Posts tagged memory
Articles and news from the latest research reports.
Alzheimer’s researchers trying brain zaps
It has the makings of a science fiction movie: zap someone’s brain with mild jolts of electricity to try to stave off the creeping memory loss of Alzheimer’s disease.
And it’s not easy. Holes are drilled into the patient’s skull so tiny wires can be implanted into just the right spot.
A dramatic shift is beginning in the frustrating struggle to find something to slow the damage of this epidemic: The first U.S. experiments with “brain pacemakers” for Alzheimer’s are getting under way. Scientists are looking beyond drugs to implants in the hunt for much-needed new treatments.
The research is in its infancy. Only a few dozen people with early-stage Alzheimer’s will be implanted in a handful of hospitals. No one knows if it might work, and if it does, how long the effects might last.
Kathy Sanford was among the first to sign up. The Ohio woman’s early-stage Alzheimer’s was gradually getting worse. She still lived independently, posting reminders to herself, but no longer could work. Medications weren’t helping.
The Connection Between Memory and Sleep
Researchers found information can be better retained with reinforcing stimuli delivered during sleep
When you’re studying for an exam, is there something you can do while you sleep to retain the information better?
"The question is, ‘What determines which information is going to be kept and which information is lost?’" says neuroscientist Ken Paller.
With support from the National Science Foundation (NSF), Paller and his team at Northwestern University are studying the connection between memory and sleep, and the possibilities of boosting memory storage while you snooze.
"We think many stages of sleep are important for memory. However, a lot of the evidence has shown that slow-wave sleep is particularly important for some types of memory," explains Paller.
Slow-wave sleep is often referred to as “deep sleep,” and consists of stages 3 and 4 of non-rapid-eye-movement sleep.
Paller’s lab group members demonstrated for Science Nation two of the tests they run on study participants. In the first experiment, the subjects learned two pieces of music in a format similar to the game Guitar Hero. During a short nap following learning, just one of the learned tunes was played softly several times, to selectively reinforce the memory for playing that tune without any reinforcement but not for the other tune. Paller wanted to know whether the test subjects could more accurately produce the tune played during sleep.
In the second exercise, the subjects were asked to memorize the location of 50 objects on a computer screen. The presentation of each object was coupled with a unique sound. During the post-learning nap, memory for the location of 25 objects was reinforced by the play-back of only 25 of the sounds. In this case, Paller wanted to know whether the subjects could remember object locations better if the associated sounds were played during sleep.
Researchers recorded electrical activity generated in the brain using EEG electrodes attached to the scalp. They thus determined whether the subjects entered “deep sleep,” and only those who did participated in the reinforcement experiments. In both experiments, participants did a better job remembering what was reinforced while they slept, compared to what was not reinforced.
"We think that memory processing happens during sleep every night," says Paller. "We’re at the beginning of finding out what types of memory can be reinforced, how large reinforcement effects can be, and what sorts of stimuli can be used to reactivate memories so that they can be better consolidated."
Paller’s goal is to better understand the fundamental brain mechanisms responsible for memory. And that, in turn, may help people with memory problems, including those who find themselves more forgetful as they age.
"We experience progressively less slow-wave sleep as we age. Of course, many brain mechanisms come into play to allow us to remember, including some processing that transpires during sleep. So, there’s a lot to figure out about how memory works, but I think it’s fair to say that the person you are when you’re awake is partly a function of what your brain does when you’re asleep," explains Paller. He says these reactivation techniques could turn out to be valuable for enhancing what people have learned.
"What is beautiful about this set of experiments is that Dr. Paller identified ‘deep sleep’ as a critical time window during which memory for specific experiences can be selectively enhanced by the method of reactivation without conscious effort," says Akaysha Tang, director of the cognitive neuroscience program in the NSF Directorate for Social, Behavioral and Economic Sciences.
"Normally, conscious rehearsal of memorized material is needed if one wants to remember something better or retain it for longer, and one has to find time to review or rehearse," continues Tang. "Dr. Paller and the members of his lab group showed that such selective enhancement could be achieved without conscious effort and without demanding more of one’s waking hours. So, instead of pulling that all-nighter to memorize the material, in the future, it may be possible to consolidate the memory by sleeping with a scientifically programmed lullaby!"
(Source: nsf.gov)
What is déjà vu and why does it happen?
Have you ever experienced a sudden feeling of familiarity while in a completely new place? Or the feeling you’ve had the exact same conversation with someone before?
This feeling of familiarity is, of course, known as déjà vu (a French term meaning “already seen”) and it’s reported to occur on an occasional basis in 60-80% of people. It’s an experience that’s almost always fleeting and it occurs at random.
So what is responsible for these feelings of familiarity?
Despite coverage in popular culture, experiences of déjà vu are poorly understood in scientific terms. Déjà vu occurs briefly, without warning and has no physical manifestations other than the announcement: “I just had déjà vu!”
Many researchers propose that the phenomenon is a memory-based experience and assume the memory centres of the brain are responsible for it.
New understanding of brain’s early spatial development
Researchers at the University of Bath have uncovered a new understanding of how the brain develops its sense of space by working with blind people.
The researchers from the University’s Department of Psychology found that people who lose their sight later in life use a different method of following directions to those who are born without sight. This means that the brain needs to have a visual experience early on in life in order to build a visual perspective, or frame of reference, to know what is where.
The researchers carried out a study with participants including those who were congenitally blind; those who became blind later in life; and others who were sighted, to learn which methods the different groups used to remember where things are.
The study revealed that people who have been sighted and then become blind use a ‘allocentric’ reference frame, meaning they remember locations as they are positioned relative to one another, and this is the same as sighted people who do this task, even when blindfolded.
In contrast congenitally blind participants preferred an ‘egocentric’ reference frame meaning they first remember a starting point at home and then store a memory of the locations from the home location. Dr Michael Proulx who led the study said the results help us to understand more about the role of a critical period for developmental vision on spatial cognition and brain organisation.
He said: “In our study we were curious as to whether having visual experience during child development was key to creating the structures in the brain to support such an allocentric reference frame. First we found an interesting difference between the congenitally blind and sighted people: although the sighted people preferred the allocentric, reference frame, the congenitally blind participants preferred the self-centred or egocentric reference frame for remembering locations.
“The important piece of the puzzle, however, was whether the late blind people would perform like the congenitally blind, showing that current visual experience matters, or like the sighted, showing the role of early visual experience. The results were clear: the late blind performed the same as the sighted participants. Therefore having the experience of vision early in life lays the groundwork in the brain for the representation of locations in a different reference frame than that found in people who never had visual experience.”
All of the participants of the study were blindfolded and then walked to the locations of objects in a large room. They were later tested on a computer with a virtual pointing task that asked them to remember objects in the room relative to the other object locations.
Dr Proulx and his colleagues are following up this finding with additional research to investigate how additional information, such as the texture or sound of the environment, might influence the frame of reference used.
This would allow for improved maps rendered in Braille or sound to be produced for visually impaired persons to use in public places, such as rail stations, or in new cities.
They are also examining the impact of visual experience on the neural basis for spatial learning and memory by examining how the congenitally blind and late blind brains represent spatial information in the absence of vision.
The pilot and autopilot within our mind-brain connection
Have you ever driven to work so deep in thought that you arrive safely yet can’t recall the drive itself? And if so, what part of “you” was detecting cars and pedestrians, making appropriate stops and turns? Although when you get to work you can’t remember the driving experience, you are likely to have exquisite memory about having planned your day.
How does one understand this common experience? This is the question posed by Professor of Biology, John Lisman and his former undergraduate student, Eliezer J. Sternberg, now in medical school, in a recent paper in the Journal of Cognitive Neuroscience. Lisman explains that once a task such as driving has become a habit, you can perform another task at the same time, such as planning your day. But looking closer at these two behaviors, driving and planning, one can see interesting differences. The Habit system that is driving you to work is non-flexible: if the new parking regulations at work require you to go left instead or right, the likelihood that you’ll go right is very high. On the other hand, if you heard yesterday that your boss has scheduled a group meeting for noon, the likehood that you’ll plan your day accordingly is high. In other words, your non-habit system is flexible.
What interests Lisman and Sternberg is the relationship of the habit/non-habit systems to concepts of conscious vs unconscious. These concepts were popularized by Freud, who posited a duality of the human mind. Behavior can be influenced by both the conscious system and unconscious system. Freud compared the mind to an iceberg——with the small conscious system above water and the larger unconscious system below. Modern cognitive neuroscience now accepts this duality.
The mind can be described as having an unconscious and conscious part. And the brain can be described as having both habit and non-habit systems. Lisman and Sternberg argue that these two views can be merged: there is a habit system of which we are unconscious and a non-habit system of which we are conscious.
This simple equation turns out to have enormous implications for research on the mind-brain connection. Experiments on consciousness are done in humans because you can ask them to report their awareness, something you can’t do with animals. On the other hand, there are many invasive procedures for studying what’s happening in the brain of animals. So how can you study consciousness in rats?
Lisman and Sternberg provide a simple answer — ask whether rats have habit and non-habits. Scientific literature demonstrates that rats indeed have both habits and non-habits. For instance, when a rat comes to a choice point on a maze (and the reward site is to left), rats display very different behavior depending on how much experience they’ve had with that maze. With relatively little experience, rats pause at the choice point and look both ways before making a decision; in contrast, a highly experienced rats zooms left without stopping. Experiments have shown that different parts of the brain are involved in these two phases. Lisman and Sternberg make two conclusions: first, that rats, like us, have conscious and unconscious parts of the brain and second, that from experiments on rats we can learn to identify the parts of the brain that mediate conscious vs unconscious processes.
In their paper, Lisman and Sternberg also discuss potential objections to their hypothesis, and suggest further tests.
(Photo: GETTY)
Eliminating useless information important to learning, making new memories
As we age, it just may be the ability to filter and eliminate old information – rather than take in the new stuff – that makes it harder to learn, scientists report.
“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.
It’s that critical weakening that appears hampered in the older brain, according to a study in the journal Scientific Reports.
The NMDA receptor in the brain’s hippocampus is like a switch for regulating learning and memory, working through subunits called NR2A and NR2B. NR2B is expressed in higher percentages in children, enabling neurons to talk a fraction of a second longer; make stronger bonds, called synapses; and optimize learning and memory. This formation of strong bonds is called long-term potentiation. The ratio shifts after puberty, so there is more NR2A and slightly reduced communication time between neurons.
When Tsien and his colleagues genetically modified mice that mimic the adult ratio – more NR2A, less NR2B – they were surprised to find the rodents were still good at making strong connections and short-term memories but had an impaired ability to weaken existing connections, called long-term depression, and to make new long-term memories as a result. It’s called information sculpting and adult ratios of NMDA receptor subunits don’t appear to be very good at it.
“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. While each neuron averages 3,000 synapses, the relentless onslaught of information and experiences necessitates some selective whittling. Insufficient sculpting, at least in their mouse, meant a reduced ability to remember things short-term – like the ticket number at a fast-food restaurant – and long-term – like remembering a favorite menu item at that restaurant. Both are impacted in Alzheimer’s and age-related dementia.
All long-term depression was not lost in the mice, rather just response to the specific electrical stimulation levels that should induce weakening of the synapse. Tsien expected to find the opposite: that long-term potentiation was weak and so was the ability to learn and make new memories. “What is abnormal is the ability to weaken existing connectivity.”
Acknowledging the leap, this impaired ability could also help explain why adults can’t learn a new language without their old accent and why older people tend to be more stuck in their ways, the memory researcher said.
“We know we lose the ability to perfectly speak a foreign language if we learn than language after the onset of sexual maturity. I can learn English but my Chinese accent is very difficult to get rid of. The question is why,” Tsien said.
Tsien and his colleagues already have learned what happens when NR2B is overexpressed. He and East China Normal University researchers announced in 2009 the development of Hobbie-J, a smarter than average rat. 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.
Doogie, Hobbie-J and their descendants have maintained superior memory as they age. Now Tsien is interested in following the NR2A over-expressing mouse to see what happens.
(Source: news.georgiahealth.edu)
Newly found ‘volume control’ in the brain promotes learning, memory
Scientists have long wondered how nerve cell activity in the brain’s hippocampus, the epicenter for learning and memory, is controlled — too much synaptic communication between neurons can trigger a seizure, and too little impairs information processing, promoting neurodegeneration. Researchers at Georgetown University Medical Center say they now have an answer. In the January 10 issue of Neuron, they report that synapses that link two different groups of nerve cells in the hippocampus serve as a kind of “volume control,” keeping neuronal activity throughout that region at a steady, optimal level.
"Think of these special synapses like the fingers of God and man touching in Michelangelo’s famous fresco in the Sistine Chapel," says the study’s senior investigator, Daniel Pak, PhD, an associate professor of pharmacology. "Now substitute the figures for two different groups of neurons that need to perform smoothly. The touching of the fingers, or synapses, controls activity levels of neurons within the hippocampus."
The hippocampus is a processing unit that receives input from the cortex and consolidates that information in terms of learning and memory. Neurons known as granule cells, located in the hippocampus’ dentate gyrus, receive transmissions from the cortex. Those granule cells then pass that information to the other set of neurons (those in the CA3 region of the hippocampus, in this study) via the synaptic fingers.
Those fingers dial up, or dial down, the volume of neurotransmission from the granule cells to the CA3 region to keep neurotransmission in the learning and memory areas of the hippocampus at an optimal flow — a concept known as homeostatic plasticity. “If granule cells try to transmit too much activity, we found, the synaptic junction tamps down the volume of transmission by weakening their connections, allowing the proper amount of information to travel to CA3 neurons,” says Pak. “If there is not enough activity being transmitted by the granule cells, the synapses become stronger, pumping up the volume to CA3 so that information flow remains constant.”
There are many such touching fingers in the hippocampus, connecting the so-called “mossy fibers” of the granule cells to neurons in the CA3 region. But importantly, not every one of the billions of neurons in the hippocampus needs to set its own level of transmission from one nerve cell to the other, says Pak.
To explain, he uses another analogy. “It had previously been thought that neurons act separately like cars, each working to keep their speed at a constant level even though signal traffic may be fast or slow. But we wondered how these neurons could process learning and memory information efficiently, while also regulating the speed by which they process and communicate that information.
"We believe, based on our study, that only the mossy fiber synapses on the CA3 neurons control the level of activity for the hippocampus — they are like the engine on a train that sets the speed for all the other cars, or neurons, attached to it," Pak says. "That frees up the other neurons to do the job they are tasked with doing — processing and encoding information in the forms of learning and memory."
Not only does the study offer a new model for how homeostatic plasticity in the hippocampus can co-exist with learning and memory, it also suggests a new therapeutic avenue to help patients with uncontrollable seizures, he says.
"The CA3 region is highly susceptible to seizures, so if we understand how homeostasis is maintained in these neurons, we could potentially manipulate the system. When there is an excessive level of CA3 neuronal activity in a patient, we could learn how to therapeutically turn it down."
(Source: eurekalert.org)
Scientists explore the illusion of memory
A memory might seem like a permanent, precious essence carved deep into the circuits of the brain. But it is not. Instead, scientists are discovering that a memory changes every time you think about it.
"Every time you recall a memory, it becomes sensitive to disruption. Often that is used to incorporate new information into it." That’s the blunt assessment from one of the world’s leading experts on memory, Dr. Eric Kandel from Columbia University.
And that means our memories are not abstract snapshots stored forever in a bulging file in our mind, but rather, they’re a collection of brain cells — neurons that undergo chemical changes every time they’re engaged.
So when we think about something from the past, the memory is called up like a computer file, reviewed and revised in subtle ways, and then sent back to the brain’s archives, now modified slightly, updated, and changed.
As scientists increasingly understand the biological process of memory, they are also learning how to interrupt it, and that means they might one day be able to ease the pain of past trauma, or alter destructive habits and addictions, as though shaking an Etch A Sketch, erasing the scribbles on the mind, and starting fresh.
In his McGill University lab, researcher Karim Nader routinely erases the memory of his laboratory rats. But first he has to give them a memory and he does that by putting them in an isolation cubicle, playing a tone, and then delivering a small electrical shock to their feet.
Study Refutes Accepted Model of Memory Formation
A study by Johns Hopkins researchers has shown that a widely accepted model of long-term memory formation — that it hinges on a single enzyme in the brain — is flawed. The new study, published in the Jan. 2 issue of Nature, found that mice lacking the enzyme that purportedly builds memory were in fact still able to form long-term memories as well as normal mice could.
“The prevailing theory is that when you learn something, you strengthen connections between your brain cells called synapses,” explains Richard Huganir, Ph.D., a professor and director of the Johns Hopkins University School of Medicine’s Solomon H. Snyder Department of Neuroscience. “The question is, how exactly does this strengthening happen?”
A research group at SUNY Downstate, led by Todd Sacktor, Ph.D., has suggested that key to the process is an enzyme they discovered, known as PKM-zeta. In 2006, Sacktor’s group made waves when it created a molecule that seemed to block the action of PKM-zeta — and only PKM-zeta. When the molecule, dubbed ZIP, was given to mice, it erased existing long-term memories. The molecule caught the attention of reporters and bloggers, who mused on the social and ethical implications of memory erasure.
But for researchers, ZIP was exciting primarily as a means for studying PKM-zeta. “Since 2006, many papers have been published on PKM-zeta and ZIP, but no one knew what PKM-zeta was acting on,” says Lenora Volk, Ph.D., a member of Huganir’s team. “We thought that learning the enzyme’s target could tell us a lot about how memories are stored and maintained.”
For the current study, Volk and fellow team member Julia Bachman made mice that lacked working PKM-zeta, so-called genetic “knockouts.” The goal was to compare the synapses of the modified mice with those of normal mice, and find clues about how the enzyme works.
But, says Volk, “what we got was not at all what we expected. We thought the strengthening capacity of the synapses would be impaired, but it wasn’t.” The brains of the mice without PKM-zeta were indistinguishable from those of other mice, she says. Additionally, the synapses of the PKM-zeta-less mice responded to the memory-erasing ZIP molecule just as the synapses of normal mice do.
The team then considered whether, in the absence of PKM-zeta, the mouse brains had honed a substitute synapse-building pathway, much in the way that a blind person learns to glean more information from her other senses. So the researchers made mice whose PKM-zeta genes functioned normally until they were given a drug that would suddenly shut the gene down. This allowed them to study PKM-zeta-less adult mice that had had no opportunity to develop a way around the loss of the gene. Still, the synapses of the so-called conditional knockout mice responded to stimuli just as synapses in normal mice did.
What this means, the researchers say, is that PKM-zeta is not the key long-term memory molecule previous studies had suggested, although it may have some role in memory. “We don’t know what this ZIP peptide is really acting on,” says Volk. “Finding out what its target is will be quite important, because then we can begin to understand at the molecular level how synapses strengthen and how memories form in response to stimuli.”
The Role of Medial Prefrontal Cortex in Memory and Decision Making
Some have claimed that the medial prefrontal cortex (mPFC) mediates decision making. Others suggest mPFC is selectively involved in the retrieval of remote long-term memory. Yet others suggests mPFC supports memory and consolidation on time scales ranging from seconds to days. How can all these roles be reconciled? We propose that the function of the mPFC is to learn associations between context, locations, events, and corresponding adaptive responses, particularly emotional responses. Thus, the ubiquitous involvement of mPFC in both memory and decision making may be due to the fact that almost all such tasks entail the ability to recall the best action or emotional response to specific events in a particular place and time. An interaction between multiple memory systems may explain the changing importance of mPFC to different types of memories over time. In particular, mPFC likely relies on the hippocampus to support rapid learning and memory consolidation.