In one ear and out the other

Remember that sound bite you heard on the radio this morning? The grocery items your spouse asked you to pick up? Chances are, you won’t.

Researchers at the University of Iowa have found that when it comes to memory, we don’t remember things we hear nearly as well as things we see or touch.

“As it turns out, there is merit to the Chinese proverb ‘I hear, and I forget; I see, and I remember,” says lead author of the study and UI graduate student, James Bigelow.

“We tend to think that the parts of our brain wired for memory are integrated. But our findings indicate our brain may use separate pathways to process information. Even more, our study suggests the brain may process auditory information differently than visual and tactile information, and alternative strategies—such as increased mental repetition—may be needed when trying to improve memory,” says Amy Poremba, associate professor in the UI Department of Psychology and corresponding author on the paper, published this week in the journal PLoS One.

Bigelow and Poremba discovered that when more than 100 UI undergraduate students were exposed to a variety of sounds, visuals, and things that could be felt, the students were least apt to remember the sounds they had heard.

In an experiment testing short-term memory, participants were asked to listen to pure tones they heard through headphones, look at various shades of red squares, and feel low-intensity vibrations by gripping an aluminum bar. Each set of tones, squares and vibrations was separated by time delays ranging from one to 32 seconds.

Although students’ memory declined across the board when time delays grew longer, the decline was much greater for sounds, and began as early as four to eight seconds after being exposed to them.

While this seems like a short time span, it’s akin to forgetting a phone number that wasn’t written down, notes Poremba. “If someone gives you a number, and you dial it right away, you are usually fine. But do anything in between, and the odds are you will have forgotten it,” she says.

In a second experiment, Bigelow and Poremba tested participants’ memory using things they might encounter on an everyday basis. Students listened to audio recordings of dogs barking, watched silent videos of a basketball game, and touched and held common objects blocked from view, such as a coffee mug. The researchers found that between an hour and a week later, students were worse at remembering the sounds they had heard, but their memory for visual scenes and tactile objects was about the same.

Both experiments suggest that the way your mind processes and stores sound may be different from the way it process and stores other types of memories. And that could have big implications for educators, design engineers, and advertisers alike.

“As teachers, we want to assume students will remember everything we say. But if you really want something to be memorable you may need to include a visual or hands-on experience, in addition to auditory information,” says Poremba.

Previous research has suggested that humans may have superior visual memory, and that hearing words associated with sounds—rather than hearing the sounds alone—may aid memory. Bigelow and Poremba’s study builds upon those findings by confirming that, indeed, we remember less of what we hear, regardless of whether sounds are linked to words.

The study also is the first to show that our ability to remember what we touch is roughly equal to our ability to remember what we see. The finding is important, because experiments with nonhuman primates such as monkeys and chimpanzees have shown that they similarly excel at visual and tactile memory tasks, but struggle with auditory tasks. Based on these observations, the authors believe humans’ weakness for remembering sounds likely has its roots in the evolution of the primate brain.

New ideas change your brain cells

A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.

Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.

In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.

“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.

It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.

“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”

Background

According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.

(Image: Shutterstock)

Mechanism behind the activation of dormant memory cells discovered

The electrical stimulation of the hippocampus in in-vivo experiments activates precisely the same receptor complexes as learning or memory recall. This has been discovered for the first time and the finding has now been published in the highly respected journal “Brain Structure Function”. “This may form the basis for the use of medications aimed at powering up dormant or less active memory cells,” says Gert Lubec, Head of Fundamental Research / Neuroproteomics at the University Department of Paediatrics and Adolescent Medicine at the MedUni Vienna. 

“This discovery has far-reaching consequences both for the molecular understanding of memory formation and the understanding of the clinical electrical stimulation, which is already possible, of areas of the brain for therapeutic purposes,” says the MedUni Vienna researcher.  Similar principles are currently already being used in the field of deep brain stimulation. With this technology, an implanted device delivers electronic impulses to the patient’s brain. This physical stimulation allows neuronal circuits to be influenced that control both behaviour and memory.

The latest findings very much form part of the highly controversial subject of “cognitive enhancement”. Scientists are currently discussing the possibility of improving mental capacity through the use of drugs - including in healthy subjects of all age groups, but especially in patients with age-related impairments of cognitive processes.

With regard to the study design, two electrodes were implanted into the brain in an animal model. One transferred electrical impulses to stimulate the hippocampus, while the other transferred the electrical signals away. “These electrical potentials are the electrical equivalent of memory and are known as LTP (Long Term Potentiation),” explains Lubec. The generation of LTP in an in-vivo experiment was accompanied by specific changes in the receptor complexes - the same receptor complexes that are also activated during learning and memory formation.

A circuit for change

To answer the seemingly simple question “Have I been here before?” we must use our memories of previous experiences to determine if our current location is familiar or novel. In a new study published in the Journal of Neuroscience researchers from the RIKEN Brain Science Institute have identified a region of the hippocampus, called CA2, which is sensitive to even small changes in a familiar context. The results provide the first clue to the contributions of CA2 to memory and may help shed light on why this area is often found to be abnormal in the schizophrenic brain.

Why does the brain remember dreams?

Some people recall a dream every morning, whereas others rarely recall one. A team led by Perrine Ruby, an Inserm Research Fellow at the Lyon Neuroscience Research Center (Inserm/CNRS/Université Claude Bernard Lyon 1), has studied the brain activity of these two types of dreamers in order to understand the differences between them. In a study published in the journal Neuropsychopharmacology, the researchers show that the temporo-parietal junction, an information-processing hub in the brain, is more active in high dream recallers. Increased activity in this brain region might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, thereby facilitating the encoding of dreams in memory.

The reason for dreaming is still a mystery for the researchers who study the difference between “high dream recallers,” who recall dreams regularly, and “low dream recallers,” who recall dreams rarely. In January 2013 (work published in the journal Cerebral Cortex), the team led by Perrine Ruby, Inserm researcher at the Lyon Neuroscience Research Center, made the following two observations: “high dream recallers” have twice as many time of wakefulness during sleep as “low dream recallers” and their brains are more reactive to auditory stimuli during sleep and wakefulness. This increased brain reactivity may promote awakenings during the night, and may thus facilitate memorisation of dreams during brief periods of wakefulness.

In this new study, the research team sought to identify which areas of the brain differentiate high and low dream recallers. They used Positron Emission Tomography (PET) to measure the spontaneous brain activity of 41 volunteers during wakefulness and sleep. The volunteers were classified into 2 groups: 21 “high dream recallers” who recalled dreams 5.2 mornings  per week in average, and 20 “low dream recallers,” who reported 2 dreams per month in average. High dream recallers, both while awake and while asleep, showed stronger spontaneous brain activity in the medial prefrontal cortex (mPFC) and in the temporo-parietal junction (TPJ), an area of the brain involved in attention orienting toward external stimuli.

What Makes Memories Last?

Prions can be notoriously destructive, spurring proteins to misfold and interfere with cellular function as they spread without control. New research, published in the open access journal PLOS Biology on February 11, 2014, from scientists at the Stowers Institute for Medical Research reveals that certain prion-like proteins, however, can be precisely controlled so that they are generated only in a specific time and place. These prion-like proteins are not involved in disease processes; rather, they are essential for creating and maintaining long-term memories.

“This protein is not toxic; it’s important for memory to persist,” says Stowers researcher Kausik Si, Ph.D., who led the study. To ensure that long-lasting memories are created only in the appropriate neural circuits, Si explains, the protein must be tightly regulated so that it adopts its prion-like form only in response to specific stimuli. He and his colleagues report on the biochemical changes that make that precision possible.

Si’s lab is focused on finding the molecular alterations that encode a memory in specific neurons as it endures for the days, months, or years—even as the cells’ proteins are degraded and renewed. Increasingly, their research is pointing toward prion-like proteins as critical regulators of long-term memory.

In 2012, Si’s group demonstrated that prion formation in nerve cells is essential for the persistence of long-term memory in fruit flies. Prions are a fitting candidate for this job because their conversion is self-sustaining: once a prion-forming protein has shifted into its prion shape, additional proteins continue to convert without any additional stimulus.

Si’s team found that in fruit flies, the prion-forming protein Orb2 is necessary for memories to persist. Flies that produce a mutated version of Orb2 that is unable to form prions learn new behaviors, but their memories are short-lived. “Beyond a day, the memories become unstable. By three days, the memory has completely disappeared,” Si explains.

In the new study, Si wanted to find out how this process could be controlled so that memories form at the right time. “We know that all experiences do not form long-term memory—somehow the nervous system has a way to discriminate. So if prion-formation is the biochemical basis of memory, it must be regulated.” Si says. “But prion formation appears to be random for all the cases we know of so far.”

Si and his colleagues knew that Orb2 existed in two forms—Orb2A and Orb2B. Orb2B is widespread throughout the fruit fly’s nervous system, but Orb2A appears only in a few neurons, at extremely low concentrations. What’s more, once it is produced, Orb2A quickly falls apart; the protein has a half-life of only about an hour.

“When Orb2A binds to the more abundant form, it triggers conversion to the prion state, acting as a seed for the conversion. Once conversion begins, it is a self-sustaining process; additional Orb2 continues to convert to the prion state, with or without Orb2A. By altering the abundance of the Orb2A seed”, Si says, “cells might regulate where, when, and how the conversion process is engaged”. But how do nerve cells control the abundance of the Orb2A seed?

Their experiments revealed that when a protein called TOB associates with Orb2A , it becomes much more stable, with a new half-life of 24 hours. This step increases the prevalence of the prion-like state and explains how Orb2’s conversion to the prion state can be confined in both time and space.

The findings raise a host of new questions for Si, who now wants to understand what happens when Orb2 enters its prion-like state, as well as where in the brain the process occurs. While unraveling these mechanisms will likely be more accessible in the fruit fly than in more complex organisms, Si points out that proteins related to Orb2 and TOB have also been found in the brains of mice and humans. He has already shown that in the sea snail Aplysia, conversion to a prion-like state facilitates long-term change in synaptic strength. “This basic mechanism appears to be conserved across species,” he notes.

Brain Implants Hold Promise Restoring Combat Memory Loss

The Pentagon is exploring the development of implantable probes that may one day help reverse some memory loss caused by brain injury.

The goal of the project, still in early stages, is to treat some of the more than 280,000 troops who have suffered brain injuries since 2000, including in combat in Iraq and Afghanistan.

The Defense Advanced Research Projects Agency is focused on wounded veterans, though some research may benefit others such as seniors with dementia or athletes with brain injuries, said Geoff Ling, a physician and deputy director of Darpa’s Defense Sciences office. It’s still far from certain that such work will result in an anti-memory-loss device. Still, word of the project is creating excitement after more than a decade of failed attempts to develop drugs to treat brain injury and memory loss.

“The way human memory works is one of the great unsolved mysteries,” said Andres Lozano, chairman of neurosurgery at the University of Toronto. “This has tremendous value from a basic science aspect. It may have huge implications for patients with disorders affecting memory, including those with dementia and Alzheimer’s disease.”

At least 1.7 million people in the U.S. are diagnosed with memory loss each year, costing the nation’s economy more than $76 billion annually, according to the most recent federal health data. The Department of Veterans Affairs estimates it will spend $4.2 billion to care for former troops with brain injuries between fiscal 2013 and 2022.

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The iPod in the head: How the brain processes musical hallucinations

Sufferers persistently perceive music, as if they were hearing it with their ears, when no music is actually being played. Initially they often mistake the experience for actual music playing and while musical hallucinations can occasionally be a symptom of a neurological or psychiatric disorder, it is usually caused by hearing loss in people who are in normal physical and mental health.

Dr Sukhbinder Kumar from the Institute of Neuroscience at Newcastle University, lead author of the paper published in Cortex said: “We found that a network of brain areas, that are usually involved in processing of melodies and retrieval of memory of music, were particularly active during hallucinations of music in the absence of any sound or music being played externally.”

Nearly one in ten people suffer from tinnitus which is technically an auditory hallucination, in which tones or buzzing noises are heard following hearing loss. However in a small number of people with hearing loss these hallucinations take the form of music, but until now the brain mechanisms underlying this process were poorly understood.

This study by researchers at Newcastle University and University College London and funded by the Wellcome Trust has looked in depth at one sufferer of the condition and pinpointed the regions of the brain involved in producing the hallucinations. These findings could lead to a better understanding of the condition and possibly treatments in the future.

Musical hallucination

Sylvia, 69, a maths teacher who is also a musician with perfect pitch, started to go deaf about 20 years ago after a viral infection. Then about eleven years later she experienced a sudden acute hearing loss and severe tinnitus and her musical hallucinations developed after this. Due to her musical knowledge Sylvia was able to notate what she was hearing.

Initially the condition was irritating and affected Sylvia’s sleep, but she learnt to live with it. “I did everything I could to get rid of them but they persisted, always in a minor key and therefore a bit depressing,” she said.

“Eventually the number of notes increased until they seemed to be parts of tunes. One day I recognized something and, once I had done so, more and more phrases from classical music appeared in my brain.”

Among the pieces of music that Sylvia was hearing in her hallucinations was Gilbert and Sullivan’s HMS Pinafore, as well as music by Bach. Amazingly Sylvia found that by playing music herself, she was able to alter the music in her hallucinations.

“I can change the hallucination playing in my head to the music I am practising. This is particularly the case with the music of Bach - the hallucination will pause and then a whole page will start to play in my head, gradually curtailing itself until just a phrase remains and is repeated.  That might then repeat a thousand times a day. It is as if I have my own internal ipod.”

Sylvia’s experience is fairly typical, though the condition occurs just as often in non-musicians, and sometimes starts abruptly rather than slowly developing as in her case.

How we hear

As Sylvia’s hallucinations could be manipulated by playing an external piece of music that allowed the researchers to understand what was happening in her brain during hallucinations. They first identified pieces of music that suppressed her hallucinations and these pieces were then played to her while her brain activity was being monitored using magnetoencephalography MEG), which measures magnetic fields around the scalp as the brain processes information.

During normal perception of music what we actually ‘hear’ is a complex interplay of the sound entering the ear and our brain’s interpretations and predictions. Normally the strength and quality of the input from the ear is so high that it dominates what we actually perceive however the brain fills in the gaps when the ears do not provide enough input.

“With hearing loss, as in Sylvia’s case, the signal from the ear becomes weak and noisy, like a poorly-tuned radio. The brain’s predictive mechanisms therefore have to work very hard to make sense of what we are hearing. What we have found is that these processes sometimes end up running away with themselves to cause hallucinations,” said author Dr William Sedley also of Newcastle University.

Dr Kumar added: “This also explains why listening to an external piece of music suppresses hallucinations. When external music is playing the signal entering her brain is much stronger and more reliable, which constrains the aberrant communication going on in the brain areas during hallucinations.”

This new understanding of musical hallucinations may provide better treatment in the future as Newcastle University’s Professor Tim Griffiths, professor of Cognitive Neurology who lead the study explained: “It might be possible to disrupt the abnormal communication between the brain areas using brain stimulation, or to use pharmacological treatments to disrupt chemical transmitters that drive communication between them.

“Better hearing aids also appear to help suppress hallucinations, so we would advise people experiencing musical hallucinations to seek medical attention, if for nothing more than to ensure they have the best available hearing aids.”

Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, says: “This case is extremely fascinating, but the condition is relatively rare. However, it is unusual cases such as this that can give us profound insights into how the brain works and, one hopes, lead to potential new treatments to improve the patient’s life.”