Neuroscience

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Posts tagged hippocampus

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Activity in dendrites is critical in memory formation Why do we remember some things and not others? In a unique imaging study, two Northwestern University researchers have discovered how neurons in the brain might allow some experiences to be remembered while others are forgotten. It turns out, if you want to remember something about your environment, you better involve your dendrites. Using a high-resolution, one-of-a-kind microscope, Daniel A. Dombeck and Mark E. J. Sheffield peered into the brain of a living animal and saw exactly what was happening in individual neurons called place cells as the animal navigated a virtual reality maze. The scientists found that, contrary to current thought, the activity of a neuron’s cell body and its dendrites can be different. They observed that when cell bodies were activated but the dendrites were not activated during an animal’s experience, a lasting memory of that experience was not formed by the neurons. This suggests that the cell body seems to represent ongoing experience, while dendrites, the treelike branches of a neuron, help to store that experience as a memory. "There are a lot of theories on memory but very little data as to how individual neurons actually store information in a behaving animal," said Dombeck, assistant professor of neurobiology in the Weinberg College of Arts and Sciences and the study’s senior author. "Now we have uncovered signals in dendrites that we think are very important for learning and memory. Our findings could explain why some experiences are remembered and others are forgotten." In the brain’s hippocampus, there are hundreds of thousands of place cells — neurons essential to the brain’s GPS system. Dombeck and Sheffield are the first to image the activity of individual dendrites in place cells. Their findings contribute to our understanding of how the brain represents the world around it and also point to dendrites as a new potential target for therapeutics to combat memory deficits and debilitating diseases, such as Alzheimer’s disease (AD). Disruption to the brain’s GPS system is one of the first symptoms of AD, with many patients unable to find their way home. Understanding how place cells and their dendrites store these types of memories could help us find new ways to treat the disease. The Northwestern study will be published Oct. 26 by the journal Nature. Neuroscientist John O’Keefe discovered place cells in 1971 (and received this year’s Nobel Prize in physiology and medicine), but it is only in the last few years that scientists, such as Dombeck and Sheffield, have been able to image these neurons that represent a map of where we are in our environment. In their study, Dombeck and Sheffield found dendrite signals that could explain how an animal can experience something without storing the experience as a memory. They saw that dendrites are not always activated when the cell body is activated in a neuron. Signals produced in the dendrites (used to store information) and signals within the neuron cell body (used to compute and transmit information) can be either highly synchronized or desynchronized depending on how well the neurons remember different features of the maze. Scientists have long believed that the neuronal tasks of computing and storing information are connected — when neurons compute information, they are also storing it, and vice versa. The Northwestern study provides evidence against this classic view of neuronal function. "We experience events all the time, which must be represented in the brain by the activity of neurons, but not all these events can be recalled later," said Mark E. J. Sheffield, a postdoctoral fellow in Dombeck’s lab and first author of the study. "A daily commute to work, for example, requires the activity of millions of neurons, but you would be hard pressed to remember what was happening halfway through your commute last Tuesday," Sheffield said. "How is it then that the neurons could be activated during the commute without storing that information in the brain? Now we may have an explanation for how this occurs." Dombeck and Sheffield built their own laser scanning microscope that can image neurons on multiple planes. They then studied individual animals navigating (on a trackball) a virtual reality maze constructed using the video game Quake II. Each lit-up structure seen in the images they took indicate a neuron firing action potentials. The activity of these neurons represents an animal’s experience of where it is in the environment, the researchers said. Whether the neurons store this experience or not appears to depend on the activity of the neurons’ dendrites. (Image credit)

Activity in dendrites is critical in memory formation

Why do we remember some things and not others? In a unique imaging study, two Northwestern University researchers have discovered how neurons in the brain might allow some experiences to be remembered while others are forgotten. It turns out, if you want to remember something about your environment, you better involve your dendrites.

Using a high-resolution, one-of-a-kind microscope, Daniel A. Dombeck and Mark E. J. Sheffield peered into the brain of a living animal and saw exactly what was happening in individual neurons called place cells as the animal navigated a virtual reality maze.

The scientists found that, contrary to current thought, the activity of a neuron’s cell body and its dendrites can be different. They observed that when cell bodies were activated but the dendrites were not activated during an animal’s experience, a lasting memory of that experience was not formed by the neurons. This suggests that the cell body seems to represent ongoing experience, while dendrites, the treelike branches of a neuron, help to store that experience as a memory.

"There are a lot of theories on memory but very little data as to how individual neurons actually store information in a behaving animal," said Dombeck, assistant professor of neurobiology in the Weinberg College of Arts and Sciences and the study’s senior author. "Now we have uncovered signals in dendrites that we think are very important for learning and memory. Our findings could explain why some experiences are remembered and others are forgotten."

In the brain’s hippocampus, there are hundreds of thousands of place cells — neurons essential to the brain’s GPS system. Dombeck and Sheffield are the first to image the activity of individual dendrites in place cells.

Their findings contribute to our understanding of how the brain represents the world around it and also point to dendrites as a new potential target for therapeutics to combat memory deficits and debilitating diseases, such as Alzheimer’s disease (AD). Disruption to the brain’s GPS system is one of the first symptoms of AD, with many patients unable to find their way home. Understanding how place cells and their dendrites store these types of memories could help us find new ways to treat the disease.

The Northwestern study will be published Oct. 26 by the journal Nature.

Neuroscientist John O’Keefe discovered place cells in 1971 (and received this year’s Nobel Prize in physiology and medicine), but it is only in the last few years that scientists, such as Dombeck and Sheffield, have been able to image these neurons that represent a map of where we are in our environment.

In their study, Dombeck and Sheffield found dendrite signals that could explain how an animal can experience something without storing the experience as a memory.

They saw that dendrites are not always activated when the cell body is activated in a neuron. Signals produced in the dendrites (used to store information) and signals within the neuron cell body (used to compute and transmit information) can be either highly synchronized or desynchronized depending on how well the neurons remember different features of the maze.

Scientists have long believed that the neuronal tasks of computing and storing information are connected — when neurons compute information, they are also storing it, and vice versa. The Northwestern study provides evidence against this classic view of neuronal function.

"We experience events all the time, which must be represented in the brain by the activity of neurons, but not all these events can be recalled later," said Mark E. J. Sheffield, a postdoctoral fellow in Dombeck’s lab and first author of the study.

"A daily commute to work, for example, requires the activity of millions of neurons, but you would be hard pressed to remember what was happening halfway through your commute last Tuesday," Sheffield said. "How is it then that the neurons could be activated during the commute without storing that information in the brain? Now we may have an explanation for how this occurs."

Dombeck and Sheffield built their own laser scanning microscope that can image neurons on multiple planes. They then studied individual animals navigating (on a trackball) a virtual reality maze constructed using the video game Quake II.

Each lit-up structure seen in the images they took indicate a neuron firing action potentials. The activity of these neurons represents an animal’s experience of where it is in the environment, the researchers said. Whether the neurons store this experience or not appears to depend on the activity of the neurons’ dendrites.

(Image credit)

Filed under place cells memory formation dendrites hippocampus neurons neuroscience science

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(Figure 1: A magnified image of a mouse brain showing memory cells (red) that can be turned ‘on’ and ‘off’ using light delivered by a fiber optic cable (black). Credit: © Susumu Tonegawa) Memories get the emotional switch Memories of experiences are encoded in the brain along with contextual and emotional information such as where the experience took place and whether it was positive or negative. This allows for the formation of memory associations that might assist in survival. Just how this positive and negative encoding occurs, however, has remained unclear. Susumu Tonegawa and colleagues from the RIKEN–MIT Center for Neural Circuit Genetics have now discovered that neurons in the hippocampus region of the brain can be artificially switched to encode memories as either positive or negative regardless of the original experience. Tonegawa’s research team used genetic techniques to mark neurons in the dorsal dentate gyrus region of the hippocampus and the basolateral complex of the amygdala (BLA) in male mice. Memories are encoded in both these regions as specific groups of activated cells called ‘engrams’, but each region encodes the memory in slightly different ways: the BLA encodes positive and negative memory ‘valence’, while the dorsal dentate gyrus encodes contextual information such as emotion. The genetic labeling, which involved using a light-sensitive ion channel called channelrhodopsin, was activated by the formation of either a positive memory, in this case exposure to females, or a negative memory associated with a foot shock. The cells that expressed this channel could be subsequently activated by exposure to light (Fig. 1); doing so induced aversive responses in mice that had experienced foot shocks, and appetitive responses in those that had experienced female interactions. The researchers then used light to activate the hippocampal or BLA neurons that had been labeled during the formation of a positive memory while exposing the mice to foot shocks. The next time the animals were tested, light activation of those hippocampal neurons that had initially induced appetitive responses instead led the mice to exhibit aversive responses. However, BLA neurons could not be switched in this way, indicating that only neurons in the hippocampus have plasticity in their encoding of positive or negative memories. The valence of hippocampal neurons, the researchers found, could be switched from both good to bad and bad to good using this technique, with the switch attributed to a change in the strength of connections between the hippocampal and BLA neurons of each engram. The findings provide new insight into how memories can be altered after they are formed. The possibility of inducing similar changes to memory valence in humans could also offer hope of a treatment for those suffering from conditions such as post-traumatic stress disorder.

(Figure 1: A magnified image of a mouse brain showing memory cells (red) that can be turned ‘on’ and ‘off’ using light delivered by a fiber optic cable (black). Credit: © Susumu Tonegawa)

Memories get the emotional switch

Memories of experiences are encoded in the brain along with contextual and emotional information such as where the experience took place and whether it was positive or negative. This allows for the formation of memory associations that might assist in survival. Just how this positive and negative encoding occurs, however, has remained unclear.

Susumu Tonegawa and colleagues from the RIKEN–MIT Center for Neural Circuit Genetics have now discovered that neurons in the hippocampus region of the brain can be artificially switched to encode memories as either positive or negative regardless of the original experience.

Tonegawa’s research team used genetic techniques to mark neurons in the dorsal dentate gyrus region of the hippocampus and the basolateral complex of the amygdala (BLA) in male mice. Memories are encoded in both these regions as specific groups of activated cells called ‘engrams’, but each region encodes the memory in slightly different ways: the BLA encodes positive and negative memory ‘valence’, while the dorsal dentate gyrus encodes contextual information such as emotion.

The genetic labeling, which involved using a light-sensitive ion channel called channelrhodopsin, was activated by the formation of either a positive memory, in this case exposure to females, or a negative memory associated with a foot shock. The cells that expressed this channel could be subsequently activated by exposure to light (Fig. 1); doing so induced aversive responses in mice that had experienced foot shocks, and appetitive responses in those that had experienced female interactions.

The researchers then used light to activate the hippocampal or BLA neurons that had been labeled during the formation of a positive memory while exposing the mice to foot shocks. The next time the animals were tested, light activation of those hippocampal neurons that had initially induced appetitive responses instead led the mice to exhibit aversive responses. However, BLA neurons could not be switched in this way, indicating that only neurons in the hippocampus have plasticity in their encoding of positive or negative memories.

The valence of hippocampal neurons, the researchers found, could be switched from both good to bad and bad to good using this technique, with the switch attributed to a change in the strength of connections between the hippocampal and BLA neurons of each engram.

The findings provide new insight into how memories can be altered after they are formed. The possibility of inducing similar changes to memory valence in humans could also offer hope of a treatment for those suffering from conditions such as post-traumatic stress disorder.

Filed under memory hippocampus neurons dentate gyrus engrams emotion neuroscience science

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(Image caption: Pictured is a mouse hippocampal neuron studded with thousands of synaptic connections (yellow). The number and location of synapses — not too many or too few — is critical to healthy brain function. The researchers found that MHCI proteins, known for their role in the immune system, also are one of the only known factors that ensure synapse density is not too high. The protein does so by inhibiting insulin receptors, which promote synapse formation. Credit: Lisa Boulanger) Immune proteins moonlight to regulate brain-cell connections When it comes to the brain, “more is better” seems like an obvious assumption. But in the case of synapses, which are the connections between brain cells, too many or too few can both disrupt brain function. Researchers from Princeton University and the University of California-San Diego (UCSD) recently found that an immune-system protein called MHCI, or major histocompatibility complex class I, moonlights in the nervous system to help regulate the number of synapses, which transmit chemical and electrical signals between neurons. The researchers report in the Journal of Neuroscience that in the brain MHCI could play an unexpected role in conditions such as Alzheimer’s disease, type II diabetes and autism. MHCI proteins are known for their role in the immune system where they present protein fragments from pathogens and cancerous cells to T cells, which are white blood cells with a central role in the body’s response to infection. This presentation allows T cells to recognize and kill infected and cancerous cells. In the brain, however, the researchers found that MHCI immune molecules are one of the only known factors that limit the density of synapses, ensuring that synapses form in the appropriate numbers necessary to support healthy brain function. MHCI limits synapse density by inhibiting insulin receptors, which regulate the body’s sugar metabolism and, in the brain, promote synapse formation. Senior author Lisa Boulanger, an assistant professor in the Department of Molecular Biology and the Princeton Neuroscience Institute (PNI), said that MHCI’s role in ensuring appropriate insulin signaling and synapse density raises the possibility that changes in the protein’s activity could contribute to conditions such Alzheimer’s disease, type II diabetes and autism. These conditions have all been associated with a complex combination of disrupted insulin-signaling pathways, changes in synapse density, and inflammation, which activates immune-system molecules such as MHCI. Patients with type II diabetes develop “insulin resistance” in which insulin receptors become incapable of responding to insulin, the reason for which is unknown, Boulanger said. Similarly, patients with Alzheimer’s disease develop insulin resistance in the brain that is so pronounced some have dubbed the disease “type III diabetes,” Boulanger said. "Our results suggest that changes in MHCI immune proteins could contribute to disorders of insulin resistance," Boulanger said. "For example, chronic inflammation is associated with type II diabetes, but the reason for this link has remained a mystery. Our results suggest that inflammation-induced changes in MHCI could have consequences for insulin signaling in neurons and maybe elsewhere." MHCI levels also are “dramatically altered” in the brains of people with Alzheimer’s disease, Boulanger said. Normal memory depends on appropriate levels of MHCI. Boulanger was senior author on a 2013 paper in the journal Learning and Memory that found that mice bred to produce less functional MHCI proteins exhibited striking changes in the function of the hippocampus, a part of the brain where some memories are formed, and had severe memory impairments. "MHCI levels are altered in the Alzheimer’s brain, and altering MHCI levels in mice disrupts memory, reduces synapse number and causes neuronal insulin resistance, all of which are core features of Alzheimer’s disease," Boulanger said. Links between MHCI and autism also are emerging, Boulanger said. People with autism have more synapses than usual in specific brain regions. In addition, several autism-associated genes regulate synapse number, often via a signaling protein known as mTOR (mammalian target of rapamycin). In their study, Boulanger and her co-authors found that mice with reduced levels of MHCI had increased insulin-receptor signaling via the mTOR pathway, and, consequently, more synapses. When elevated mTOR signaling was reduced in MHCI-deficient mice, normal synapse density was restored. Thus, Boulanger said, MHCI and autism-associated genes appear to converge on the mTOR-synapse regulation pathway. This is intriguing given that inflammation during pregnancy, which alters MHCI levels in the fetal brain, may slightly increase the risk of autism in genetically predisposed individuals, she said. "Up-regulating MHCI is essential for the maternal immune response, but changing MHCI activity in the fetal brain when synaptic connections are being formed could potentially affect synapse density," Boulanger said. Ben Barres, a professor of neurobiology, developmental biology and neurology at the Stanford University School of Medicine, said that while it is known that both insulin-receptor signaling increases synapse density, and MHCI signaling decreases it, the researchers are the first to show that MHCI actually affects insulin receptors to control synapse density. "The idea that there could be a direct interaction between these two signaling systems comes as a great surprise," said Barres, who was not involved in the research. "This discovery not only will lead to new insight into how brain circuitry develops but to new insight into declining brain function that occurs with aging." Particularly, the research suggests a possible functional connection between type II diabetes and Alzheimer’s disease, Barres said. "Type II diabetes has recently emerged as a risk factor for Alzheimer’s disease but it has not been clear what the connection is to the synapse loss experienced with Alzheimer’s disease," he said. "Given that type II diabetes is accompanied by decreased insulin responsiveness, it may be that the MHCI signaling becomes able to overcome normal insulin signaling and contribute to synapse decline in this disease." Research during the past 15 years has shown that MHCI lives a prolific double-life in the brain, Boulanger said. The brain is “immune privileged,” meaning the immune system doesn’t respond as rapidly or effectively to perceived threats in the brain. Dozens of studies have shown, however, that MHCI is not only present throughout the healthy brain, but is essential for normal brain development and function, Boulanger said. A 2013 paper from her lab published in the journal Molecular and Cellular Neuroscience showed that MHCI is even present in the fetal-mouse brain, at a stage when the immune system is not yet mature. "Many people thought that immune molecules like MHCI must be missing from the brain," Boulanger said. "It turns out that MHCI immune proteins do operate in the brain — they just do something completely different. The dual roles of these proteins in the immune system and nervous system may allow them to mediate both harmful and beneficial interactions between the two systems."

(Image caption: Pictured is a mouse hippocampal neuron studded with thousands of synaptic connections (yellow). The number and location of synapses — not too many or too few — is critical to healthy brain function. The researchers found that MHCI proteins, known for their role in the immune system, also are one of the only known factors that ensure synapse density is not too high. The protein does so by inhibiting insulin receptors, which promote synapse formation. Credit: Lisa Boulanger)

Immune proteins moonlight to regulate brain-cell connections

When it comes to the brain, “more is better” seems like an obvious assumption. But in the case of synapses, which are the connections between brain cells, too many or too few can both disrupt brain function.

Researchers from Princeton University and the University of California-San Diego (UCSD) recently found that an immune-system protein called MHCI, or major histocompatibility complex class I, moonlights in the nervous system to help regulate the number of synapses, which transmit chemical and electrical signals between neurons. The researchers report in the Journal of Neuroscience that in the brain MHCI could play an unexpected role in conditions such as Alzheimer’s disease, type II diabetes and autism.

MHCI proteins are known for their role in the immune system where they present protein fragments from pathogens and cancerous cells to T cells, which are white blood cells with a central role in the body’s response to infection. This presentation allows T cells to recognize and kill infected and cancerous cells.

In the brain, however, the researchers found that MHCI immune molecules are one of the only known factors that limit the density of synapses, ensuring that synapses form in the appropriate numbers necessary to support healthy brain function. MHCI limits synapse density by inhibiting insulin receptors, which regulate the body’s sugar metabolism and, in the brain, promote synapse formation.

Senior author Lisa Boulanger, an assistant professor in the Department of Molecular Biology and the Princeton Neuroscience Institute (PNI), said that MHCI’s role in ensuring appropriate insulin signaling and synapse density raises the possibility that changes in the protein’s activity could contribute to conditions such Alzheimer’s disease, type II diabetes and autism. These conditions have all been associated with a complex combination of disrupted insulin-signaling pathways, changes in synapse density, and inflammation, which activates immune-system molecules such as MHCI.

Patients with type II diabetes develop “insulin resistance” in which insulin receptors become incapable of responding to insulin, the reason for which is unknown, Boulanger said. Similarly, patients with Alzheimer’s disease develop insulin resistance in the brain that is so pronounced some have dubbed the disease “type III diabetes,” Boulanger said.

"Our results suggest that changes in MHCI immune proteins could contribute to disorders of insulin resistance," Boulanger said. "For example, chronic inflammation is associated with type II diabetes, but the reason for this link has remained a mystery. Our results suggest that inflammation-induced changes in MHCI could have consequences for insulin signaling in neurons and maybe elsewhere."

MHCI levels also are “dramatically altered” in the brains of people with Alzheimer’s disease, Boulanger said. Normal memory depends on appropriate levels of MHCI. Boulanger was senior author on a 2013 paper in the journal Learning and Memory that found that mice bred to produce less functional MHCI proteins exhibited striking changes in the function of the hippocampus, a part of the brain where some memories are formed, and had severe memory impairments.

"MHCI levels are altered in the Alzheimer’s brain, and altering MHCI levels in mice disrupts memory, reduces synapse number and causes neuronal insulin resistance, all of which are core features of Alzheimer’s disease," Boulanger said.

Links between MHCI and autism also are emerging, Boulanger said. People with autism have more synapses than usual in specific brain regions. In addition, several autism-associated genes regulate synapse number, often via a signaling protein known as mTOR (mammalian target of rapamycin). In their study, Boulanger and her co-authors found that mice with reduced levels of MHCI had increased insulin-receptor signaling via the mTOR pathway, and, consequently, more synapses. When elevated mTOR signaling was reduced in MHCI-deficient mice, normal synapse density was restored.

Thus, Boulanger said, MHCI and autism-associated genes appear to converge on the mTOR-synapse regulation pathway. This is intriguing given that inflammation during pregnancy, which alters MHCI levels in the fetal brain, may slightly increase the risk of autism in genetically predisposed individuals, she said.

"Up-regulating MHCI is essential for the maternal immune response, but changing MHCI activity in the fetal brain when synaptic connections are being formed could potentially affect synapse density," Boulanger said.

Ben Barres, a professor of neurobiology, developmental biology and neurology at the Stanford University School of Medicine, said that while it is known that both insulin-receptor signaling increases synapse density, and MHCI signaling decreases it, the researchers are the first to show that MHCI actually affects insulin receptors to control synapse density.

"The idea that there could be a direct interaction between these two signaling systems comes as a great surprise," said Barres, who was not involved in the research. "This discovery not only will lead to new insight into how brain circuitry develops but to new insight into declining brain function that occurs with aging."

Particularly, the research suggests a possible functional connection between type II diabetes and Alzheimer’s disease, Barres said.

"Type II diabetes has recently emerged as a risk factor for Alzheimer’s disease but it has not been clear what the connection is to the synapse loss experienced with Alzheimer’s disease," he said. "Given that type II diabetes is accompanied by decreased insulin responsiveness, it may be that the MHCI signaling becomes able to overcome normal insulin signaling and contribute to synapse decline in this disease."

Research during the past 15 years has shown that MHCI lives a prolific double-life in the brain, Boulanger said. The brain is “immune privileged,” meaning the immune system doesn’t respond as rapidly or effectively to perceived threats in the brain. Dozens of studies have shown, however, that MHCI is not only present throughout the healthy brain, but is essential for normal brain development and function, Boulanger said. A 2013 paper from her lab published in the journal Molecular and Cellular Neuroscience showed that MHCI is even present in the fetal-mouse brain, at a stage when the immune system is not yet mature.

"Many people thought that immune molecules like MHCI must be missing from the brain," Boulanger said. "It turns out that MHCI immune proteins do operate in the brain — they just do something completely different. The dual roles of these proteins in the immune system and nervous system may allow them to mediate both harmful and beneficial interactions between the two systems."

Filed under brain cells synapses MHCI immune system insulin hippocampus neuroscience science

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Physical exercise in old age can stimulate brain fitness, but effect decreases with advancing age Physical exercise in old age can improve brain perfusion as well as certain memory skills. This is the finding of Magdeburg neuroscientists who studied men and women aged between 60 and 77. In younger individuals regular training on a treadmill tended to improve cerebral blood flow and visual memory. However, trial participants who were older than 70 years of age tended to show no benefit of exercise. Thus, the study also indicates that the benefits of exercise may be limited by advancing age. Researchers of the German Center for Neurodegenerative Diseases (DZNE), the University of Magdeburg and the Leibniz Institute for Neurobiology have published these results in the current edition of the journal “Molecular Psychiatry”. Scientists at the Karolinska Institute in Stockholm and the Max Planck Institute for Human Development were also involved in the study. The 40 test volunteers were healthy for their age, sedentary when the study commenced and divided into two groups. About half of the study participants exercised regularly on a treadmill for 3 months. The other individuals merely performed muscle relaxation sessions. In 7 out of 9 members of the exercise group who were not more than 70 years old, the training improved physical fitness and also tended to increase perfusion in the hippocampus – an area of the brain which is important for memory function. The increased perfusion was accompanied by improved visual memory: at the end of the study, these individuals found it easier to memorize abstract images than at the beginning of the training program. These effects were largely absent in older volunteers who participated in the workout as well as in the members of the control group. The study included extensive tests of the volunteers’ physical condition and memory. Furthermore, the study participants were examined by magnetic resonance imaging (MRI). This technique enables detailed insights into the interior of the brain. Exercising against dementia Physical exercise is known to have considerable health benefits: the effects on the body have been researched extensively, the effects on brain function less so. An increase in brain perfusion through physical exercise had previously only been demonstrated empirically in younger people. The new study shows that some ageing brains also retain this ability to adapt, even though it seems to decrease with advancing age. Furthermore, the results indicate that changes in memory performance resulting from physical exercise are closely linked to changes in brain perfusion. “Ultimately, we aim to develop measures to purposefully counteract dementia such as Alzheimer’s disease. This is why we want to understand the effects of physical exercise on the brain and the related neurobiological mechanisms. This is essential for developing treatments that are truly effective,” is how Professor Emrah Düzel, site speaker of the DZNE in Magdeburg and director of the Institute of Cognitive Neurology and Dementia Research at the University of Magdeburg, explains the background to the study. The goal: new brain cells The researchers’ goal is to cause new nerve cells to grow in the brain. This is how they intend to counter the loss of neurons typical of dementia. “The human brain is able to change and evolve throughout our lives. New nerve cells can form even in adult brains,” says Düzel. “Our aim is to stimulate this so-called neurogenesis. We don’t yet know whether our training methods promote the development of new brain cells. However, fundamental research shows that the formation of new brain cells often goes hand in hand with improved brain perfusion.” Changes in the hippocampus Indeed, it did turn out that the treadmill exercise sessions caused more blood to reach the hippocampus in younger participants. “This improves the supply of oxygen and nutrients and may also have other positive effects on the brain’s metabolism,” says the neuroscientist. “However, we have also seen that the effect of the training decreases with age. It is less effective in people aged over 70 than in people in their early 60s. It will be an important goal of our research to understand the causes for this and to find remedies.” Düzel adds: “It is encouraging to see that visual memory improved as brain perfusion increased. However, effective treatments would also have to affect other brain functions. In our study, the effect was limited to visual short-term memory.” A combined training for body and mind Other experiments are now under way in Magdeburg in which test participants are sent on an unusual kind of scavenger hunt: they are assigned the task of finding objects concealed in a computer-generated landscape which is pictured on a large screen. Movement control in this virtual world is done with the help of a treadmill. “This complex situation makes high demands on motor skills and sense of orientation,” explains Düzel. “It challenges both the brain as well as the muscles.” In the long term, the scientists aim to include people in the early stages of Alzheimer’s disease in their study program. “We are looking for ways of delaying or even stopping the progression of the disease. And we are also researching methods of prevention,” emphasizes Düzel. “Connecting physical activity and mental exercise may have a broad impact, and combined training might become a therapeutic approach. However, this has yet to be shown. In fact, our current results suggest that we may need pharmacological treatments to make exercise more effective.”

Physical exercise in old age can stimulate brain fitness, but effect decreases with advancing age

Physical exercise in old age can improve brain perfusion as well as certain memory skills. This is the finding of Magdeburg neuroscientists who studied men and women aged between 60 and 77. In younger individuals regular training on a treadmill tended to improve cerebral blood flow and visual memory. However, trial participants who were older than 70 years of age tended to show no benefit of exercise. Thus, the study also indicates that the benefits of exercise may be limited by advancing age. Researchers of the German Center for Neurodegenerative Diseases (DZNE), the University of Magdeburg and the Leibniz Institute for Neurobiology have published these results in the current edition of the journal “Molecular Psychiatry”. Scientists at the Karolinska Institute in Stockholm and the Max Planck Institute for Human Development were also involved in the study.

The 40 test volunteers were healthy for their age, sedentary when the study commenced and divided into two groups. About half of the study participants exercised regularly on a treadmill for 3 months. The other individuals merely performed muscle relaxation sessions. In 7 out of 9 members of the exercise group who were not more than 70 years old, the training improved physical fitness and also tended to increase perfusion in the hippocampus – an area of the brain which is important for memory function. The increased perfusion was accompanied by improved visual memory: at the end of the study, these individuals found it easier to memorize abstract images than at the beginning of the training program. These effects were largely absent in older volunteers who participated in the workout as well as in the members of the control group.

The study included extensive tests of the volunteers’ physical condition and memory. Furthermore, the study participants were examined by magnetic resonance imaging (MRI). This technique enables detailed insights into the interior of the brain.

Exercising against dementia

Physical exercise is known to have considerable health benefits: the effects on the body have been researched extensively, the effects on brain function less so. An increase in brain perfusion through physical exercise had previously only been demonstrated empirically in younger people. The new study shows that some ageing brains also retain this ability to adapt, even though it seems to decrease with advancing age. Furthermore, the results indicate that changes in memory performance resulting from physical exercise are closely linked to changes in brain perfusion.

“Ultimately, we aim to develop measures to purposefully counteract dementia such as Alzheimer’s disease. This is why we want to understand the effects of physical exercise on the brain and the related neurobiological mechanisms. This is essential for developing treatments that are truly effective,” is how Professor Emrah Düzel, site speaker of the DZNE in Magdeburg and director of the Institute of Cognitive Neurology and Dementia Research at the University of Magdeburg, explains the background to the study.

The goal: new brain cells

The researchers’ goal is to cause new nerve cells to grow in the brain. This is how they intend to counter the loss of neurons typical of dementia. “The human brain is able to change and evolve throughout our lives. New nerve cells can form even in adult brains,” says Düzel. “Our aim is to stimulate this so-called neurogenesis. We don’t yet know whether our training methods promote the development of new brain cells. However, fundamental research shows that the formation of new brain cells often goes hand in hand with improved brain perfusion.”

Changes in the hippocampus

Indeed, it did turn out that the treadmill exercise sessions caused more blood to reach the hippocampus in younger participants. “This improves the supply of oxygen and nutrients and may also have other positive effects on the brain’s metabolism,” says the neuroscientist. “However, we have also seen that the effect of the training decreases with age. It is less effective in people aged over 70 than in people in their early 60s. It will be an important goal of our research to understand the causes for this and to find remedies.”

Düzel adds: “It is encouraging to see that visual memory improved as brain perfusion increased. However, effective treatments would also have to affect other brain functions. In our study, the effect was limited to visual short-term memory.”

A combined training for body and mind

Other experiments are now under way in Magdeburg in which test participants are sent on an unusual kind of scavenger hunt: they are assigned the task of finding objects concealed in a computer-generated landscape which is pictured on a large screen. Movement control in this virtual world is done with the help of a treadmill. “This complex situation makes high demands on motor skills and sense of orientation,” explains Düzel. “It challenges both the brain as well as the muscles.”

In the long term, the scientists aim to include people in the early stages of Alzheimer’s disease in their study program. “We are looking for ways of delaying or even stopping the progression of the disease. And we are also researching methods of prevention,” emphasizes Düzel. “Connecting physical activity and mental exercise may have a broad impact, and combined training might become a therapeutic approach. However, this has yet to be shown. In fact, our current results suggest that we may need pharmacological treatments to make exercise more effective.”

Filed under physical activity exercise aging dementia memory hippocampus brain cells neuroscience science

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Mental Rest and Reflection Boost Learning A new study, which may have implications for approaches to education, finds that brain mechanisms engaged when people allow their minds to rest and reflect on things they’ve learned before may boost later learning. Scientists have already established that resting the mind, as in daydreaming, helps strengthen memories of events and retention of information. In a new twist, researchers at The University of Texas at Austin have shown that the right kind of mental rest, which strengthens and consolidates memories from recent learning tasks, helps boost future learning. The results appear online this week in the journal Proceedings of the National Academy of Sciences. Margaret Schlichting, a graduate student researcher, and Alison Preston, an associate professor of psychology and neuroscience, gave participants in the study two learning tasks in which participants were asked to memorize different series of associated photo pairs. Between the tasks, participants rested and could think about anything they chose, but brain scans found that the ones who used that time to reflect on what they had learned earlier in the day fared better on tests pertaining to what they learned later, especially where small threads of information between the two tasks overlapped. Participants seemed to be making connections that helped them absorb information later on, even if it was only loosely related to something they learned before. "We’ve shown for the first time that how the brain processes information during rest can improve future learning," says Preston. "We think replaying memories during rest makes those earlier memories stronger, not just impacting the original content, but impacting the memories to come. Until now, many scientists assumed that prior memories are more likely to interfere with new learning. This new study shows that at least in some situations, the opposite is true. "Nothing happens in isolation," says Preston. "When you are learning something new, you bring to mind all of the things you know that are related to that new information. In doing so, you embed the new information into your existing knowledge." Preston described how this new understanding might help teachers design more effective ways of teaching. Imagine a college professor is teaching students about how neurons communicate in the human brain, a process that shares some common features with an electric power grid. The professor might first cue the students to remember things they learned in a high school physics class about how electricity is conducted by wires. "A professor might first get them thinking about the properties of electricity," says Preston. "Not necessarily in lecture form, but by asking questions to get students to recall what they already know. Then, the professor might begin the lecture on neuronal communication. By prompting them beforehand, the professor might help them reactivate relevant knowledge and make the new material more digestible for them." This research was conducted with adult participants. The researchers will next study whether a similar dynamic is at work with children.

Mental Rest and Reflection Boost Learning

A new study, which may have implications for approaches to education, finds that brain mechanisms engaged when people allow their minds to rest and reflect on things they’ve learned before may boost later learning.

Scientists have already established that resting the mind, as in daydreaming, helps strengthen memories of events and retention of information. In a new twist, researchers at The University of Texas at Austin have shown that the right kind of mental rest, which strengthens and consolidates memories from recent learning tasks, helps boost future learning.

The results appear online this week in the journal Proceedings of the National Academy of Sciences.

Margaret Schlichting, a graduate student researcher, and Alison Preston, an associate professor of psychology and neuroscience, gave participants in the study two learning tasks in which participants were asked to memorize different series of associated photo pairs. Between the tasks, participants rested and could think about anything they chose, but brain scans found that the ones who used that time to reflect on what they had learned earlier in the day fared better on tests pertaining to what they learned later, especially where small threads of information between the two tasks overlapped. Participants seemed to be making connections that helped them absorb information later on, even if it was only loosely related to something they learned before.

"We’ve shown for the first time that how the brain processes information during rest can improve future learning," says Preston. "We think replaying memories during rest makes those earlier memories stronger, not just impacting the original content, but impacting the memories to come.

Until now, many scientists assumed that prior memories are more likely to interfere with new learning. This new study shows that at least in some situations, the opposite is true.

"Nothing happens in isolation," says Preston. "When you are learning something new, you bring to mind all of the things you know that are related to that new information. In doing so, you embed the new information into your existing knowledge."

Preston described how this new understanding might help teachers design more effective ways of teaching. Imagine a college professor is teaching students about how neurons communicate in the human brain, a process that shares some common features with an electric power grid. The professor might first cue the students to remember things they learned in a high school physics class about how electricity is conducted by wires.

"A professor might first get them thinking about the properties of electricity," says Preston. "Not necessarily in lecture form, but by asking questions to get students to recall what they already know. Then, the professor might begin the lecture on neuronal communication. By prompting them beforehand, the professor might help them reactivate relevant knowledge and make the new material more digestible for them."

This research was conducted with adult participants. The researchers will next study whether a similar dynamic is at work with children.

Filed under learning hippocampus mental rest memory psychology neuroscience science

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Brain surgery through the cheek For those most severely affected, treating epilepsy means drilling through the skull deep into the brain to destroy the small area where the seizures originate – invasive, dangerous and with a long recovery period. Five years ago, a team of Vanderbilt engineers wondered: Is it possible to address epileptic seizures in a less invasive way? They decided it would be possible. Because the area of the brain involved is the hippocampus, which is located at the bottom of the brain, they could develop a robotic device that pokes through the cheek and enters the brain from underneath which avoids having to drill through the skull and is much closer to the target area. To do so, however, meant developing a shape-memory alloy needle that can be precisely steered along a curving path and a robotic platform that can operate inside the powerful magnetic field created by an MRI scanner. The engineers have developed a working prototype, which was unveiled in a live demonstration this week at the Fluid Power Innovation and Research Conference in Nashville by David Comber, the graduate student in mechanical engineering who did much of the design work. The business end of the device is a 1.14 mm nickel-titanium needle that operates like a mechanical pencil, with concentric tubes, some of which are curved, that allow the tip to follow a curved path into the brain. (Unlike many common metals, nickel-titanium is compatible with MRIs). Using compressed air, a robotic platform controllably steers and advances the needle segments a millimeter at a time. According to Comber, they have measured the accuracy of the system in the lab and found that it is better than 1.18 mm, which is considered sufficient for such an operation. In addition, the needle is inserted in tiny, millimeter steps so the surgeon can track its position by taking successive MRI scans. According to Associate Professor of Mechanical Engineering Eric Barth, who headed the project, the next stage in the surgical robot’s development is testing it with cadavers. He estimates it could be in operating rooms within the next decade. To come up with the design, the team began with capabilities that they already had. “I’ve done a lot of work in my career on the control of pneumatic systems,” Barth said. “We knew we had this ability to have a robot in the MRI scanner, doing something in a way that other robots could not. Then we thought, ‘What can we do that would have the highest impact?’” At the same time, Associate Professor of Mechanical Engineering Robert Webster had developed a system of steerable surgical needles. “The idea for this came about when Eric and I were talking in the hallway one day and we figured that his expertise in pneumatics was perfect for the MRI environment and could be combined with the steerable needles I’d been working on,” said Webster. The engineers identified epilepsy surgery as an ideal, high-impact application through discussions with Associate Professor of Neurological Surgery Joseph Neimat. They learned that currently neuroscientists use the through-the-cheek approach to implant electrodes in the brain to track brain activity and identify the location where the epileptic fits originate. But the straight needles they use can’t reach the source region, so they must drill through the skull and insert the needle used to destroy the misbehaving neurons through the top of the head. Comber and Barth shadowed Neimat through brain surgeries to understand how their device would work in practice. “The systems we have now that let us introduce probes into the brain – they deal with straight lines and are only manually guided,” Neimat said. “To have a system with a curved needle and unlimited access would make surgeries minimally invasive. We could do a dramatic surgery with nothing more than a needle stick to the cheek.” The engineers have designed the system so that much of it can be made using 3-D printing in order to keep the price low. This was achieved by collaborating with Jonathon Slightam and Vito Gervasi at the Milwaukee School of Engineering who specialize in novel applications for additive manufacturing.

Brain surgery through the cheek

For those most severely affected, treating epilepsy means drilling through the skull deep into the brain to destroy the small area where the seizures originate – invasive, dangerous and with a long recovery period.

Five years ago, a team of Vanderbilt engineers wondered: Is it possible to address epileptic seizures in a less invasive way? They decided it would be possible. Because the area of the brain involved is the hippocampus, which is located at the bottom of the brain, they could develop a robotic device that pokes through the cheek and enters the brain from underneath which avoids having to drill through the skull and is much closer to the target area.

To do so, however, meant developing a shape-memory alloy needle that can be precisely steered along a curving path and a robotic platform that can operate inside the powerful magnetic field created by an MRI scanner.

The engineers have developed a working prototype, which was unveiled in a live demonstration this week at the Fluid Power Innovation and Research Conference in Nashville by David Comber, the graduate student in mechanical engineering who did much of the design work.

The business end of the device is a 1.14 mm nickel-titanium needle that operates like a mechanical pencil, with concentric tubes, some of which are curved, that allow the tip to follow a curved path into the brain. (Unlike many common metals, nickel-titanium is compatible with MRIs). Using compressed air, a robotic platform controllably steers and advances the needle segments a millimeter at a time.

According to Comber, they have measured the accuracy of the system in the lab and found that it is better than 1.18 mm, which is considered sufficient for such an operation. In addition, the needle is inserted in tiny, millimeter steps so the surgeon can track its position by taking successive MRI scans.

According to Associate Professor of Mechanical Engineering Eric Barth, who headed the project, the next stage in the surgical robot’s development is testing it with cadavers. He estimates it could be in operating rooms within the next decade.

To come up with the design, the team began with capabilities that they already had.

“I’ve done a lot of work in my career on the control of pneumatic systems,” Barth said. “We knew we had this ability to have a robot in the MRI scanner, doing something in a way that other robots could not. Then we thought, ‘What can we do that would have the highest impact?’”

At the same time, Associate Professor of Mechanical Engineering Robert Webster had developed a system of steerable surgical needles. “The idea for this came about when Eric and I were talking in the hallway one day and we figured that his expertise in pneumatics was perfect for the MRI environment and could be combined with the steerable needles I’d been working on,” said Webster.

The engineers identified epilepsy surgery as an ideal, high-impact application through discussions with Associate Professor of Neurological Surgery Joseph Neimat. They learned that currently neuroscientists use the through-the-cheek approach to implant electrodes in the brain to track brain activity and identify the location where the epileptic fits originate. But the straight needles they use can’t reach the source region, so they must drill through the skull and insert the needle used to destroy the misbehaving neurons through the top of the head.

Comber and Barth shadowed Neimat through brain surgeries to understand how their device would work in practice.

“The systems we have now that let us introduce probes into the brain – they deal with straight lines and are only manually guided,” Neimat said. “To have a system with a curved needle and unlimited access would make surgeries minimally invasive. We could do a dramatic surgery with nothing more than a needle stick to the cheek.”

The engineers have designed the system so that much of it can be made using 3-D printing in order to keep the price low. This was achieved by collaborating with Jonathon Slightam and Vito Gervasi at the Milwaukee School of Engineering who specialize in novel applications for additive manufacturing.

Filed under brain surgery epilepsy hippocampus robotics 3D printing neuroscience technology science

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Manipulating memory with light Just look into the light: not quite, but researchers at the UC Davis Center for Neuroscience and Department of Psychology have used light to erase specific memories in mice, and proved a basic theory of how different parts of the brain work together to retrieve episodic memories. Optogenetics, pioneered by Karl Diesseroth at Stanford University, is a new technique for manipulating and studying nerve cells using light. The techniques of optogenetics are rapidly becoming the standard method for investigating brain function. Kazumasa Tanaka, Brian Wiltgen and colleagues at UC Davis applied the technique to test a long-standing idea about memory retrieval. For about 40 years, Wiltgen said, neuroscientists have theorized that retrieving episodic memories — memories about specific places and events — involves coordinated activity between the cerebral cortex and the hippocampus, a small structure deep in the brain. "The theory is that learning involves processing in the cortex, and the hippocampus reproduces this pattern of activity during retrieval, allowing you to re-experience the event," Wiltgen said. If the hippocampus is damaged, patients can lose decades of memories. But this model has been difficult to test directly, until the arrival of optogenetics. Wiltgen and Tanaka used mice genetically modified so that when nerve cells are activated, they both fluoresce green and express a protein that allows the cells to be switched off by light. They were therefore able both to follow exactly which nerve cells in the cortex and hippocampus were activated in learning and memory retrieval, and switch them off with light directed through a fiber-optic cable. They trained the mice by placing them in a cage where they got a mild electric shock. Normally, mice placed in a new environment will nose around and explore. But when placed in a cage where they have previously received a shock, they freeze in place in a “fear response.” Tanaka and Wiltgen first showed that they could label the cells involved in learning and demonstrate that they were reactivated during memory recall. Then they were able to switch off the specific nerve cells in the hippocampus, and show that the mice lost their memories of the unpleasant event. They were also able to show that turning off other cells in the hippocampus did not affect retrieval of that memory, and to follow fibers from the hippocampus to specific cells in the cortex. "The cortex can’t do it alone, it needs input from the hippocampus," Wiltgen said. "This has been a fundamental assumption in our field for a long time and Kazu’s data provides the first direct evidence that it is true." They could also see how the specific cells in the cortex were connected to the amygdala, a structure in the brain that is involved in emotion and in generating the freezing response.

Manipulating memory with light

Just look into the light: not quite, but researchers at the UC Davis Center for Neuroscience and Department of Psychology have used light to erase specific memories in mice, and proved a basic theory of how different parts of the brain work together to retrieve episodic memories.

Optogenetics, pioneered by Karl Diesseroth at Stanford University, is a new technique for manipulating and studying nerve cells using light. The techniques of optogenetics are rapidly becoming the standard method for investigating brain function.

Kazumasa Tanaka, Brian Wiltgen and colleagues at UC Davis applied the technique to test a long-standing idea about memory retrieval. For about 40 years, Wiltgen said, neuroscientists have theorized that retrieving episodic memories — memories about specific places and events — involves coordinated activity between the cerebral cortex and the hippocampus, a small structure deep in the brain.

"The theory is that learning involves processing in the cortex, and the hippocampus reproduces this pattern of activity during retrieval, allowing you to re-experience the event," Wiltgen said. If the hippocampus is damaged, patients can lose decades of memories.

But this model has been difficult to test directly, until the arrival of optogenetics.

Wiltgen and Tanaka used mice genetically modified so that when nerve cells are activated, they both fluoresce green and express a protein that allows the cells to be switched off by light. They were therefore able both to follow exactly which nerve cells in the cortex and hippocampus were activated in learning and memory retrieval, and switch them off with light directed through a fiber-optic cable.

They trained the mice by placing them in a cage where they got a mild electric shock. Normally, mice placed in a new environment will nose around and explore. But when placed in a cage where they have previously received a shock, they freeze in place in a “fear response.”

Tanaka and Wiltgen first showed that they could label the cells involved in learning and demonstrate that they were reactivated during memory recall. Then they were able to switch off the specific nerve cells in the hippocampus, and show that the mice lost their memories of the unpleasant event. They were also able to show that turning off other cells in the hippocampus did not affect retrieval of that memory, and to follow fibers from the hippocampus to specific cells in the cortex.

"The cortex can’t do it alone, it needs input from the hippocampus," Wiltgen said. "This has been a fundamental assumption in our field for a long time and Kazu’s data provides the first direct evidence that it is true."

They could also see how the specific cells in the cortex were connected to the amygdala, a structure in the brain that is involved in emotion and in generating the freezing response.

Filed under optogenetics memory hippocampus cerebral cortex nerve cells neuroscience science

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Mining big data yields Alzheimer’s discovery

Scientists at The University of Manchester have used a new way of working to identify a new gene linked to neurodegenerative diseases such as Alzheimer’s. The discovery fills in another piece of the jigsaw when it comes to identifying people most at risk of developing the condition.

image

Researcher David Ashbrook and colleagues from the UK and USA used two of the world’s largest collections of scientific data to compare the genes in mice and humans. Using brain scans from the ENIGMA Consortium and genetic information from The Mouse Brain Library, he was able to identify a novel gene, MGST3 that regulates the size of the hippocampus in both mouse and human, which is linked to a group of neurodegenerative diseases. The study has just been published in the journal BMC Genomics.

David, who works in Dr Reinmar Hager’s lab at the Faculty of Life Sciences, says: “There is already the ‘reserve hypothesis’ that a person with a bigger hippocampus will have more of it to lose before the symptoms of Alzheimer’s are spotted. By using ENIGMA to look at hippocampus size in humans and the corresponding genes and then matching those with genes in mice from the BXD system held in the Mouse Brain Library database we could identify this specific gene that influences neurological diseases.”

He continues: “Ultimately this could provide another biomarker in the toolkit for identifying those at greatest risk of developing diseases such as Alzheimer’s.”

Dr Hager, senior author of the study, says: “What is critical about this research is that we have not only been able to identify this specific gene but also the networks it uses to influence a disease like Alzheimer’s. We believe this information will be incredibly useful for future studies looking at treatments and preventative measures.”

The ENIGMA Consortium is led by Professor Paul Thompson based at the University of California, Los Angeles, and contains brain images and gene information from nearly 25,000 subjects. The Mouse Brain Library, established by Professor Robert Williams based at the University of Tennessee Health Science Center, contains data on over 10,000 brains and numerical data from just over 20,000 mice. 

David explains why combining the information held by both databases is so useful: “The key advantage of working this way is that it is much easier to identify a genetic variant in mice as they live in such controlled environments. By taking the information from mice and comparing it to human gene information we can identify the same variant much more quickly.”

And David thinks this way of working will be used more often in the future: “We are living in a big data world thanks to the likes of the Human Genome Project and post-genome technologies. A lot of that information is now widely shared so by mining what we already know we can learn so much more, advancing our knowledge of diseases and ultimately improving detection and treatment.”

(Source: manchester.ac.uk)

Filed under alzheimer's disease MGST3 hippocampus brain structure genomics genetics neuroscience science

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Sugar Linked to Memory Problems in Adolescent Rats

Studying rats as model subjects, scientists found that adolescents were at an increased risk of suffering negative health effects from sugar-sweetened beverage consumption.

Adolescent rats that freely consumed large quantities of liquid solutions containing sugar or high-fructose corn syrup (HFCS) in concentrations comparable to popular sugar-sweetened beverages experienced memory problems and brain inflammation, and became pre-diabetic, according to a new study from USC. Neither adult rats fed the sugary drinks nor adolescent rats who did not consume sugar had the same issues.

“The brain is especially vulnerable to dietary influences during critical periods of development, like adolescence,” said Scott Kanoski, corresponding author of the study and an assistant professor at the USC Dornsife College of Letters, Arts and Sciences.

Kanoski collaborated with USC’s Ted Hsu, Vaibhav Konanur, Lilly Taing, Ryan Usui, Brandon Kayser, and Michael Goran. Their study, which tested a total of 76 rats, was published online by the journal Hippocampus on Sept. 23.

About 35 to 40 percent of the rats’ caloric intake was from sugar or HFCS. For comparason, added sugars make up about 17 percent of the total caloric intake of teens in the U.S. on average, according to the CDC.

The rats were then tested in mazes that probe their spatial memory ability. Adolescent rats that had consumed the sugary beverages, particularly HFCS, performed worse on the test than any other group – which may be the result of the neuroinflammation detected in the hippocampus, Kanoski said.

The hippocampus is a part of the temporal lobe located deep within the brain that controls memory formation. People with Alzheimer’s Disease and other dementias often suffer damage to the hippocampus.

“Consuming a diet high in added sugars not only can lead to weight gain and metabolic disturbances, but can also negatively impact our neural functioning and cognitive ability.” Kanoski said. Next, Kanoski and his team plant to see how different monosaccharides (simple sugars) and HFCS affect the brain.

(Source: pressroom.usc.edu)

Filed under hippocampus memory sugar cognitive function adolescence neuroscience science

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(Image caption: 3D image of the hippocampus of a rat. Credit: M. Pyka) A glimpse into the 3D brain People who wish to know how memory works are forced to take a glimpse into the brain. They can now do so without bloodshed: RUB researchers have developed a new method for creating 3D models of memory-relevant brain structures. They published their results in the trade journal “Frontiers in Neuroanatomy”. Sea Horse gave the hippocampus the name The way neurons are interconnected in the brain is very complicated. This holds especially true for the cells of the hippocampus. It is one of the oldest brain regions and its form resembles a sea horse (hippocampus in Latin). The hippocampus enables us to navigate space securely and to form personal memories. So far, the anatomic knowledge of the networks inside the hippocampus and its connection to the rest of the brain has left scientists guessing which information arrived where and when. Signals spread through the brain Accordingly, Dr Martin Pyka and his colleagues from the Mercator Research Group have developed a method which facilitates the reconstruction of the brain’s anatomic data as a 3D model on the computer. This approach is quite unique, because it enables automatic calculation of the neural interconnection on the basis of their position inside the space and their projection directions. Biologically feasible network structures can thus be generated more easily than it used to be the case with the method available to date. Deploying 3D models, the researchers use this technique to monitor the way neural signals spread throughout the network time-wise. They have, for example, found evidence that the hippocampus’ form and size could explain why neurons in those networks fire in certain frequencies. Information become memories In future, this method may help us understand how animals, for example, combine various information to form memories within the hippocampus, in order to memorise food sources or dangers and to remember them in certain situations.

(Image caption: 3D image of the hippocampus of a rat. Credit: M. Pyka)

A glimpse into the 3D brain

People who wish to know how memory works are forced to take a glimpse into the brain. They can now do so without bloodshed: RUB researchers have developed a new method for creating 3D models of memory-relevant brain structures. They published their results in the trade journal “Frontiers in Neuroanatomy”.

Sea Horse gave the hippocampus the name

The way neurons are interconnected in the brain is very complicated. This holds especially true for the cells of the hippocampus. It is one of the oldest brain regions and its form resembles a sea horse (hippocampus in Latin). The hippocampus enables us to navigate space securely and to form personal memories. So far, the anatomic knowledge of the networks inside the hippocampus and its connection to the rest of the brain has left scientists guessing which information arrived where and when.

Signals spread through the brain

Accordingly, Dr Martin Pyka and his colleagues from the Mercator Research Group have developed a method which facilitates the reconstruction of the brain’s anatomic data as a 3D model on the computer. This approach is quite unique, because it enables automatic calculation of the neural interconnection on the basis of their position inside the space and their projection directions. Biologically feasible network structures can thus be generated more easily than it used to be the case with the method available to date. Deploying 3D models, the researchers use this technique to monitor the way neural signals spread throughout the network time-wise. They have, for example, found evidence that the hippocampus’ form and size could explain why neurons in those networks fire in certain frequencies.

Information become memories

In future, this method may help us understand how animals, for example, combine various information to form memories within the hippocampus, in order to memorise food sources or dangers and to remember them in certain situations.

Filed under 3d model hippocampus memory neurons brain structure neuroscience science

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