Neuroscience

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Posts tagged memory

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Memory relies on astrocytes, the brain’s lesser known cells
When you’re expecting something—like the meal you’ve ordered at a restaurant—or when something captures your interest, unique electrical rhythms sweep through your brain.
These waves are called gamma oscillations and they reflect a symphony of cells—both excitatory and inhibitory—playing together in an orchestrated way. Though their role has been debated, gamma waves have been associated with higher-level brain function, and disturbances in the patterns have been tied to schizophrenia, Alzheimer’s disease, autism, epilepsy and other disorders.
Now, new research from the Salk Institute shows that little known supportive cells in the brain known as astrocytes may in fact be major players that control these waves.
In a study published July 28 in the Proceedings of the National Academy of Sciences, Salk researchers report a new, unexpected strategy to turn down gamma oscillations, by disabling not neurons but astrocytes—cells type traditionally thought to provide more of a support role in the brain. In the process, the team showed that astrocytes, and the gamma oscillations they help shape, are critical for some forms of memory.
"This is what could be called a smoking gun," says co-author Terrence Sejnowski, head of the Computational Neurobiology Laboratory at the Salk Institute for Biological Sciences and a Howard Hughes Medical Institute investigator. "There are hundreds of papers linking gamma oscillations with attention and memory, but they are all correlational. This is the first time we have been able to do a causal experiment, where we selectively block gamma oscillations and show that it has a highly specific impact on how the brain interacts with the world."
A collaboration among the labs of Salk professors Sejnowski, Inder Verma and Stephen Heinemann found that activity in the form of calcium signaling in astrocytes immediately preceded gamma oscillations in the brains of mice. This suggested that astrocytes, which use many of the same chemical signals as neurons, could be influencing these oscillations.
To test their theory, the group used a virus carrying tetanus toxin to disable the release of chemicals released selectively from astrocytes, effectively eliminating the cells’ ability to communicate with neighboring cells. Neurons were unaffected by the toxin.
After adding a chemical to trigger gamma waves in the animals’ brains, the researchers found that brain tissue with disabled astrocytes produced shorter gamma waves than in tissue containing healthy cells. And after adding three genes that would allow the researchers to selectively turn on and off the tetanus toxin in astrocytes at will, they found that gamma waves were dampened in mice whose astrocytes were blocked from signaling. Turning off the toxin reversed this effect.
The mice with the modified astrocytes seemed perfectly healthy. But after several cognitive tests, the researchers found that they failed in one major area: novel object recognition. A healthy mouse spent more time with a new item placed in its environment than it did with familiar items, as expected.
In contrast, the group’s new mutant mouse treated all objects the same. “That turned out to be a spectacular result in the sense that novel object recognition memory was not just impaired, it was gone—as if we were deleting this one form of memory, leaving others intact,” Sejnowski says.
The results were surprising, in part because astrocytes operate on a seconds- or longer timescale whereas neurons signal far faster, on the millisecond scale. Because of that slower speed, no one suspected astrocytes were involved in the high-speed brain activity needed to make quick decisions.
"What I thought quite unique was the idea that astrocytes, traditionally considered only guardians and supporters of neurons and other cells, are also involved in the processing of information and in other cognitive behavior," says Verma, a professor in the Laboratory of Genetics and American Cancer Society Professor.
It’s not that astrocytes are quick—they’re still slower than neurons. But the new evidence suggests that astrocytes are actively supplying the right environment for gamma waves to occur, which in turn makes the brain more likely to learn and change the strength of its neuronal connections.
Sejnowski says that the behavioral result is just the tip of the iceberg. “The recognition system is hugely important,” he says, adding that it includes recognizing other people, places, facts and things that happened in the past. With this new discovery, scientists can begin to better understand the role of gamma waves in recognition memory, he adds.

Memory relies on astrocytes, the brain’s lesser known cells

When you’re expecting something—like the meal you’ve ordered at a restaurant—or when something captures your interest, unique electrical rhythms sweep through your brain.

These waves are called gamma oscillations and they reflect a symphony of cells—both excitatory and inhibitory—playing together in an orchestrated way. Though their role has been debated, gamma waves have been associated with higher-level brain function, and disturbances in the patterns have been tied to schizophrenia, Alzheimer’s disease, autism, epilepsy and other disorders.

Now, new research from the Salk Institute shows that little known supportive cells in the brain known as astrocytes may in fact be major players that control these waves.

In a study published July 28 in the Proceedings of the National Academy of Sciences, Salk researchers report a new, unexpected strategy to turn down gamma oscillations, by disabling not neurons but astrocytes—cells type traditionally thought to provide more of a support role in the brain. In the process, the team showed that astrocytes, and the gamma oscillations they help shape, are critical for some forms of memory.

"This is what could be called a smoking gun," says co-author Terrence Sejnowski, head of the Computational Neurobiology Laboratory at the Salk Institute for Biological Sciences and a Howard Hughes Medical Institute investigator. "There are hundreds of papers linking gamma oscillations with attention and memory, but they are all correlational. This is the first time we have been able to do a causal experiment, where we selectively block gamma oscillations and show that it has a highly specific impact on how the brain interacts with the world."

A collaboration among the labs of Salk professors Sejnowski, Inder Verma and Stephen Heinemann found that activity in the form of calcium signaling in astrocytes immediately preceded gamma oscillations in the brains of mice. This suggested that astrocytes, which use many of the same chemical signals as neurons, could be influencing these oscillations.

To test their theory, the group used a virus carrying tetanus toxin to disable the release of chemicals released selectively from astrocytes, effectively eliminating the cells’ ability to communicate with neighboring cells. Neurons were unaffected by the toxin.

After adding a chemical to trigger gamma waves in the animals’ brains, the researchers found that brain tissue with disabled astrocytes produced shorter gamma waves than in tissue containing healthy cells. And after adding three genes that would allow the researchers to selectively turn on and off the tetanus toxin in astrocytes at will, they found that gamma waves were dampened in mice whose astrocytes were blocked from signaling. Turning off the toxin reversed this effect.

The mice with the modified astrocytes seemed perfectly healthy. But after several cognitive tests, the researchers found that they failed in one major area: novel object recognition. A healthy mouse spent more time with a new item placed in its environment than it did with familiar items, as expected.

In contrast, the group’s new mutant mouse treated all objects the same. “That turned out to be a spectacular result in the sense that novel object recognition memory was not just impaired, it was gone—as if we were deleting this one form of memory, leaving others intact,” Sejnowski says.

The results were surprising, in part because astrocytes operate on a seconds- or longer timescale whereas neurons signal far faster, on the millisecond scale. Because of that slower speed, no one suspected astrocytes were involved in the high-speed brain activity needed to make quick decisions.

"What I thought quite unique was the idea that astrocytes, traditionally considered only guardians and supporters of neurons and other cells, are also involved in the processing of information and in other cognitive behavior," says Verma, a professor in the Laboratory of Genetics and American Cancer Society Professor.

It’s not that astrocytes are quick—they’re still slower than neurons. But the new evidence suggests that astrocytes are actively supplying the right environment for gamma waves to occur, which in turn makes the brain more likely to learn and change the strength of its neuronal connections.

Sejnowski says that the behavioral result is just the tip of the iceberg. “The recognition system is hugely important,” he says, adding that it includes recognizing other people, places, facts and things that happened in the past. With this new discovery, scientists can begin to better understand the role of gamma waves in recognition memory, he adds.

Filed under astrocytes memory gamma oscillations neuroscience science

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(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)
A protein couple controls flow of information into the brain’s memory center
Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.
Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.
Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.
In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”
A pair of helpers
Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”
This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.
Long-term effect
The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.
However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”
The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.
Fast sequence of signals
However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.
Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.
“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”
Sensitive balance
Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”
Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)

A protein couple controls flow of information into the brain’s memory center

Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.

Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.

Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.

In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”

A pair of helpers

Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”

This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.

Long-term effect

The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.

However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”

The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.

Fast sequence of signals

However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.

Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.

“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”

Sensitive balance

Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”

Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

Filed under AMPA receptors glutamate neurons hippocampus granule cells memory neuroscience science

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Targeting the brain to treat obesity

Unlocking the secrets to better treating the pernicious disorders of obesity and dementia reside in the brain, according to a paper from American University’s Center for Behavioral Neuroscience. In the paper, researchers make the case for treating obesity with therapies aimed at areas of the brain responsible for memory and learning. Furthermore, treatments that focus on the hippocampus could play a role in reducing certain dementias.

"In the struggle to treat these diseases, therapies and preventive measures often fall short. This is a new way for providers who treat people with weight problems and for researchers who study dementias to think about obesity and cognitive decline," said Prof. Terry Davidson, center director and lead study author.

In the paper, published in the journal Physiology & Behavior, Davidson and colleague Ashley A. Martin review research findings linking obesity with cognitive decline, including the center’s findings about the “vicious cycle” model, which explains how weight-challenged individuals who suffer from particular kinds of cognitive impairment are more susceptible to overeating.

Obesity, Memory Deficits and Lasting Effects

It is widely accepted that overconsumption of dietary fats, sugar and sweeteners can cause obesity. These types of dietary factors are also linked to cognitive dysfunction. Foods that are risk factors for cognitive impairment (i.e., foods high in saturated fats and simple carbohydrates that make up the modern Western diet) are so widespread and readily available in today’s food environment, their consumption is all but encouraged, Davidson said.

Across age groups, evidence reveals links between excess food intake, body weight and cognitive dysfunction. Childhood obesity and consumption of the Western diet can have lasting effects, as seen through the normal aging process, cognitive deficits and brain pathologies. Several analyses of cases of mild cognitive impairment progressing to full-blown cases of Alzheimer’s disease show that the first signs of brain disease can occur at least 50 years prior to the emergence of serious cognitive dysfunction. These signs originate in the hippocampus, the area of the brain where memory, learning, decision making, behavior control and other cognitive functions come into play.

Still, most research on the role of the brain in obesity focuses on areas thought to be involved with hunger motivation (e.g., hypothalamus), taste (e.g., brain stem), reinforcement (e.g., striatum) and reward (e.g., nucleus accumbens) or with hormonal or metabolic disorders. This research has not yet been successful in generating therapies that are effective in treating or preventing obesity, Davidson says.

Vicious Cycle

Experiments in rats by Davidson and colleagues show that overconsumption of the Western diet can damage or change the blood-brain barrier, the tight network of blood vessels protecting the brain and substrates for cognition. Certain kinds of dementias are known to arise from the breakdown in these brain substrates.

"Breakdown in the blood-brain barrier is more rationale for treating obesity as a learning and memory disorder," Davidson said. "Treating obesity successfully may also reduce the incidence of dementias, because the deterioration in the brain is often produced by the same diets that promote obesity."

The “vicious cycle” model AU researchers put forth says eating a Western diet high in saturated fats, sugar and simple carbohydrates produces pathologies in brain structures and circuits, ultimately changing brain pathways and disrupting cognitive abilities.

It works like this: People become less able to resist temptation when they encounter environmental cues (e.g., food itself or the sight of McDonald’s Golden Arches) that remind them of the pleasures of consumption. They then eat more of the same type of foods that produce the pathological changes in the brain, leading to progressive deterioration in those areas and impairments in cognitive processes important for providing control over one’s thoughts and behaviors. These cognitive impairments can weaken a person’s ability to resist thinking about food, making them more easily distracted by food cues in the environment and more susceptible to overeating and weight gain.

"People have known at least since the time of Hippocrates that one key to a healthy life is to eat in moderation. Yet many of us are unable to follow that good advice," Davidson said. "Our work suggests that new therapeutic interventions that target brain regions involved with learning and memory may lead to success in controlling both the urge to eat, as well as the undesirable consequences produced by overeating."

(Source: eurekalert.org)

Filed under obesity cognitive decline memory western diet hippocampus neuroscience science

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Missing sleep may hurt your memory
Lack of sleep, already considered a public health epidemic, can also lead to errors in memory, finds a new study by researchers at Michigan State University and the University of California, Irvine.
The study, published online in the journal Psychological Science, found participants deprived of a night’s sleep were more likely to flub the details of a simulated burglary they were shown in a series of images.
Distorted memory can have serious consequences in areas such as criminal justice, where eyewitness misidentifications are thought to be the leading cause of wrongful convictions in the United States.
“We found memory distortion is greater after sleep deprivation,” said Kimberly Fenn, MSU associate professor of psychology and co-investigator on the study. “And people are getting less sleep each night than they ever have.”
The Centers for Disease Control and Prevention calls insufficient sleep an epidemic and said it’s linked to vehicle crashes, industrial disasters and chronic diseases such as hypertension and diabetes.
The researchers conducted experiments at MSU and UC-Irvine to gauge the effect of insufficient sleep on memory. The results: Participants who were kept awake for 24 hours – and even those who got five or fewer hours of sleep – were more likely to mix up event details than participants who were well rested.
“People who repeatedly get low amounts of sleep every night could be more prone in the long run to develop these forms of memory distortion,” Fenn said. “It’s not just a full night of sleep deprivation that puts them at risk.”

Missing sleep may hurt your memory

Lack of sleep, already considered a public health epidemic, can also lead to errors in memory, finds a new study by researchers at Michigan State University and the University of California, Irvine.

The study, published online in the journal Psychological Science, found participants deprived of a night’s sleep were more likely to flub the details of a simulated burglary they were shown in a series of images.

Distorted memory can have serious consequences in areas such as criminal justice, where eyewitness misidentifications are thought to be the leading cause of wrongful convictions in the United States.

“We found memory distortion is greater after sleep deprivation,” said Kimberly Fenn, MSU associate professor of psychology and co-investigator on the study. “And people are getting less sleep each night than they ever have.”

The Centers for Disease Control and Prevention calls insufficient sleep an epidemic and said it’s linked to vehicle crashes, industrial disasters and chronic diseases such as hypertension and diabetes.

The researchers conducted experiments at MSU and UC-Irvine to gauge the effect of insufficient sleep on memory. The results: Participants who were kept awake for 24 hours – and even those who got five or fewer hours of sleep – were more likely to mix up event details than participants who were well rested.

“People who repeatedly get low amounts of sleep every night could be more prone in the long run to develop these forms of memory distortion,” Fenn said. “It’s not just a full night of sleep deprivation that puts them at risk.”

Filed under sleep sleep deprivation memory false memory psychology neuroscience science

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Rhymes can inspire reasoning during the third trimester in the womb

Mozart, Beethoven or even Shakespeare — pregnant mothers have been known to expose their babies to many forms of auditory stimulation. But according to researchers at the University of Florida, all a baby really needs is the music of mom’s voice.

image

Research published in the most recent issue of the journal Infant Behavior and Development shows that babies in utero begin to respond to the rhythm of a nursery rhyme — showing evidence of learning — by 34 weeks of pregnancy and are capable of remembering a set rhyme until just prior to birth. Nursing researcher Charlene Krueger and her team studied pregnant women who recited a rhyme to their babies three times a day for six weeks, beginning at 28 weeks’ gestational age, which is the start of the third trimester of pregnancy.

“The mother’s voice is the predominant source of sensory stimulation in the developing fetus,” said Krueger, an associate professor in the UF College of Nursing. “This research highlights just how sophisticated the third trimester fetus really is and suggests that a mother’s voice is involved in the development of early learning and memory capabilities. This could potentially affect how we approach the care and stimulation of the preterm infant.”

Krueger’s team recruited 32 pregnant women during their 28th week of pregnancy, as determined by fetal ultrasound. The participants were between 18 and 39 years of age, spoke English as a primary language and were pregnant with their first baby. Once recruited, the women were randomly assigned to either an experimental or a control group. The mean age of the women in the group was 25. In addition, 68 percent of the women were white, 28 percent were black and 4 percent were of another race or ethnicity.

From 28 to 34 weeks of pregnancy, all mothers in the study recited a passage or nursery rhyme out loud twice a day and then came in for testing at 28, 32, 33 and 34 weeks’ gestation. To determine whether the fetus could remember the pattern of speech at 34 weeks of age, all mothers were asked to stop speaking the passage. Then the fetuses were tested again at 36 and 38 weeks’ gestational age.

During testing, researchers used a fetal heart monitor, similar to what is used during traditional labor and delivery, to record heart rate and determine any changes. Researchers interpret a small heart rate deceleration in the fetus as an indicator of learning or familiarity with a stimulus.

At testing, the fetuses in the experimental group were played a recording of the same rhyme their mother had been reciting at home but spoken by a female stranger. Those in the control group heard a different rhyme also spoken by a stranger. This was to help determine if the fetus was responding simply to its mother’s voice or to a familiar pattern of speech, which is a more difficult task, Krueger said.

The researchers found that the fetus’ heart rate began to respond to the familiar rhyme recited by a stranger’s voice by 34 weeks of gestational age — once the mother had spoken the rhyme out loud at home for six weeks. They continued to respond with a small cardiac deceleration for as long as four weeks after the mother had stopped saying the rhyme until about 38 weeks. At 38 weeks, there was a statistically significant difference between the two groups in responding to the strangers’ recited rhymes — the experimental group who heard the original rhyme responded with a deeper and more sustained cardiac deceleration, whereas the control group who heard a new rhyme responded with a cardiac acceleration.

Further research is needed to more fully understand how ongoing development affects learning and memory, Krueger said. Her aim is to recognize how this type of research can influence care in preterm infants and their long-term outcomes.

“This study helped us understand more about how early a fetus could learn a passage of speech and whether the passage could be remembered weeks later even without daily exposure to it,” Krueger said. “This could have implications to those preterm infants who are born before 37 weeks of age and the impact an intervention such as their mother’s voice may have on influencing better outcomes in this high-risk population.”

(Source: news.ufl.edu)

Filed under pregnancy fetus memory learning reasoning child development neuroscience science

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Preschoolers Can Reflect on What They Don’t Know

Contrary to previous assumptions, researchers find that preschoolers are able to gauge the strength of their memories and make decisions based on their self-assessments. The study findings are published in Psychological Science, a journal of the Association for Psychological Science.

image

“Previously, developmental researchers assumed that preschoolers did not introspect much on their mental states, and were not able to reflect on their own uncertainty when problem solving,” says psychological scientist Emily Hembacher of the University of California, Davis, lead author of the study. “This is partly because young children are not usually able to tell us much about their own mental processes due to verbal limitations.”

In several previous studies in their lab, Hembacher and co-author Simona Ghetti observed that preschoolers reported feeling uncertain after giving wrong answers during tasks, suggesting the preschoolers were capable of metacognition — the ability to evaluate one’s own thoughts and mental states.

The researchers decided to examine preschoolers’ metacognition about their memories, given its importance for learning.  They investigated whether kids could assess their confidence in their memories and use those assessments in deciding whether to exclude answers they had generated but were unsure of when given the option.

Eighty-one children ages 3, 4, and 5 participated in the study.  The preschoolers viewed a series of drawings of various items, such as a piano or a balloon.  Half of the images were presented once, and the other half were shown twice.  Next, the children were presented with a pair of images: one they had seen, and a new one they had not seen.  The children were instructed to pick which image they’d seen before in the previous task.

After making their choice, the preschoolers rated how confident they were that their choice was correct.  They then sorted their answers into two boxes.  One box was for the responses that children were confident about and wanted researchers to evaluate for a prize.  The other one was for responses the children thought might be mistaken and that they didn’t want researchers to see.

The data revealed that only 4- and 5-year-olds reported being less confident in their incorrect than their correct memory responses.  They were also more confident about images they’d seen twice, suggesting that they could distinguish between stronger and weaker memories. Older preschoolers were also more likely to decide whether they wanted researchers to see their answers based on their confidence level.

Although 3-year-olds didn’t display the same kind of metacognitive capability on individual responses, the data showed that 3-year-olds who had scored well reported higher confidence overall than kids who hadn’t scored as well.

When the researchers analyzed just the correct answers, they found that preschoolers of all ages sorted responses they weren’t as confident about to the box they didn’t want researchers to evaluate.  So, while they may not be as advanced as their older peers, even children as young as 3 seem to display some ability to reflect on their own knowledge.

The findings contribute to research on the reliability of children’s eyewitness testimony in a court of law, and they carry important implications for educational practices.

“Previous emphasis on the development of metacognition during middle childhood has influenced education practices aimed at strengthening children’s monitoring and control of their own learning,” says Hembacher. “Now we know that some of these ideas may be adapted to meet preschoolers’ learning needs.”

(Source: psychologicalscience.org)

Filed under learning memory child development confidence preschoolers psychology neuroscience

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Researcher shows how stress hormones promote brain’s building of negative memories
When a person experiences a devastating loss or tragic event, why does every detail seem burned into memory whereas a host of positive experiences simply fade away?
It’s a bit more complicated than scientists originally thought, according to a study recently published in the journal Neuroscience by ASU researcher Sabrina Segal.
When people experience a traumatic event, the body releases two major stress hormones: norepinephrine and cortisol. Norepinephrine boosts heart rate and controls the fight-or-flight response, commonly rising when individuals feel threatened or experience highly emotional reactions. It is chemically similar to the hormone epinephrine – better known as adrenaline.
In the brain, norepinephrine in turn functions as a powerful neurotransmitter or chemical messenger that can enhance memory.
Research on cortisol has demonstrated that this hormone can also have a powerful effect on strengthening memories. However, studies in humans up until now have been inconclusive – with cortisol sometimes enhancing memory, while at other times having no effect.
A key factor in whether cortisol has an effect on strengthening certain memories may rely on activation of norepinephrine during learning, a finding previously reported in studies with rats.
In her study, Segal, an assistant research professor at the Institute for Interdisciplinary Salivary Bioscience Research at ASU, and her colleagues at the University of California-Irvine showed that human memory enhancement functions in a similar way.
Conducted in the laboratory of Larry Cahill at U.C. Irvine, Segal’s study included 39 women who viewed 144 images from the International Affective Picture Set. This set is a standardized picture set used by researchers to elicit a range of responses, from neutral to strong emotional reactions, upon view.
Segal and her colleagues gave each of the study’s subjects either a dose of hydrocortisone – to simulate stress – or a placebo just prior to viewing the picture set. Each woman then rated her feelings at the time she was viewing the image, in addition to giving saliva samples before and after. One week later, a surprise recall test was administered.
What Segal’s team found was that “negative experiences are more readily remembered when an event is traumatic enough to release cortisol after the event, and only if norepinephrine is released during or shortly after the event.”
“This study provides a key component to better understanding how traumatic memories may be strengthened in women,” Segal added, “because it suggests that if we can lower norepinephrine levels immediately following a traumatic event, we may be able to prevent this memory enhancing mechanism from occurring, regardless of how much cortisol is released following a traumatic event.”
Further studies are needed to explore to what extent the relationship between these two stress hormones differ depending on whether you are male or female, particularly because women are twice as likely to develop disorders from stress and trauma that affect memory, such as in Posttraumatic Stress Disorder (PTSD). In the meantime, the team’s findings are a first step toward a better understanding of neurobiological mechanisms that underlie traumatic disorders, such as PTSD.
(Image: Wikimedia Commons)

Researcher shows how stress hormones promote brain’s building of negative memories

When a person experiences a devastating loss or tragic event, why does every detail seem burned into memory whereas a host of positive experiences simply fade away?

It’s a bit more complicated than scientists originally thought, according to a study recently published in the journal Neuroscience by ASU researcher Sabrina Segal.

When people experience a traumatic event, the body releases two major stress hormones: norepinephrine and cortisol. Norepinephrine boosts heart rate and controls the fight-or-flight response, commonly rising when individuals feel threatened or experience highly emotional reactions. It is chemically similar to the hormone epinephrine – better known as adrenaline.

In the brain, norepinephrine in turn functions as a powerful neurotransmitter or chemical messenger that can enhance memory.

Research on cortisol has demonstrated that this hormone can also have a powerful effect on strengthening memories. However, studies in humans up until now have been inconclusive – with cortisol sometimes enhancing memory, while at other times having no effect.

A key factor in whether cortisol has an effect on strengthening certain memories may rely on activation of norepinephrine during learning, a finding previously reported in studies with rats.

In her study, Segal, an assistant research professor at the Institute for Interdisciplinary Salivary Bioscience Research at ASU, and her colleagues at the University of California-Irvine showed that human memory enhancement functions in a similar way.

Conducted in the laboratory of Larry Cahill at U.C. Irvine, Segal’s study included 39 women who viewed 144 images from the International Affective Picture Set. This set is a standardized picture set used by researchers to elicit a range of responses, from neutral to strong emotional reactions, upon view.

Segal and her colleagues gave each of the study’s subjects either a dose of hydrocortisone – to simulate stress – or a placebo just prior to viewing the picture set. Each woman then rated her feelings at the time she was viewing the image, in addition to giving saliva samples before and after. One week later, a surprise recall test was administered.

What Segal’s team found was that “negative experiences are more readily remembered when an event is traumatic enough to release cortisol after the event, and only if norepinephrine is released during or shortly after the event.”

“This study provides a key component to better understanding how traumatic memories may be strengthened in women,” Segal added, “because it suggests that if we can lower norepinephrine levels immediately following a traumatic event, we may be able to prevent this memory enhancing mechanism from occurring, regardless of how much cortisol is released following a traumatic event.”

Further studies are needed to explore to what extent the relationship between these two stress hormones differ depending on whether you are male or female, particularly because women are twice as likely to develop disorders from stress and trauma that affect memory, such as in Posttraumatic Stress Disorder (PTSD). In the meantime, the team’s findings are a first step toward a better understanding of neurobiological mechanisms that underlie traumatic disorders, such as PTSD.

(Image: Wikimedia Commons)

Filed under stress negative emotions PTSD memory learning norepinephrine cortisol neuroscience science

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Study Links Enzyme to Alzheimer’s Disease 
Unclogging the body’s protein disposal system may improve memory in patients with Alzheimer’s disease (AD), according to a study from scientists at Kyungpook National University in Korea published in The Journal of Experimental Medicine.
In AD, various biochemical functions of brain cells go awry, leading to progressive neuronal damage and eventual memory loss. One example is the cellular disposal system, called autophagy, which is disrupted in patients with AD, causing the accumulation of toxic protein plaques characteristic of the disease. Jae-sung Bae and colleagues had earlier noted that the brains of AD patients have elevated levels of an enzyme called acid sphingomyelinase (ASM), which breaks down cell membrane lipids prevalent in the myelin sheath that coats nerve endings. But whether increased ASM directly contributes to AD (and if so, how) was unclear.
The group now finds that these two defects are linked. In mice with AD-like disease, elevated ASM activity clogged up the autophagy machinery resulting in the accumulation of undigested cellular waste. Reducing levels of ASM restored autophagy, lessened brain pathology, and improved learning and memory in the mice. Provided these results hold true in humans, interfering with ASM activity might prove to be an effective way to slow—and possibly reverse—neurodegeneration in patients with AD.

Study Links Enzyme to Alzheimer’s Disease

Unclogging the body’s protein disposal system may improve memory in patients with Alzheimer’s disease (AD), according to a study from scientists at Kyungpook National University in Korea published in The Journal of Experimental Medicine.

In AD, various biochemical functions of brain cells go awry, leading to progressive neuronal damage and eventual memory loss. One example is the cellular disposal system, called autophagy, which is disrupted in patients with AD, causing the accumulation of toxic protein plaques characteristic of the disease. Jae-sung Bae and colleagues had earlier noted that the brains of AD patients have elevated levels of an enzyme called acid sphingomyelinase (ASM), which breaks down cell membrane lipids prevalent in the myelin sheath that coats nerve endings. But whether increased ASM directly contributes to AD (and if so, how) was unclear.

The group now finds that these two defects are linked. In mice with AD-like disease, elevated ASM activity clogged up the autophagy machinery resulting in the accumulation of undigested cellular waste. Reducing levels of ASM restored autophagy, lessened brain pathology, and improved learning and memory in the mice. Provided these results hold true in humans, interfering with ASM activity might prove to be an effective way to slow—and possibly reverse—neurodegeneration in patients with AD.

Filed under alzheimer's disease autophagy acid sphingomyelinase memory neuroscience science

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Transplantation of healthy new brain cells reverses learning and memory loss in Alzheimer’s disease model

A new study from the Gladstone Institutes has revealed a way to alleviate the learning and memory deficits caused by apoE4, the most important genetic risk factor for Alzheimer’s disease, improving cognition to normal levels in aged mice.

In the study, which was conducted in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors—early-stage brain cells that have the capacity to develop into mature inhibitory neurons—into two mouse models of Alzheimer’s disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer’s. The transplants helped to replenish the brain by replacing cells lost due to apoE4, regulating brain activity and improving learning and memory abilities.

“This is the first time transplantation of inhibitory neuron progenitors has been used in aged Alzheimer’s disease models,” said first author Leslie Tong, a graduate student at the Gladstone Institutes and UCSF. “Working with older animals can be challenging from a technical standpoint, and it was amazing to see that the cells not only survived but affected activity and behavior.”

The success of the treatment in older mice, which corresponded to late adulthood in humans, is particularly important, as this would be the age that would be targeted were this method ever to be used therapeutically in people.

“This is a very important proof of concept study,” said senior author Yadong Huang, MD, PhD, an associate investigator at Gladstone Institutes and associate professor of neurology and pathology at UCSF. “The fact that we see a functional integration of these cells into the hippocampal circuitry and a complete rescue of learning and memory deficits in an aged model of Alzheimer’s disease is very exciting.” 

A balance of excitatory and inhibitory activity in the brain is essential for normal function. However, in the apoE4 model of Alzheimer’s disease—a genetic risk factor that is carried by approximately 25% of the population and is involved in 60-75% of all Alzheimer’s cases—this balance gets disrupted due to a decline in inhibitory regulator cells that are essential in maintaining normal brain activity. The hippocampus, an important memory center in the brain, is particularly affected by this loss of inhibitory neurons, resulting in an increase in network activation that is thought to contribute to the learning and memory deficits characteristic of Alzheimer’s disease. The accumulation of amyloid beta in the brain has also been linked to this imbalance between excitatory and inhibitory activity in the brain.

In the current study, the researchers hoped that by grafting inhibitory neuron progenitors into the hippocampus of aged apoE4 mice, they would be able to combat these effects, replacing the lost cells and restoring normal function to the area. Remarkably, these new inhibitory neurons survived in the hippocampus, enhancing inhibitory signaling and rescuing impairments in learning and memory.

In addition, when these inhibitory progenitor cells were transplanted into apoE4 mice with an accumulation of amyloid beta, prior deficits were alleviated. However, the new inhibitory neurons did not affect amyloid beta levels, suggesting that the cognitive enhancement did not occur as a result of amyloid clearance, and amyloid did not impair the integration of the transplant.

According to Dr. Huang, the potential implications for these findings extend beyond the current methods used. “Stem cell therapy in humans is still a long way off. However, this study tells us that if there is any way we can enhance inhibitory neuron function in the hippocampus, like through the development of small molecule compounds, it may be beneficial for Alzheimer disease patients.”

(Source: gladstoneinstitutes.org)

Filed under alzheimer's disease apoE4 hippocampus memory learning brain activity neuroscience science

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Can Games, Puzzles Keep Aging Minds Sharp?
Older adults who enjoy mentally stimulating games may have bigger brains and sharper thinking skills than their peers, new research suggests.
The study looked at the connection between playing games such as puzzles, crosswords, cards and checkers and mental acuity for adults in their 50s and 60s.
Researchers found that people who played those games at least every other day performed better on tests of memory and other mental functions. And, based on MRI scans, they had greater tissue mass in brain areas involved in memory.
Read more
(Image: Alamy)

Can Games, Puzzles Keep Aging Minds Sharp?

Older adults who enjoy mentally stimulating games may have bigger brains and sharper thinking skills than their peers, new research suggests.

The study looked at the connection between playing games such as puzzles, crosswords, cards and checkers and mental acuity for adults in their 50s and 60s.

Researchers found that people who played those games at least every other day performed better on tests of memory and other mental functions. And, based on MRI scans, they had greater tissue mass in brain areas involved in memory.

Read more

(Image: Alamy)

Filed under aging memory mental exercise cognitive stimulation psychology neuroscience science

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