scientists could exploit these findings to devise artificial neurons that are more energy-efficient.  “This trick of the brain absolutely points to a way to design better computers,” says Sejnowski. “Using probabilistic transmission turns out to be as accurate and require much less energy for both computers and brains.”

How your brain distinguishes safety from danger

Columbia University researchers have successfully identified the cellular network that allows mice to remember which environments are safe and which are dangerous. The study also looks into what happens when these neurons are tampered with, offering insight into how conditions such as PTDS, panic attacks and anxiety disorders can be treated.

This is an image showing LRIP inhibitory neurons (in green) extending from the entorhinal cortex (lower right) into the hippocampus. LRIPs have been found to be part of a sophisticated mechanism that is critical to the formation of contextual memories.
Image via sciencedaily

The brain’s capacity to learn and encode memories are two cornerstone tools for any animal’s survival. Contextual memories (those that form during particular experiences) form the basis for appropriate fear responses in dangerous settings and help avoiding such situations in the future.

Just remembering that a particular setting or series of events ultimately led to danger and estimating whether an environment is safe or poses a threat are two very different things however. Earlier research found that contextual memories form and remain encoded in two separate but highly interconnected brain areas — the hippocampus and the entorhinal cortex — involved in memory and navigation.

Two of the connections between these areas have well documented roles and ways of functioning, but the third such bundle of neurons had scientists puzzling over what ts role actually was.

“Neurons in the entorhinal cortex wind their way into the hippocampus via two distinct routes, or pathways,” explained PhD Jayeeta Basu, first author of the paper.

“It is thought that contextual memories are formed when these two pathways became activated as part of a carefully timed sequence. But a few years ago, scientists discovered a third pathway that linked the two regions whose purpose was unknown.”

There are two “flavors” of neurons; around 80% of them are excitatory meaning they carry signals over long distances in the brain, often across whole brain regions, with the other 20% being inhibitory — they function locally to slow or halt excitatory activity. What was so unusual about the neurons in this recently discovered third pathway was that they acted across a relatively long distance, but were also inhibitory. So scientists called them long-range inhibitory projections, or LRIPs.

This new study aimed to investigate the role LRIPs played in the processes of learning and memory formation. To this end, the team first temporarily inhibited their activity in mice, then placed the animals in a room where they were subjected to a brief electric shock delivered through the floor. When returned to the room 24 hours later, the mice showed signs of fear, indicating that they remembered the electric shock. The scientists concluded that LRIPs weren’t involved in the formation of “fearful memories.”

When placed in a completely different room however, the mice again showed signs of fear, suggesting that their fear of the electric shock generalized from the initial room to a different context. Control-group mice showed signs of fear when placed in the initial chamber but not in the second one, revealing the role of LRIPs in distinguishing between dangerous or benign environments.

Brain imaging techniques and electrical recordings from unaltered mice revealed the role of the connection in much more precise detail. When a stimulus such as sound, light or footshock activates the LRIPs, neurons fire an inhibitory signal from the entorhinal cortex to the hippocampus. This LRIP signal silences a set of inhibitory cells in the hippocampus, allowing other neurons to activate and ultimately generating a memory.

It’s a bit confusing but this series of signals is only a part of a larger and even more convoluted gating mechanism, evidenced by a short 20-millisecnd delay between the activation of the LRIPs and the arrival of inhibitory signals to the hippocampus.

“This brief delay enables the electrical signals to flow into the hippocampus in an elegant, precisely timed sequence, which is ultimately what allows the memory to form and be stored with the appropriate specificity so that it can be recalled accurately,” said senior author Dr. Siegelbaum.

“Without this delay, fearful memories lack specificity and accuracy, preventing the brain from appropriately distinguishing danger from safety.”

“The implications of these findings for the human brain, while preliminary, are intriguing,” said PhD co-author Attila Losonczy.

“The study suggests that any alterations in these pathways activity–particularly a disruption of the timed delay–may contribute to pathological forms of fear response, such as posttraumatic stress, anxiety, or panic disorders.”

The paper, titled “Gating of hippocampal activity, plasticity, and memory by entorhinal cortex long-range inhibition” is available online here.

 

Rats dream of getting to a brighter future

It’s not just us humans that dream of a better future – rats do too. When rats rest, their brains imagine a favorable future such as a tasty treat, a new study by UCL researchers found.

Image via Like Cool.

Researchers wanted to see what happens in the rats’ brain as they sleep, so they first monitored them as they looked at some delicious but inaccessible food. They then monitored them as they rested, and ultimately, as they finally received the desired food. They then did the same thing as the rats were sleeping, and found that their brains were mimicking walking to and from the desired food.

“During exploration, mammals rapidly form a map of the environment in their hippocampus,” says senior author Dr Hugo Spiers (UCL Experimental Psychology). “During sleep or rest, the hippocampus replays journeys through this map which may help strengthen the memory. It has been speculated that such replay might form the content of dreams. Whether or not rats experience this brain activity as dreams is still unclear, as we would need to ask them to be sure! Our new results show that during rest the hippocampus also constructs fragments of a future yet to happen. Because the rat and human hippocampus are similar, this may explain why patients with damage to their hippocampus struggle to imagine future events.”

The study not only revealed an amazing fact about rats, but could also help humans with damage to the hippocampus who can’t imagine the future. The hippocampus is a major component of the brains of humans and other vertebrates which plays a major role in memory and spatial navigation. But there might be more to the hippocampus than what we currently believe.

“What’s really interesting is that the hippocampus is normally thought of as being important for memory, with place cells storing details about locations you’ve visited,” explains co-lead author Dr Freyja Ólafsdóttir (UCL Biosciences). “What’s surprising here is that we see the hippocampus planning for the future, actually rehearsing totally novel journeys that the animals need to take in order to reach the food.”

Their results indicate that the hippocampus may plan routes that have not yet happened – a dream route that would lead them to the food. This is also an indication that thinking about the future is not restricted to humans – something which biologists thought for a long time.

“What we don’t know at the moment is what these neural simulations are actually for,” says co-lead author Dr Caswell Barry (UCL Biosciences). “It seems possible this process is a way of evaluating the available options to determine which is the most likely to end in reward, thinking it through if you like. We don’t know that for sure though and something we’d like to do in the future is try to establish a link between this apparent planning and what the animals do next.”

 

Light/Moderate Alcohol Consumption associated with better Memory in Later Life

Alcohol is generally regarded as unhealthy, with a myriad of long-term negative effects and even short term negative effects. But there are still many things we don’t understand about how alcohol interacts with out bodies. For example, a 2011 Texas research found that alcohol consumption helps some areas of our brain remember better, while a 2005 study showed that moderate alcohol consumption lowers the risk of type 2 diabetes. Now, a new study suggests that low or moderate alcohol consumption is correlated with higher episodic memory and larger hippocampal brain volume.

A glass of wine may do wonders for your health – but more will certainly harm it. Image via The Telegraph.

“The findings from this study provide new evidence that hippocampal volume may contribute to the observed differences in episodic memory among older adults and late life alcohol consumption status”, authors write in the study.

Now, let’s just settle one thing right off the bat – correlation does not imply causation. The fact that alcohol consumption is correlated with better episodic memory doesn’t mean that the alcohol is the cause here. This being said, previous studies conducted on animals have also suggested that moderate alcohol consumption could promote generation of new nerve cells in the hippocampus. The hippocampus one of the crucial parts of the brain, responsible for storing memory and navigating through space. While it’s pretty clear that the hippocampus is involved in many other things, it’s still not clear what those things are. What is clear is that during Alzheimer’s disease, this is the area which suffers the most damage.

Now, this study has found not only that light consumption of alcohol is not detrimental, but that it can in fact help your brain.

“There were no significant differences in cognitive functioning and regional brain volumes during late life according to reported midlife alcohol consumption status,” said lead author Brian Downer. “This may be due to the fact that adults who are able to continue consuming alcohol into old age are healthier, and therefore have higher cognition and larger regional brain volumes, than people who had to decrease their alcohol consumption due to unfavourable health outcomes.”

What is important to keep in mind here is that while low alcohol consumption may have some benefits, extended periods of abusing alcohol is well known to cause damage to the brain. So, to sum it up, no one is saying “Don’t drink alcohol at all” – it’s just that if you want to drink, one or two glasses is more than enough.

Journal Reference: Downer B, Jiang Y, Zanjani F, Fardo D. Effects of Alcohol Consumption on Cognition and Regional Brain Volumes Among Older Adults. Am J Alzheimers Dis Other Demen. 2014 Sep 7.

baby_brain

Baby brains grow to half the adult size in just 90 days

baby_brain

Researchers performed MRI scans on babies to see how their brains developed from birth to later stages. Their findings reveal the explosive growth of the human brain following birth: in just 90 days, the baby brain grows by 64% its initial size reaching half the adult size.

[ALSO READ] Baby brains benefit from music, even before they walk

They grow up so fast

Traditionally, brain growth is followed the old fashioned way using a measuring tape. This way, doctors casually record skull, and consequently brain growth and if any deviations from a known patterns are encountered, they then further investigate. For instance, premature babies have a smaller brain and develop slower than those delivered at term. As we all know, skulls vary in shape and size and they’re not the best metric for gauging brain size.

[INTERESTING] Babies can tell two languages apart as early as seven months of age

Lucky for scientists, there are MRI scanners. Researchers at University of California scanned the brains of 87 babies, healthy and delivered at term, from birth until three months of age. They saw the most rapid changes immediately after birth – newborn brains grew at an average rate of 1% a day. This slowed to 0.4% per day at the end of the 90-day period. The highest growth rate among brain structures was for the cerebellum, an area of the brain involved in movement. Oppositely, the hippocampus which is responsible for memory formation and retrieval showed the least growth. Apparently, in its early stages the brain wants to concentrate resources on getting the heck out – ‘guh, guh, dadah’ is enough for now.

 

“This is the first time anyone has published accurate data about how babies’ brains grow that is not based on post-mortem studies or less effective scanning methods,” Dr Martin Ward Platt, a consultant paediatrician at the Royal Victoria Infirmary in Newcastle.

“The study should provide us with useful information as this is an important time in development.

“We know, for example, if there are difficulties around the time of birth, a baby’s growth can fall away in the first few months.”

[RELATED] Why you don’t have memories before age 3-4 

By closely following brain development in its early formation days, researchers hope to spot clues that might help them  identify early signs of developmental disorders such as autism.Scientists will now investigate whether alcohol and drug consumption during pregnancy alters brain size at birth. Findings appeared in JAMA Neurology.

 

Photo: neuroanthropology.net -

Erasing traumatic memories using gene therapy

Photo: neuroanthropology.net -

Photo: neuroanthropology.net –

It’s estimated that some 8 million people in the United States suffer from post-traumatic stress disorder (PTSD), causing great angst, depression and poor social integration. There are numerous therapies and techniques designed to help patients recover and banish the specters that lurk in the deepest recesses of their minds, haunting them. A common psychotherapy is fighting fear with fear, by having the patient face his ordeal: basically, the patient is introduced in an environment where the trauma is re-lived. The basis is that as the patient relieves past traumatic events, this time in a controlled and safe environment, he may have a chance at overcoming it.

For many, the memories of their traumas, be them war scenes or child abuse, are so deeply entrenched that therapy fails. The older these memories are, the more difficult the therapy becomes. Now, MIT neuroscientists are  proposing a novel way of accessing and re-editing traumas by erasing the old memory to replace it with a fresh, safe one. Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory, along with colleagues, studied the effects of a drug called a HDAC2 inhibitor on mice.

Previously, scientists demonstrated that when new memories are formed  the chromatin in neurons — DNA packaged with proteins — undergoes remodeling to facilitate the activation of certain genes required to create new memories. The MIT researchers wanted to see what happens in the case of the chromatin modifications that occur when previously acquired memories are extinguished. First, the researchers purposely induced a conditioned fear-response into  mice by placing them in a specific environment, where a mild electrical shock was applied. Then, the researchers attempted to recondition the mice by repeatedly placing them inside the environment, this time shock free.

[RELATED] Possibility of erasing unwanted memories emerges 

They found that during the first 24 hours of trauma,  extensive chromatin remodeling occurred during the reconditioning. For several hours after the mice were placed back in the feared chamber, there was a dramatic increase in histone acetylation of memory-related genes, caused by inactivation of the protein HDAC2. That histone acetylation makes genes more accessible, turning on the processes needed to form new memories or overwrite old ones.

Erasing bad memories

Mice which had memories older than 30 days, however, showed no change in histone acetylation. In other words, re-exposure to trauma can work effectively by changing the primary emotional response to it, as a result of erasing the previous memory, but there’s only a short window of opportunity available.

“If you do something within this window of time, then you have the possibility of modifying the memory or forming a new trace of memory that actually instructs the animal that this is not such a dangerous place,”   says Tsai. “However, the older the memory is, the harder it is to really change that memory.”

Based on these findings, the MIT scientists chose to experiment with a HDAC2 inhibitor, which can cause structural changes in the brain, essentially making it more plastic increasing the possibility that very strong new memories will override old, traumatic memories. Mice with trauma memories older than 30 days were treated with this inhibitor and subjected to the same re-conditioning technique. This time, their traumatic memories were extinguished just as easily as in the mice with 24-hour-old memories.

Moreover, the HDAC2 inhibitor treatment seems to turn on a group of genes, which in turn, eventually, activate other genes necessary for memory formation. In the hippocampus, the part of the brain where memory are stored, the number of neuron connections was found to be greater and stronger than usual.

“Our experiments really strongly argue that either the old memories are permanently being modified, or a new much more potent memory is formed that completely overwrites the old memory,” Tsai says.

“This could be a very promising way to bring older memories back, process them in the hippocampus, and then extinguish them with the correct paradigm,” says Jelena Radulovic, a professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine who was not part of the research team.

There are already FDA approved drugs that contain HDAC2 inhibitors, used for cancer treatments. Tsai hopes that, considering this, a human clinical trial might commence soon to see how well an HDAC2 psychotherapy might fair. The results were reported in a paper published in the journal Cell.

Meditation Could Slow the Progress of Alzheimer’s

Meditation has been shown to have an impact on brain activity, decreasing beta waves and impacting each part differently. Activity in the frontal and parietal lobe slows down, while the flow of information to the thalamus is reduced. This can lead to positive side effects such as improved focus, better memory, and a reduction in anxiety. According to a new study conducted at Beth Israel Deaconess Medical Centre, meditation’s impact on the brain could play an important role in slowing down the progression of Alzheimer’s disease and other cognitive disorders.

Stress, Anxiety, and Dementia

 

Image via Sukadev Bretz, @Flickr.

As people age, their cognitive ability may deteriorate. This can range from mild forgetfulness indicative of aging, to more serious signs of dementia. According to researcher Rebecca Erwin Wells, MD, MPH, approximately 50% of those diagnosed with a mild cognitive impairment may go on to develop dementia within five years of this diagnosis. There is also a link between stress and Alzheimer’s disease. This study was conducted to determine if the practice of stress reduction through meditation might help to delay or stop this progression.

The Study and its Results

The study evaluated 14 adults already diagnosed with mild cognitive impairment, who were broken into two groups. One group met for two hours each week to participate in meditation and yoga, over a period of eight weeks. They were also encouraged to practice at home each day, and participated in a day-long mindfulness retreat. The second group received normal treatment, without the meditation and mindfulness practice. All of the participants had an MRI at the beginning of the study, as well as after eight weeks to see if there were changes in brain activity.

Memory tests were also conducted at the beginning and end of the study. Although there were few differences between the two groups in memory, there was a difference in the MRI imaging results. Although both groups experienced some atrophy of the hippocampus, the area responsible for learning and memory, those who practiced meditation experienced this to a lesser degree. This suggests that an intervention with practices such as meditation and yoga could potentially impact the areas of the brain that are most vulnerable to cognitive disorders such as Alzheimer’s.

Future Implications

While this study was small in scope, it backs up what many alternative therapy practitioners believe; that meditation can improve brain function and significantly reduce stress. If you look at aged care courses at Now Learning or in many universities, meditation is often suggested as a possible therapy for aging patients. Meditation is a simple intervention, with extremely minimal negative side effects. If it could help delay the symptoms of Alzheimer’s even for a short period of time, this can improve the quality of life of aging patients. At the moment, there are no therapies to prevent the progression to dementia, which makes this link worth investigating in greater depth.

tsien

As we age learning is hampered because our brains can’t filter useless information as before

Children are veritable knowledge sponges that can appropriate an intense amount of skills in a short amount of time. As we age, starting from the end of puberty, people seem to loose their ability of learning new skills as intense as children do. For instance, if a 30 year old French man decided to starting learning English, even if he were to study, work and live in London, for decades maybe, chances are he wouldn’t be able to lose his French accent.

tsienResearchers believe this steady decline in the ability of learning and making new memories is caused not by a decrease in our capacity of absorbing new information, but rather by a hindering in the human’s brain capacity of filtering and eliminating old information like before.

“When you are young, your brain is able to strengthen certain connections and weaken certain connections to make new memories,” said Dr. Joe Z. Tsien, neuroscientist at the Medical College of Georgia at Georgia Regents University and Co-Director of the GRU Brain & Behavior Discovery Institute.

For older brains, this ability is diminished. The Georgia Regents University researchers refer to the NMDA receptor in the brain’s hippocampus – a major component of the brain primarily responsible for transferring information from short-term to long-term, basically facilitating memory) – which acts as a switch for regulating learning and memory, working through subunits called NR2A and NR2B.

When NR2B is over-expressed with respect to NR2A – such as the case with children – neurons communicate between themselves a bit longer than those in adult brains, where the opposite case is in place (more NR2B than NR2A). This leads to stronger bonds between neurons – synapses – and a better ability to learn.

“What is abnormal is the ability to weaken existing connectivity,” Tsien.

The scientists tested this theory and engineered mice with more NR2A, less NR2B – mimicking the adult human brain ratio – and found the rodents were still good at making strong connections and short-term memories but had an impaired ability to weaken existing connections. This weakened the ability of making new long-term memories as a result, too. The whole process is called information sculpting by the scientists. “If you only make synapses stronger and never get rid of the noise or less useful information then it’s a problem,” said Tsien, the study’s corresponding author.

The researchers weren’t surprised to find that hampering of the ability to weaken existing connectivity is a more important factor leading to poorer learning and memory-making ability than previously thought. Tsien and colleagues had known for a while what an overexpressed NR2B might entail. In 2009 the scientists announced they had engineered a smarter than average rat called Hobbie-J, while a decade earlier Tsien reported in the journal Nature the development of a smart mouse dubbed Doogie using the same techniques to over-express the NR2B gene in the hippocampus.

The study findings were reported in the journal Scientific Reports.

source: Georgia Health

An image of a transgenic mouse hippocampus.

Memories are stored in specific brain cells, MIT Inception-like research finds

An image of a transgenic mouse hippocampus.

An image of a transgenic mouse hippocampus.

When the brain deems an experience meaningful enough, it will transfer that information from short-term storage, where typically information like where you put your car keys or the phone number of a person you just met gets stored temporarily, to your long-term memory, offering the possibility to be accessed at a later time. Neurologists claim this recording is made in the brain by strengthening the connections between groups of neurons that participate in encoding the experience, a pattern of connections which is referred to as an engram. These engrams will typically stay dormant unless they’re stimulated by a cue, which will evoke the event back into memory.

This explains why a song playing in the background might instantly transport you back to a special event tied to the track or the sweet scent of a freshly baked pie might transport you back in time to when you were a child. There are a myriad of such “anchors” dispersed though out our neural network, however the existence of engrams beyond their hypothetical nature has been debated for a while, as their exact mechanism and location has been a focus of persistent research for many decades. Now, a recent research conducted by scientists at MIT which made use of optogenetics demonstrates that memories are indeed stored in specific brain cells.

“We demonstrate that behavior based on high-level cognition, such as the expression of a specific memory, can be generated in a mammal by highly specific physical activation of a specific small subpopulation of brain cells, in this case by light,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience at MIT and lead author of the study reported online today in the journal Nature. “This is the rigorously designed 21st-century test of Canadian neurosurgeon Wilder Penfield’s early-1900s accidental observation suggesting that mind is based on matter.”

A breakthrough in neuroscience

Dr. Penfield is one of the most influential figures in neurosurgery, a pioneer in the field whose legacy includes, among others, the first maps of the sensory and motor cortices of the brain showing their connections to the various limbs and organs of the body, still used today, unaltered. He was a man inherently concerned with the various subterfuges of the human mind, and dedicated his life to understanding how the brain works and whether there is any scientific basis that might acknowledge the existence of the human soul. One of his most groundbreaking works is the elaboration of the Montreal Procedure, a controversial surgery in which he treated epilepsy patients by severing nerve cells in the brain where the seizures originated. The operation would take place under local-anesthesia, as the patient’s collaboration was deemed indispensable. Penfield would destroy only the affected nerve cells by the disease, as he stimulated the brain with tiny jolts of electricity and observed the patient’s response. While probing nerve cells in the hippocampus, the region of the brain responsible for memory formation and storage, some patients would report vivid and complex recollections of past events.

Many discussions followed around these sort of events, but until now, it wasn’t scientifically proven that the simple reactivation of nerve cells in the hippocampus could cause memory recall.

To test their hypothesis, the MIT researchers identified the particular brain cells in the hippocampus that were active only when a mouse was learning about a new environment. They then proceeded in identifying which genes were activated in those cells, and added the gene for channelrhodopsin-2 (ChR2), a light-activated protein used in optogenetic indispensable for the present research, to a genetically engineered mouse.

“We thought we could use this new technology to directly test the hypothesis about memory encoding and storage in a mimicry experiment,” says co-author Xu Liu, a postdoc in Tonegawa’s lab.

“We wanted to artificially activate a memory without the usual required sensory experience, which provides experimental evidence that even ephemeral phenomena, such as personal memories, reside in the physical machinery of the brain,” adds co-author Steve Ramirez, a graduate student in Tonegawa’s lab.

Inception: fear induced on command

The scientists next labelled a population of hippocampal dentate gyrus neurons, using tiny optical fibers to deliver pulses of light to the neurons. Finally, the mice were introduced to an environment and were left to accustom themselves for a few minutes of exploration. A mild food shock was induced all of sudden, which caused the mice to fear the particular environment. The brain cells activated during this fear conditioning became tagged with ChR2. Later, the mice were introduced in a totally different environment, with an obviously different maze and of another smell, and were left there to explore. A pulse of light was triggered onto the neurons involved in the first experience, which lead to the fear memory getting switched on; the mice quickly entered a defensive, immobile crouch. This is called fear conditioning.

“Our results show that memories really do reside in very specific brain cells,” Liu says, “and simply by reactivating these cells by physical means, such as light, an entire memory can be recalled.”

Activation of cells labelled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context specific.

“This remarkable work exhibits the power of combining the latest technologies to attack one of neurobiology’s central problems,” says Charles Stevens, a professor in the 
Molecular Neurobiology Laboratory at the Salk Institute who was not involved in this research. “Showing that the reactivation of those nerve cells that were active during learning can reproduce the learned behavior is surely a milestone.”

The method may also have applications in the study of neurodegenerative and neuropsychiatric disorders. “The more we know about the moving pieces that make up our brains,” Ramirez says, “the better equipped we are to figure out what happens when brain pieces break down.”

source

neuron

Why the brain gets slower as we get older

From a certain age onward, humans seem to process information at a slower pace – learning new things becomes more difficult, remembering where you put the car keys seems to give headaches, and it gets ever worse as we age even more. Neuroscientists at the University of Bristol studying dysfunctional neural communication in Alzheimer patients demonstrated that the number one likely culprit to blame are the sodium channels, which are integral membrane proteins that have a direct influence on the degree of neural excitation. Although, the research was targeted on Alzheimer patients, the scientists found that the same degradation of Na+ channels in the brains of older, otherwise healthy individuals causes a loss of cognitive performance .

To encode and transmit information, the brain uses electrical signals. The researchers, lead by Professor Andy Randall and Dr Jon Brown from the University’s School of Physiology and Pharmacology, studied the electrical activity of the brain by recording the electrical signal in the hippocampus‘ cells, which plays a crucial role in the consolidation of short-term memory to long-term memory and spatial navigation. What the researchers were basically looking for was to determine the degree of neural excitation, whose main characteristic is the action potential.

“Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer’s disease. We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells”, said Professor Randall.

neuronAn action potential is a brief, large electrical signal which instantly branches out in the rest of the cell, until it reaches the edge and activates the synapses made with the myriad of neighboring neurons. As we age, these action potentials are harder to trigger, and this relative reluctance arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurons.

With this in mind, scientists might be able to develop treatments or drugs which could open more sodium channels, and thus improve cognitive abilities.

“Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.”

[SciGuru] image credit