Posts tagged memory
Articles and news from the latest research reports.
Are concussions related to Alzheimer’s disease?
A new study suggests that a history of concussion involving at least a momentary loss of consciousness may be related to the buildup of Alzheimer’s-associated plaques in the brain. The research is published in the December 26, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.
"Interestingly, in people with a history of concussion, a difference in the amount of brain plaques was found only in those with memory and thinking problems, not in those who were cognitively normal," said study author Michelle Mielke, PhD, with Mayo Clinic in Rochester, Minn.
For the study, people from Olmsted County in Minnesota were given brain scans; these included 448 people without any signs of memory problems and 141 people with memory and thinking problems called mild cognitive impairment. Participants, who were all age 70 or older, were also asked about whether they had ever experienced a brain injury that involved any loss of consciousness or memory.
Of the 448 people without any thinking or memory problems, 17 percent reported a brain injury and 18 percent of the 141 with memory and thinking difficulties reported a concussion or head trauma.
The study found no difference in any brain scan measures among the people without memory and thinking impairments, whether or not they had head trauma. However, people with memory and thinking impairments and a history of head trauma had levels of amyloid plaques an average of 18 percent higher than those with no head trauma history.
"Our results add merit to the idea that concussion and Alzheimer’s disease brain pathology may be related," said Mielke. "However, the fact that we did not find a relationship in those without memory and thinking problems suggests that any association between head trauma and amyloid is complex."
Take note students: Mice that ‘cram’ for exams remember less
It’s been more than 100 years since German psychologist Hermann Ebbinghaus determined that learning interspersed with rest created longer-lasting memories than so-called cramming, or learning without rest intervals.
Yet it’s only much more recently that scientists have begun to understand the underlying molecular mechanisms for this phenomenon. In a study published Monday in the journal PNAS, researchers examined the physical changes in the brain cells of mice while “training” their eyes to keep track of a moving image.
Researchers examined the horizontal optokinetic response, or HOKR, in mice to determine what rest interval was best suited to increasing their memory.
HOKR is what makes it possible for a rider in a train to visually track the moving scenery. While the process is unconscious, it involves frequent, minute eye movements.
Mice were fastened to a device that immobilized their heads and then were made to look at a revolving, checkered image that triggered the eye response. A high speed camera was used to determine when the tracking began and when it stopped.
While the eyes of lab mice are initially unable to track the revolving image at a high speed, they eventually adapt to faster and faster movement. This tracking ability is retained for a period of time before it is forgotten.
Some of the mice were allowed to rest between training sessions, while others were not. Researchers noted clear differences between the mice that were given rest time “spacing” and those that received no breaks, or “massed training.”
"One hour of spacing produced the highest memory retention at 24 hours, which lasted for one month," wrote lead study author Wajeeha Aziz, a molecular physiologist at the National Institute for Physiological Sciences in Okazaki, Japan, and her colleagues.
"Surprisingly, massed training also produced long-term memory…. However, this occurred slowly over days, and the memory lasted for only one week."
Researchers compared brain tissue from the two groups of trained mice and with those of mice that received no training. They found that both groups of trained mice had reduced synapses in a specific type of nerve cell, Purkinje neurons.
However, spacing the training appeared to make these structural changes in synapses occur more quickly, the authors said.
"Further investigations are needed to elucidate the precise molecular mechanisms that regulate the temporal features of long-lasting memory, and the structural modifications of synapses provides an indispensable readout for such studies," the authors concluded.
Researchers find ECT can rid the mind of selected memory
A team of researchers working in the Netherlands has found that partial selective memory deletion can be achieved using Electroconvulsive Therapy (ECT). In their paper published in the journal Nature Neuroscience, the team describes a memory experiment they conducted with the assistance of severely depressed people who had already consented to undergoing ECT and found that such treatment could be used to at least partially erase memories of a specified event.
Scientists have known since 1968 (thanks to experiments conducted by psychologist Donald Lewis) that applying a shock to the brain of a rat can cause it to forget something unpleasant it had remembered. Subsequent experiments have found that memories can be blunted using repetitive type therapies or by injecting drugs such as propranolol into the brain. The one element all such findings have in common is that they must be applied during a time when a person is attempting to recall a certain event. Scientists hope that such research may lead to new ways to treat PTSD and other memory related mental ailments. In this new effort the researchers explored the idea of erasing specific memories using ECT.
Currently, people with severe depression who don’t respond to any other type of treatment are offered ECT as a last resort. It has a remarkably good success rate (approximately 86 percent rate of remission) but causes some degree of memory loss. In the Netherlands study, the team enlisted the assistance of 39 such patients who had already agreed to undergo ECT. Instead of receiving just the standard treatment, however, the volunteers were asked to watch two slide shows (along with narration) —both of which contained unsettling content. A week later the participants were divided into three groups—two to get the shock treatment and one to serve as a control group—all were asked to remember and describe one of the traumatic events described in the slide shows. Afterwards, one of the groups was given ECT and then the next day was asked to recount both stores. The other non-control group was given ECT and then were asked right afterwards to recount the unpleasant stories. The control group was asked to try to recount both stories as well.
In comparing the results between the groups, the researchers found that the first group that had been quizzed a day after receiving ECT had difficulty recalling the first story, which they had recounted prior to ECT, but remembered most of second. The second group that received ECT were able to recall both stories equally well, and the third—the control group—were able to remember both stories better than either of the groups that had received ECT.
The experiment suggests that it is possible to selectively erase short term memory in a controlled environment. Much more research will have to be conducted to determine if it would work in real world situations.
Researchers identify gene that influences the ability to remember faces
New findings suggest the oxytocin receptor, a gene known to influence mother-infant bonding and pair bonding in monogamous species, also plays a special role in the ability to remember faces. This research has important implications for disorders in which social information processing is disrupted, including autism spectrum disorder. In addition, the finding may lead to new strategies for improving social cognition in several psychiatric disorders.
A team of researchers from Yerkes National Primate Research Center at Emory University in Atlanta, the University College London in the United Kingdom and University of Tampere in Finland made the discovery, which will be published in an online Early Edition of Proceedings of the National Academy of Sciences.
According to author Larry Young, PhD, of Yerkes, the Department of Psychiatry in Emory’s School of Medicine and Emory’s Center for Translational Social Neuroscience (CTSN), this is the first study to demonstrate that variation in the oxytocin receptor gene influences face recognition skills. He and co-author David Skuse point out the implication that oxytocin plays an important role in promoting our ability to recognize one another, yet about one-third of the population possesses only the genetic variant that negatively impacts that ability. They say this finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.
Skuse is with the Institute of Child Health, University College London, and the Great Ormond Street Hospital for Children, NHS Foundation Trust, London.
Young, Skuse and their research team studied 198 families with a single autistic child because these families were known to show a wide range of variability in facial recognition skills; two-thirds of the families were from the United Kingdom, and the remainder from Finland.
The Emory researchers previously found the oxytocin receptor is essential for olfactory-based social recognition in rodents, like mice and voles, and wondered whether the same gene could also be involved in human face recognition. They examined the influence of subtle differences in oxytocin receptor gene structure on face memory competence in the parents, non-autistic siblings and autistic child, and discovered a single change in the DNA of the oxytocin receptor had a big impact on face memory skills in the families. According to Young, this finding implies that oxytocin likely plays an important role more generally in social information processing, which is disrupted in disorders such as autism.
Additionally, this study is remarkable for its evolutionary aspect. Rodents use odors for social recognition while humans use visual facial cues. This suggests an ancient conservation in genetic and neural architectures involved in social information processing that transcends the sensory modalities used from mouse to man.
Skuse credits Young’s previous research that found mice with a mutated oxytocin receptor failed to recognize mice they previously encountered. “This led us to pursue more information about facial recognition and the implications for disorders in which social information processing is disrupted.” Young adds the team will continue working together to pursue strategies for improving social cognition in psychiatric disorders based on the current findings.
Study Shows Where Alzheimer’s Starts and How It Spreads
Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer’s disease and in mouse models of the disease, Columbia University Medical Center (CUMC) researchers have clarified three fundamental issues about Alzheimer’s: where it starts, why it starts there, and how it spreads. In addition to advancing understanding of Alzheimer’s, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journal Nature Neuroscience.
“It has been known for years that Alzheimer’s starts in a brain region known as the entorhinal cortex,” said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer’s Disease Research Center. “But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected.”
The study also shows that, over time, Alzheimer’s spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer’s spreads “functionally,” that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.
A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. “The LEC is especially vulnerable to Alzheimer’s because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer’s,” said co-senior author Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.
In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP). All of the adults were free of dementia at the time of enrollment.
“Dr. Richard Mayeux’s WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer’s disease,” said Dr. Small. “This study has given us a unique opportunity to image and characterize patients with Alzheimer’s in its earliest, preclinical stage.”
The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer’s disease. An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) — a measure of metabolic activity — in the LEC compared with that of the 84 adults who were free of dementia.
A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer’s.
To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small’s lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.
The study has implications for both research and treatment. “Now that we’ve pinpointed where Alzheimer’s starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer’s at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions,” said Dr. Small. In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer’s drugs during the disease’s early stages.
The logistics of learning
Learning requires constant reconfiguration of the connections between nerve cells. Two new studies now yield new insights into the molecular mechanisms that underlie the learning process.
Learning and memory are made possible by the incessant reorganization of nerve connections in the brain. Both processes are based on targeted modifications of the functional interfaces between nerve cells – the so-called synapses – which alter their form, molecular composition and functional properties. In effect, connections between cells that are frequently co-activated together are progressively altered so that they respond to subsequent signals more rapidly and more strongly. This way, information can be encoded in patterns of synaptic activity and promptly recalled when needed. The converse is also true: learned behaviors can be lost by disuse, because inactive synapses are themselves less likely to transmit an incoming impulse, leading to the decay of such connections.
How exactly an individual synapse is altered without simultaneously affecting nearby nerve cells or other synapses on the same cell is a question that is central to Michael Kiebler’s research. Kiebler, a biochemist, holds the Chair of Cell Biology in the Faculty of Medicine at LMU. “It is now clear that the changes take place in the cell that is stimulated by synaptic input – the post-synaptic cell – and in particular in its so-called dendritic spines,” he says, “and particles that are known as “neuronal RNA granules” deliver mRNA molecules to these sites“. These mRNAs represent the blueprints for the synthesis of the proteins responsible for reconfiguring the synapses. Kiebler‘s team has developed a model, which postulates that these granules migrate from dendrite to dendrite, and release their mRNAs specifically at sites that are repeatedly activated. This would ensure that the relevant proteins are synthesized only where they are needed within the cell.
In spite of the potential significance of the model, the molecular mechanisms required for its realization have remained obscure. mRNA-binding proteins, including Staufen2 (Stau2) and Barentsz, are essential components of the granules, and Kiebler’s team, in collaboration with Giulio Superti-Furga’s group (CeMM, Vienna), have now used specific antibodies to isolate and characterize neuronal granules that contain either Stau2 or Barentsz.
Surprising diversity
It has generally been assumed that all neuronal RNA granules have essentially similar compositions. However, the new findings indicate that this is not the case. A comparison between Stau2- and Barentsz-containing granules reveals that they differ in about two-thirds of their proteins. “This suggests that the RNA granules are highly heterogeneous and dynamic in their composition,” says Kiebler. “And that makes sense to me, because it would mean that the granules can perform different functions depending on which mRNAs they carry.” Furthermore, the researchers have shown that the granules contain virtually none of the factors known to promote the translation of mRNAs into proteins. On the contrary, they include many molecules that repress protein synthesis. This in turn implies that the process of mRNA transport is uncoupled from the subsequent production of the proteins they encode.
In a complementary study, Kiebler’s team also characterized the mRNA cargoes associated with the granules. “Until now, none of the RNA molecules present in Stau2-containing granules in mammalian nerve cells had been defined, but we have now been able to identify many specific mRNAs,” Kiebler explains. Further experiments revealed that Stau2 stabilizes the mRNAs, allowing them to be used more often for the production of proteins. Moreover, the researchers have shown that specialized structures within these mRNAs, called “Staufen-Recognized Structures” (SRS), are essential for their recognition and stabilization by Stau2. “This allows us to propose a molecular mechanism for RNA recognition for the first time,” says Kiebler.
Taken together, the two new papers (1, 2) provide novel insights into the molecular mechanisms that underlie learning and memory. The scientists now want to dissect out the details in future studies. “In the long term, we are particularly interested in the question of how an activated synapse can alter the state of the granules and induce the production of protein,” Kiebler notes. It is becoming increasingly clear that RNA-binding proteins play essential roles in nerve cells. Disruption of their action can lead to neurodegenerative diseases and neurological dysfunction. Clearly, not only classical conditions such as Alzheimer‘s or Parkinson’s disease, in which RNA-binding proteins are always involved, but also cognitive defects or age-associated impairment of learning ability must be viewed in this context,” Kiebler concludes.
(Source: en.uni-muenchen.de)
Brain Area Attacked by Alzheimer’s Links Learning and Rewards
One of the first areas of the brain to be attacked by Alzheimer’s disease is more active when the brain isn’t working very hard, and quiets down during the brain’s peak performance.
The question that Duke University graduate student Sarah Heilbronner wanted to resolve was whether this brain region, called the posterior cingulate cortex, or PCC, actively dampens cognitive performance, say by allowing the mind to wander, or is instead monitoring performance and trying to improve it when needed.
If the PCC were monitoring and improving performance, increased activity there would be the result of poor performance, not the cause of it.
The PCC connects to both learning and reward systems, Heilbronner said, and is a part of the “default mode network.” It lies along a mid-line between the ears, where many structures related to rewards can be found. “It’s kind of a nexus for multiple systems,” said Heilbronner, who is currently a postdoctoral researcher in neuroanatomy at the University of Rochester.
"As this area begins to deteriorate, people begin to show the early signs of cognitive decline — problems learning and remembering things, getting lost, trouble planning — that ultimately manifest as outright dementia," said Michael Platt, director of the Duke Institute for Brain Sciences, who supervised Heilbronner’s 2012 dissertation. Their findings appear Dec. 18 in the journal Neuron.
Heilbronner’s experiment to better understand the PCC’s role in learning and remembering relied on two rhesus macaque monkeys fitted with electrodes to read out the activity of individual neurons in their brains. Their task was akin to playing video games with their eyes. The monkeys were shown a series of photographs each day marked with dots at the upper left and lower right corners. To get a rewarding squirt of juice, they had to move their gaze to the correct target dot on a photo, and they learned by trial and error which dot would yield the reward for each photo.
Each day, they were shown up to 12 photos from an assortment of Heilbronner’s vacation snaps at Yellowstone National Park and the Grand Canyon. Some of each day’s images were familiar with a known reward target, and others were new. As the monkeys responded with their gaze, the researchers watched the activity of dozens of neurons in each monkey’s brain immediately following correct and incorrect responses. They also altered the amount of juice dispensed in some cases, creating a sense of high-reward and low-reward answers.
If the PCC actively dampened performance, the researchers would expect to see it active before a choice is made or the feedback is received. Instead, they saw it working after the feedback, lasting sometimes until the next image was presented. Neurons in the PCC responded strongly when the monkeys needed to learn something new, especially when they made errors or didn’t earn enough reward to keep motivated.
The researchers also ran the task after administering a drug, muscimol, that impaired the function of the PCC temporarily during testing. With the center inactivated by the drug, the monkeys could recall earlier learning regardless of the size of the reward. Learning a new item was still possible when the reward was large, but the monkeys couldn’t learn anything new when rewards were small. “Maybe it didn’t seem worth it,” Heilbronner said.
The dampening experiment also reinforced what the researchers had seen in the timing of the PCC’s response. If this center’s role is to let the mind wander, performance should have improved when the muscimol was administered, but the opposite was true.
Heilbronner concludes that the PCC summons more resources for a challenging cognitive task. So rather than being the cause of poor performance on a task, PCC actually steps in during a challenge to improve the situation.
"This study tells us that a healthy PCC is required for monitoring performance and keeping motivated during learning, particularly when problems are challenging," Platt said.
Heilbronner is now interested in finding out whether the PCC is more important to learning than it is to recall, and how motivation interacts with PCC abnormalities seen in Alzheimer’s disease.
‘Chemobrain’ linked to disrupted brain networks
For some cancer patients, the mental fogginess that develops with chemotherapy lingers long after treatment ends. Now research in breast cancer patients may offer an explanation.
Patients who experience “chemobrain” following treatment for breast cancer show disruptions in brain networks that are not present in patients who do not report cognitive difficulties, according to researchers at Washington University School of Medicine in St. Louis.
Results of the small study were reported Thursday, Dec. 12 at a poster presentation at the San Antonio Breast Cancer Symposium.
According to the researchers, many breast cancer patients who receive chemotherapy report long-term problems with memory, attention, learning, visual-spatial skills and other forms of information processing. The brain mechanisms contributing to these difficulties are poorly understood.
The investigators used an imaging technique called resting state functional-connectivity magnetic resonance imaging (rs-fcMRI) to assess the wiring among regions of the brain in 28 patients treated at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University. Fifteen patients reported they were “extremely” or “strongly” affected by cognitive difficulties. The remaining 13 reported no cognitive impairment.
The imaging studies suggest that standard chemotherapy given to breast cancer patients may alter connectivity in brain networks, especially in the frontal parietal control regions responsible for executive function, attention and decision-making.
“Chemobrain is most likely a global phenomenon in the brain, but a set of regions involved in executive control, called the frontal-parietal network, is perhaps the most affected brain system,” said Jay F. Piccirillo, MD, professor of otolaryngology and a member of the research team with expertise in the use of brain imaging to study tinnitus, or phantom noise. “We’re confirming previous studies that also have shown this. And we’re developing a solid multidisciplinary working group at Washington University to determine how we can help these women.”
Other studies also have used neuroimaging techniques to observe the neural disruptions associated with Alzheimer’s disease, depression and stroke. Washington University researchers are beginning to investigate whether cancer patients experiencing chemobrain may benefit from therapies similar to those that help patients with other cognitive disorders.
(Source: news.wustl.edu)
Synaptic mechanisms of brain waves
Team at IST Austria examines synaptic mechanisms of rhythmic brain waves • Achievement possible through custom-design tools developed in collaboration with the institute’s Miba machine shop
How information is processed and encoded in the brain is a central question in neuroscience, as it is essential for high cognitive function such as learning and memory. Theta-gamma oscillations are “brain waves” observed in the hippocampus of behaving rats, a brain region involved in learning and memory. In rodents, theta-gamma oscillations are associated with information processing during exploration and spatial navigation. However, the underlying synaptic mechanisms have so far remained unclear. In research published this week in the journal Neuron, postdoc Alejandro Pernía-Andrade and Professor Peter Jonas, both at the Institute of Science and Technology Austria (IST Austria), discovered the synaptic mechanisms underlying oscillations at the dentate gyrus (main entrance of the hippocampus). Furthermore, the researchers suggest a role for these oscillations in the coding of information by the dentate gyrus principal neurons. Thus, these findings contribute to a better understanding of how information is processed in the brain.
Brain oscillations are, in fact, rhythmic changes in voltage in the extracellular space, referred to as electrical brain signals associated with the processing of information. These electrical signals are similar to those seen in electro-encephalographic recordings (EEG) in humans. Pernía-Andrade and Jonas observed these oscillations in a brain region called the hippocampus in behaving rats, and recorded oscillations occurring in this area using extracellular probes. To understand how oscillations are generated and which synaptic events trigger these oscillations, the researchers looked at synaptic transmission in granule cells (principal cells at the main entrance of the hippocampus) from both the extracellular (oscillations) and the intracellular perspectives (synaptic currents and neuronal firing), and then correlated the two. They discovered that excitatory and inhibitory synaptic signals contributed to different frequencies of oscillations, with excitation from the entorhinal cortex generating theta oscillations and inhibition by local dentate gyrus interneurons generating gamma oscillations. Together, excitation and inhibition provide the rhythmic signals of oscillations. It has been speculated that oscillations may help the dentate gyrus to encode information by acting as reference signals in temporal coding. Pernía-Andrade and Jonas now show that granule cell neurons send signals only at specific times in the cycle of oscillations. This so-called “phase locking” is necessary if oscillations are to function as reference signals in temporal coding.
The precise, high-resolution recording from granule cells necessary for these discoveries was possible only through technological innovations by Pernía-Andrade and Jonas, as previously no equipment was available to record synaptic signals in active rats in such high resolution. They are the result of a collaboration with the Miba machine shop, IST Austria’s electrical and mechanical SSU (Scientific Service Unit). Adapting commercially available equipment and custom-designing tools, Pernía-Andrade, Jonas and Todor Asenov, manager of the Miba machine shop, produced the first tools for precise biophysical analysis in active rats. This research is therefore not only a scientific advance but also represents a significant technological and conceptual progress in the quest to understand neuronal behavior under natural conditions.
(Source: ist.ac.at)
Turning off major memory switch dulls memories
A faultily formed memory sounds like hitting random notes on a keyboard while a proper one sounds more like a song, scientists say.
When they turned off a major switch for learning and memory, brain cells communicated, but the relationship was superficial, said Dr. Joe Tsien, neuroscientist at the Medical College of Georgia at Georgia Regents University and Co-Director of the GRU Brain & Behavior Discovery Institute.
“We have begun to crack the neural code, which allows us to look in real time at how thoughts happen and how memories are made,” Tsien said. “That has enabled us to understand for the first time how and whether the right keys are struck at the right time and in the right place and manner to make the beautiful sound of coherent memories and to compare what happens when a key element is missing.”
With the NMDA receptor intact, chatter reverberates, associations are made and helpful memories – like how touching a hot stove results in a burn – are easily retrieved.
“You see a face and think of a name, you see your office, and you think you need to work; everything is associative,” said Tsien, corresponding author of the study in the journal PLOS ONE. “But in mice lacking an NMDA receptor, you can tell the memory patterns are dull and dissociated.”
Using the century-old Pavlovian conditioning model that first showed how repetition creates association, they found that mice lacking a functioning NMDA receptor in the hippocampus, the brain’s center of learning and memory, could not recollect even something fearful.
When they played a tone, followed 20 seconds later by a mild foot shock, normal mice quickly made the association, down to the timing. The connection essentially never registered with mice lacking the NMDA receptor. Healthy brain recalling memories and Amnesic brain recalling contextual memories
“They form the initial patterns, but don’t rehearse them,” said Tsien. “Their tones are flat, the association is poor, while everything we register in the healthy brain is associative.” To illustrate just how flat, Postdoctoral Fellow Hui Kuang assigned musical notes to the memory activity of each, which resulted in random noise by the NMDA knockout mice compared to a dynamic rhythm from normal mice.
“By knowing what these patterns look like and what they mean, you can use this signature to measure, for example, during aging, why we begin to lose memory and to identify and test drugs that are truly effective at aiding memory,” Tsien said.
“You can tell whether there is an issue with reverberation, whether your brain is repeating what you need to remember, or repeats it but somehow stores it badly, so it’s not associated with the right things. This study has revealed a lot of fascinating details about what neuroscientists call the brain’s neural code” Tsien said.”
He wants to look at how aging affects these processes as a next step. The research team also is looking at Doogie, a mouse genetically bred by Tsien and his team in 1999 to be exceptionally smart, to see if they can also learn more about how super memories are made and what they look like.
This ability to decode how and what the brain is remembering, should one day help physicians better assess and treat conditions such as Alzheimer’s and schizophrenia, Tsien said. They may find that some answers are already out there, such as drugs that boost reverberation, or a stimulant like caffeine to help retrieve a memory, Tsien said.
His team first reported decoding brain cell conversations as memories were formed and recalled in PLOS ONE in 2009. As with the new study, they used a computational algorithm to translate the neuronal conversations into some of the first pictures of what memories look like.