Research into Turning Off Pain Receptors Progressing

‘Off switch’ for pain discovered: Activating the adenosine A3 receptor subtype is key to powerful pain relief

Date:
November 26, 2014
Source:
Saint Louis University Medical Center
Summary:
A way to block a pain pathway in animal models of chronic neuropathic pain has been discovered by researchers, suggesting a promising new approach to pain relief.
Pain is an enormous problem. As an unmet medical need, pain causes suffering and comes with a multi-billion dollar societal cost. Current treatments are problematic because they cause intolerable side effects, diminish quality of life and do not sufficiently quell pain.
Credit: © Feng Yu / Fotolia
In research published in the medical journal Brain, Saint Louis University researcher Daniela Salvemini, Ph.D. and colleagues within SLU, the National Institutes of Health (NIH) and other academic institutions have discovered a way to block a pain pathway in animal models of chronic neuropathic pain including pain caused by chemotherapeutic agents and bone cancer pain suggesting a promising new approach to pain relief.

The scientific efforts led by Salvemini, who is professor of pharmacological and physiological sciences at SLU, demonstrated that turning on a receptor in the brain and spinal cord counteracts chronic nerve pain in male and female rodents. Activating the A3 receptor — either by its native chemical stimulator, the small molecule adenosine, or by powerful synthetic small molecule drugs invented at the NIH — prevents or reverses pain that develops slowly from nerve damage without causing analgesic tolerance or intrinsic reward (unlike opioids).

An Unmet Medical Need

Pain is an enormous problem. As an unmet medical need, pain causes suffering and comes with a multi-billion dollar societal cost. Current treatments are problematic because they cause intolerable side effects, diminish quality of life and do not sufficiently quell pain.

The most successful pharmacological approaches for the treatment of chronic pain rely on certain “pathways”: circuits involving opioid, adrenergic, and calcium channels.

For the past decade, scientists have tried to take advantage of these known pathways — the series of interactions between molecular-level components that lead to pain. While adenosine had shown potential for pain-killing in humans, researchers had not yet successfully leveraged this particular pain pathway because the targeted receptors engaged many side effects.

A Key to Pain Relief

In this research, Salvemini and colleagues have demonstrated that activation of the A3 adenosine receptor subtype is key in mediating the pain relieving effects of adenosine.

“It has long been appreciated that harnessing the potent pain-killing effects of adenosine could provide a breakthrough step towards an effective treatment for chronic pain,” Salvemini said. “Our findings suggest that this goal may be achieved by focusing future work on the A3AR pathway, in particular, as its activation provides robust pain reduction across several types of pain.”

Researchers are excited to note that A3AR agonists are already in advanced clinical trials as anti-inflammatory and anticancer agents and show good safety profiles. “These studies suggest that A3AR activation by highly selective small molecular weight A3AR agonists such as MRS5698 activates a pain-reducing pathway supporting the idea that we could develop A3AR agonists as possible new therapeutics to treat chronic pain,” Salvemini said.


Story Source:

The above story is based on materials provided by Saint Louis University Medical Center. Note: Materials may be edited for content and length.


Journal Reference:

  1. J. W. Little, A. Ford, A. M. Symons-Liguori, Z. Chen, K. Janes, T. Doyle, J. Xie, L. Luongo, D. K. Tosh, S. Maione, K. Bannister, A. H. Dickenson, T. W. Vanderah, F. Porreca, K. A. Jacobson, D. Salvemini. Endogenous adenosine A3 receptor activation selectively alleviates persistent pain states. Brain, 2014; DOI:10.1093/brain/awu330

Cite This Page:

Saint Louis University Medical Center. “‘Off switch’ for pain discovered: Activating the adenosine A3 receptor subtype is key to powerful pain relief.” ScienceDaily. ScienceDaily, 26 November 2014. <www.sciencedaily.com/releases/2014/11/141126132639.htm>.

Jetpack Designed at ASU Assists in Running/Sprinting

Jetpack enables soldiers to sprint at Olympic speeds (VIDEO)

Researchers at Arizona State University with the help of DARPA are working on a new take on the science fiction-inspired jetpack. Unlike jetpacks of yesterday, this literally puts the wind at your back, enabling soldiers to run faster than ever before, sprinting at Olympic speeds.

“If you think of a Navy SEAL or an Army soldier that has to get in somewhere quick and do whatever they’ve gotta do, but maybe get out of there just as quickly, so these devices can really help soldiers to not only accomplish their goals and succeed in their missions, but potentially save human lives as well,” said ASU student Jason Kerestes.

Do you think steps like these will materialize in “future soldier” projects? And how much do you want a jetpack right this freakin’ minute, right?

The jetpack part of the larger ASU Research Matters project.

[Business Insider via Predator Intelligence/Facebook]

Pill may be coming that can reset the body’s clock

  • Researchers have found a mechanism that controls how people react to long-haul travel or working irregular hours
  • Tests on mice revealed an enzyme which controls their body clock 
  • By deleting the gene which produces the enzyme scientists reset this clock 
  • Although human genes can’t be deleted, scientists are working on a pill that blocks it from producing the enzyme
  • This pill could be on the shelves within five years, said researchers

By BEN SPENCER

 

A pill to treat jet lag could be on the shelves within five years, thanks to a discovery which allows scientists to reset the human body clock.

Researchers at Manchester University have found the mechanism that governs how people react to long-haul travel or working irregular hours.

Their tests on specially bred mice revealed an enzyme which controls how the body’s clock can be reset.

 
During tests, researchers at Manchester University found a gene that produces an enzyme which controls how the body's clock can be reset. Drug companies are using the discovery to develop a pill to ease the impact of sleep deprivation, jet lag and changes to daily routine. Stock image pictured

 

During tests, researchers at Manchester University found a gene that produces an enzyme which controls how the body’s clock can be reset. Drug companies are using the discovery to develop a pill to ease the impact of sleep deprivation, jet lag and changes to daily routine. Stock image pictured

 

HOW WOULD THE PILL WORK?

 

The researchers discovered the gene which produces an enzyme that controls part of the circadian clock.

They then deleted the gene in mice to stop them producing the enzyme, called casein kinase 1epsilon. 

The team studied the mice for changes by timing the lights switches in their cages to replicate a weekend flight to New York.

The mice without the crucial enzyme adapted much faster to the new day-night pattern and displayed much smaller metabolic disruption.

Deleting the gene would not be possible in humans, but the finding has allowed pharmaceutical firms to investigate a pill to block the enzyme.

Drug companies are using the discovery to develop a pill to ease the impact of sleep deprivation, jet lag and changes to daily routine. 

Dr David Bechtold, who led the research, said a treatment could even be ready within five or ten years.

 Pharmaceutical giant Pfizer, which collaborated with the Manchester team, has a treatment in pre-clinical development, and other companies are thought to be investigating other lines of research for similar products.

Dr Bechtold told the MailOnline: ‘The drugs that we have used are amenable for development, they will work and it is a matter of optimising them for clinical use. 

‘This development opens a line of work which could very realistically lead to human treatment.

‘Within five to ten years the availability of drugs which can be used to target the body clock in people will start to become a reality.’

 
Using mice, stock image pictured, researchers discovered that if they deleted the gene, it would stop the mice producing the enzyme, called casein kinase 1epsilon. Deleting the gene would not be possible in humans, but the finding has allowed pharmaceutical firms to investigate ways to block it

 

Using mice, stock image pictured, researchers discovered that if they deleted the gene, it would stop the mice producing the enzyme, called casein kinase 1epsilon. Deleting the gene would not be possible in humans, but the finding has allowed pharmaceutical firms to investigate ways to block it

 

WHAT CAUSES JET LAG?

 

Nearly all living things have an internal mechanism – known as the circadian rhythm or body clock – which synchronises bodily functions to the 24-hour pattern of the Earth’s rotation.

In humans and other mammals, the clock is regulated by the bodily senses – most importantly the way the eye perceives light and dark and the way skin feels temperature changes.

When we work late, or travel to different time zones, the light our body expects to see – based on how long we’ve been awake – for example, is different, and this causes our body clock to fall out of sync. 

This causes the feeling of jet lag. 

But the pressures of modern living mean we are now increasingly working against our clocks and risking long term health problems from metabolic disease.

Separate studies have found that people who work night shifts or who get too little sleep are more susceptible to diseases including depression, cancer, diabetes and dementia. 

The researchers discovered the gene which produces an enzyme that controls part of the circadian clock. They deleted the gene in mice to stop them producing the enzyme, called casein kinase 1epsilon.

The team studied the mice for changes by timing the lights switches in their cages to replicate a weekend flight to New York.

The mice without the crucial enzyme adapted much faster to the new day-night pattern and displayed much smaller metabolic disruption.

Deleting the gene would not be possible in humans, but the finding has allowed pharmaceutical firms to investigate a pill to block the enzyme.

Dr Bechtold, whose research is published in the journal Current Biology, said: ‘By tackling this enzyme we can wind the body clock back or forwards, we can modulate the clock.

‘So jet lag could be eliminated by using inhibitors on the family of enzymes which sets the speed of the clock.

He added: ‘We already know that modern society poses many challenges to our health and wellbeing – things that are viewed as commonplace, such as shift-work, sleep deprivation, and jet lag disrupt our body’s clocks.

‘We are not genetically predisposed to quickly adapt to shift-work or long-haul flights, and as so our bodies’ clocks are built to resist such rapid changes.

‘Unfortunately, we must deal with these issues today, and there is very clear evidence that disruption of our body clocks has real and negative consequences for our health.

‘As this work progresses in clinical terms, we may be able to enhance the clock’s ability to deal with shift work, and importantly understand how maladaptation of the clock contributes to diseases such as diabetes and chronic inflammation.’

Read more: http://www.dailymail.co.uk/sciencetech/article-2585340/Getting-rid-jet-lag-soon-simple-taking-pill-Scientists-way-reset-body-clocks-long-flights.html#ixzz2wXPpr0Ia 
Follow us: @MailOnline on Twitter | DailyMail on Facebook

 

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10 Amazing Man-made Substances

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SIMON BURGESS JUNE 20, 2013

We all know that mankind is capable of genius. But if you scratch the surface of what we can come up with, even those of us who have already discovered chocolate-covered pretzels can be blown away. For instance, did you know that we have …

10One-Way Bulletproof Glass

iStock_000012515233Small

The problems of the ultra-rich are different than yours or mine. Going by the market forces that gave us this entry, the ultra-rich worry about the fact that the bulletproof glass that may save their lives would also stop them from shooting back.

Enter one way ballistic glass: it stops bullets from one side only, allowing return fire. How is this wizardry achieved, you ask? By sandwiching two sheets of different plastics together — a brittle acrylic layer, and a softer, more elastic, polycarbonate layer. The acrylic forms a very hard surface under pressure. When a bullet strikes this side, the layer flattens it before shattering, dissipating its energy. It is then possible for the shock-absorbing back layer to contain the bullet (and the shards of acrylic) without breaking.

When shot from the other side however, the bullet hits the polycarbonate first, stretching it initially. This bending shatters the brittle acrylic behind, leaving no resistance once the bullet punches through, thus allowing the target to become the shooter. But don’t get too cocky — you just put a hole in your shield.

9Liquid Glass

Once upon a time, dish soap didn’t exist. In the past, pans were washed with soda, vinegar, silver sand, Vim or wire wool, but a new spray-on coating could save plenty of labor and make dish soap itself obsolete. Liquid Glass combines silicon dioxide with water or ethanol to make a spray that dries to form a layer of “flexible, super-durable glass“. The layer is invisible (500 times thinner than a human hair), non-toxic and repels liquids.

Liquid Glass would eliminate the need for scrubbing, and make most cleaning products unnecessary, because it also renders surfaces anti-bacterial. Microbes landing on the surface have a hard time staying there. Throw out your bleach and simply turn on to sterilize a kitchen sink. This means that in medical applications, a treated surface could be sterilised with only hot water, with no need for chemical disinfectants.

The coating can be used to treat plants fungal infections and to seal corks for better bottle seals. We aren’t trying to sell it here (promise!), but this stuff repels liquids, is non-toxic, flexible, anti-bacterial, breathable, durable and invisible. Oh, and its also dirt cheap. Either it’s a miracle, or the fine print is invisible, too. Time will tell.

8Amorphous Metal

Amorphous metal is a material that is allowing golf clubs to hit harder, bullets to strike with more force, engines and surgical knives to last longer. Contrary to its name, it combines the usual strength of metal with the surface hardness of glass. In the video above, two ball bearings are bounced, one on steel and one on amorphous metal. The bearing bounces much higher off the amorphous metal and keeps going for an uncomfortably long time.

The impact of the bearing actually leaves many small “pits” in the steel, meaning the steel absorbs and dissipates the energy of the impact. The amorphous metal is smooth however, meaning that all the energy of the impact is transmitted back to the bearing, causing the higher bounce.

Most metals have a crystalline atomic structure, which is very ordered and repetitive. Under impacts or other stress, planes of atoms in the metal can permanently ‘slip’ to form visible dents. Amorphous metal has a disordered, random atomic structure, meaning such slips are prevented and the atoms rebound to their initial position.

7Starlite

A plastic with incredible heat resistance, Starlite’s quality as a thermal insulator is actually so staggering that for a while people just assumed its inventor was deluded. Then, following the above TV spot, the British Atomic Weapons Establishment (AWE) got in touch. They subjected it to nuclear-flash-level bursts of heat, up to the level of 75 Hiroshimas. The sample was fine, if a little charred. One scientist remarked “Normally, we do a test every couple of hours because we have to wait for [the material] to cool down. We’re doing it every 10 minutes, and it’s sat there laughing at us.”

Unlike other high-performance insulators, Starlite produces no toxic fumes under heat and is also incredibly lightweight. The potential applications in space shuttles, firefighting suits, airliners or military use are endless, but Starlite has never left the lab. Inventor Maurice Ward died in 2011 without ever patenting or licensing his creation. All that is widely known is that it consists of “up to 21 organic polymers and copolymers, and small quantities of ceramics”.

6Aerogel

aerogel-grass-spines

First, imagine a porous substance of such low density that a 2.5 centimeter (1 in) cube of it could have the internal surface area of an entire football field. Next, stop taxing your imagination and accept that such a substance already exists. More a category than a specific material, Aerogel is a shape that certain substances can be molded into whose low mass makes it one of the greatest insulators we have (an Aerogel window 2.5 cm (1 in) thick has the heat-protective quality of a window that is 25 cm (10 in) thick.

All the lightest substances known to man are Aerogels. Silica Aerogel — essentially dried silicon gel — weighs only 3 times more than air. However, whilst being very brittle it can also support over 1000 times its own weight.Graphene Aerogel (pictured above) is made from carbon, and its solid component is 7 times lighter than air.

It has a spongy texture, and can be made simultaneously hydrophobic (repels water), and lipophilic (absorbs oil). For this reason it is being hyped as a method to mop up oil spills, because its massive internal surface area means it can absorb 900 times it owns weight. And its spongy texture means that once filled with oil, it can be ‘wrung out’, slung back in the water, and filled again. And you thought carbon was totally useless.

5DMSO

Corner-Brook-226

DMSO is a chemical solvent, originally a byproduct of wood pulping. It existed for almost 100 years before its medical potential was realized in the 1960s. A certain Dr Jacobs discovered that it penetrated skin quickly and deeplywithout damaging tissue. This means huge potential for carrying drugs across membranes and into the body without breaking skin, removing the danger of infection.

It has benefits of its own, reducing the inflammation associated with sprains, arthritis & burns and providing immediate pain relief that can last up to six hours. It also penetrates finger and toenails, meaning it can be used to deliver anti-fungal medications.

Unfortunately, DMSO has had its problems. When its medicinal potential was discovered, it was already commercially available as an industrial chemical. This wide availability also soured its appeal in the eyes of the drug companies — if they couldn’t patent and monopolize it, there would be no profit potential. Also, the fact that side effects include a strong case of garlic breath further reduces marketability, meaning DMSO is mostly used only within veterinary medicine.

4Carbon Nanotubes

sharma-obesity-metastasizing-cancer

A carbon nanotube is effectively a one-atom-thick sheet of carbon rolled into a cylinder. At a molecular level, the result looks like a roll of chicken wire and is the strongest material known to science. Six times lighter than steel and potentially hundreds of times stronger, the tubes also conduct heat more effectively than diamond and conduct electricity more effectively than copper.

Being so thin, they are naturally invisible to the naked eye, and a collection of nanotubes in their raw state looks similar to a petri dish full of soot. To be able to harness their mechanical (and electronic) properties requires the ‘spinning’ of many trillions of these invisible strings, which wasn’t possible until relatively recently.

One of the more striking potential uses is making cables for an elevator into outer space (a fairly old and, until recently, totally impractical idea, due to the impossibility of making a 100,000 kilometer (62,000 mile) lift cable that wouldn’t collapse under its own weight). They could also be used to cure cancer — thousands can fit into an individual cell, and coating them with folic acid causes them to target and bind with cancer cells. The tubes would then be heated with an infrared laser, ideally causing those cells to die. Other uses include stronger, lighter body armor, more efficient windmill blades on wind farms, and making the slickest cheese slicer you can imagine.

3Pykrete

154A

In 1942, the Brits had a problem. They needed aircraft carriers to help combat German U-Boats, but there was no spare steel to build any. A man called Geoffrey Pyke thought that maybe a huge floating ice island might be the answer, but this idea had been suggested (and then ridiculed and dumped) two years previously. Ice may be cheap, but it also shatters without much provocation or eventually melts.

However, a couple of New York scientists hit upon a mixture of ice and wood pulp that not only floated, but was as bullet-resistant as brick, shatterproof and didn’t melt. The material could be machined like wood, or cast into shapes like a metal. In water, an insulating shell of wet wood pulp would form, preventing further melting, and any ship made from it could theoretically be repaired whilst still at sea.

But for all its surprising qualities, Pykrete was ultimately not fit for its intended purpose. A 1,000-ton scale model was quickly built and kept frozen by a single-horsepower motor, but it was found that the ice would sag over time unless kept to a temperate of -16 degrees F, which would require a complicated system of ducts. It was also pointed out that the large amount of wood pulp required would be enough to seriously affect paper production. Pykrete ultimately remained a creative, fascinating and unworkable failure.

2BacillaFilla

Cracked-Concrete

Concrete ages over time, taking on the sickly polluted-grey look we all know and developing fractures in the process. Repairs are time-consuming and expensive — if the foundation of a building cracks, there’s often no easy way of fixing it. Many buildings in earthquake zones have been simply torn down for this reason.

But a group of students at Newcastle University (UK) have produced a genetically modified microbe, that has been “programmed to swim down fine cracks in concrete [and produce] a mixture of calcium carbonate and bacterial glue … to ‘knit’ the building back together”.

The “programming” of the BacillaFilla spores mean they only start germinating on contact with concrete, can sense when they reach the bottom of cracks (repair isn’t activated until they do), harden to the same strength as the surrounding concrete, and have a built-in self destruct gene to stop them going rogue and producing massive concrete tumors. There are also environmental implications — 5% of all man-made carbon dioxide is from the production of concrete. It is hoped the spores will be able to prolong the life of structures that would be very costly to rebuild.

1D3O

Impact protection has always been a difficult problem — how do you make something that offers real protection without becoming too heavy or inflexible?Plastic knee-pads, for example, restrict movement and can still transmit impacts to bone.

D30 offers an ingenious fix to this problem. It’s a material made of ‘intelligent molecules’ that move freely (like Play-Doh) under gentle pressure, but lock upwhen struck hard. Jackets are already on the market containing D30 pads that offer flexibility, as well as protection from the tarmac, baseball bats or fists you might accidentally walk into. The pads are low-profile, making the jackets suitable for stuntmen or even police.

The material actually works on a familiar principle, similar to the mixture of cornstarch and water you remember from elementary-school science experiments. (Some people even fill pools with the stuff.)

Memory implantation is now officially real

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Memory implantation is now officially real1SEXPAND

The movie Inception is getting closer to reality. By planting false memories into the minds of mice, neuroscientists at MIT have created the first artificially implanted memories. And they’ve brought us closer to understanding the fallibility of human recollection.

When we experience something, say a trip to the park, a memory of the event is stored in a constellation of interconnected neurons in our brains called an “engram,” or memory trace. When you recall that trip to the park, neurons in the engram become active. Reactivate those neurons artificially, the theory goes, and you can bring the memory bubbling to the surface of someone’s psyche.

In the 1940s, Canadian neurosurgeon Wilder Penfield delivered electrical shocks to the temporal lobes of patients about to undergo brain surgery, and his subjects reported the sudden recollection of specific memories. While Penfield’s methods were too crude to isolate a single engram, they provided more evidence for the memory-trace hypothesis. And they also pointed to a brain region, the temporal lobe, as a repository for episodic memories. Today, we know that these memories are actually stored in a sea-horse shaped region of the temporal lobe called the hippocampus.

How To Implant a Memory

In a study published in the latest issue of Science, a team of researchers led by MIT neuroscientist and Nobel Laureate Susumu Tonegawa demonstrates its ability to isolate and activate engrams in a mouse’s memory-rich hippocampus. The researchers go on to implant false memories in the mouse’s mind, causing it to recall experiences that have never actually occurred. Here’s how they did it.

Memory implantation is now officially realSEXPAND

First, Tonegawa and his team genetically engineered mice capable of expressing a protein called Channelrhodopsin-2 (ChR2). Importantly, the protein was expressed exclusively in the hippocampus, and only in neurons involved in memory formation. This allowed Tonegawa and his team to effectively label only the brain cells encoding for a specific engram. Place a mouse in a safe environment (Chamber A, the blue box above), and the brain cells encoding for the memory of this environment express ChR2 (the white dots).

Memory implantation is now officially realSEXPAND

Here’s the brilliant bit. ChR2 is a light-sensitive protein; shine a light on it with the tip of an optical fiber that’s been securely implanted in the brain, and cells that express it become activated. The technique – known as “optogenetics” – is among the most useful to emerge in the field of neuroscience in recent memory, and Tonegawa and his colleagues use it here to great effect. By placing the animal in a second, entirely different environment (Chamber B, the red box) and delivering light to the hippocampus, the researchers could reactivate the engram established in Chamber A, forcing the mouse to recall its experience while situated in the entirely novel environment of Chamber B.

Next comes the memory implantation. While the mouse is busy recalling the first environment, the researchers deliver a mild electrical shock to the rodent’s feet. The shock conditions fear into the mouse. Past research has shown that if one shocks a mouse in a specific environment frequently enough, it will freeze in trepidation when reintroduced to the environment at a later date. But what happens when a mouse in one environment is shocked while recalling a different, previous environment – one in which it received no foot shock?

Memory implantation is now officially realSEXPAND

Incredibly, when Tonegawa and his colleagues placed the mouse back into Chamber A, it stopped in its tracks, evincing behavioral signs of fear. The mouse’s reaction indicates it had formed a false fear-memory associated with Chamber A while standing in Chamber B. A false memory had been successfully incepted by manipulating the very neural connections involved in the mouse’s true memory. Mice later placed in Chamber B also froze in their tracks, though not as readily as those that had been shocked in Chamber B without having their memory of Chamber A activated.

“Now that we can reactivate and change the contents of memories in the brain, we can begin asking questions that were once the realm of philosophy,” said study co-author Steve Ramirez in a statement. He added:

Are there multiple conditions that lead to the formation of false memories? Can false memories for both pleasurable and aversive events be artificially created? What about false memories for more than just contexts — false memories for objects, food or other mice? These are the once seemingly sci-fi questions that can now be experimentally tackled in the lab.

Will Our Memories Ever Be Trustworthy?

If Ramirez’s study sounds familiar, don’t worry; you don’t have an implanted memory of it. A study published last year by Aleena Garner and her colleagues at UC San Diegofollowed a very similar experimental protocol, but failed to see increased freezing in mice re-exposed to either Chamber A orChamber B. Instead, the mice are believed to have formed what Garner and her team call a “hybrid” memory, one that could only be retrieved by combining “elements of both the… artificial stimulation and the natural sensory cues from the [fear-conditioning environment.]” If either condition were presented independently, the mice would carry on about their business — as though they had forgotten to be afraid.

“A key difference in [Garner’s system],” write Ramirez and Xu Liu, first authors on the present paper, is that “cells in the entire forebrain were labeled and reactivated over an extended period by a synthetic ligand.” Ramirez and Liu therefore hypothesize that activating neurons across larger areas of the brain and for longer periods of time may favor the formation of a memory “which may not be easily retrievable by the cues associated with each individual memory.” In contrast, they argue, activating smaller populations of neurons for shorter periods of time “may favor the formation of two distinct (false and genuine) memories,” as observed in the present study.

“Whether it’s a false or genuine memory,” said Tonegawa in a statement, “the brain’s neural mechanism underlying the recall of the memory is the same.” Ramirez expands on his colleague’s point:

These kinds of experiments show us just how reconstructive the process of memory actually is. Memory is not a carbon copy, but rather a reconstruction, of the world we’ve experienced. Our hope is that, by proposing a neural explanation for how false memories may be generated, down the line we can use this kind of knowledge to inform, say, a courtroom about just how unreliable things like eyewitness testimony can actually be.

Understanding how memories – false or otherwise – form in the first place could help us understand why human recollection is so untrustworthy.

The researchers’ findings are published in the latest issue of Science.