ScienceDaily (Feb. 27, 2009) — Advanced imaging reveals surprising effects on astrocyte signaling networks. The impact of the amyloid plaques that appear in the brains of patients with Alzheimer's disease may extend beyond the deposits' effects on neurons – the cells that transmit electrochemical signals throughout the nervous system.
In an article in the Feb. 27 issue of Science, researchers from the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND) report that amyloid plaques may also increase the activity of astrocytes, star-shaped nervous system cells traditionally considered to provide a supporting role in normal brain function. They also show that amyloid-induced astrocyte hyperactivity extends throughout the brain rather than being confined to regions directly adjacent to plaques.
"Our work suggests that amyloid plaques might have a more complex role in altering brain function than we had thought," says Kishore Kuchibhotla of MGH-MIND, lead author of the Science article. "Plaques develop rapidly and have been shown to cause relatively acute, localized neuro-toxicity.
We show that astrocytes could provide a network mechanism that may stretch the impact of plaques to more distant areas of the brain."
Astrocytes were long considered to provide passive support to neurons, but in the early 1990s it was discovered in cell culture that they also could transmit signals by means of transient increases in calcium levels that move from cell to cell in a wave-like manner. These calcium waves travel relatively long distances in response to a variety of external stimuli. Since astrocytes are so abundant – making up about half the volume of the brain – and found throughout the brain, the MGH investigators hypothesized that their function may also be affected by the presence of amyloid plaques.
Using cutting-edge imaging techniques that give a real-time view of the activity of brain cells in living mice, the investigators labeled astrocytes with a dye that lights up when a cell is active and shuts off when it is not. They were surprised to see astrocytes flicker on and off at much higher rates in transgenic mice with an abundance of plaques than in plaque-free animals. T
he plaque-associated astrocyte activity appeared to be synchronized and passed to distant areas of the brain in a wave-like fashion. Another imaging technology revealed that resting calcium levels were elevated throughout the astrocyte network of animals with plaques but not in normal mice.
Blocking the activity of neurons did not reduce astrocyte activity, indicating that amyloid's known impact on neuronal activity was not responsible for its apparent effects on astrocytes.
"This is the first clear evidence in a live animal model that amyloid plaques perturb calcium signaling across the astrocyte network via a neuron-independent mechanism," says Kuchibhotla. "It has been suggested that these intercellular calcium waves, which previously had been observed only in response to some sort of external stimulus, indicate the existence of or response to a traumatic insult. Our data support this hypothesis, but whether the calcium signals we observed actually protect or harm cells remains to be determined.
"We've only begun to scratch the surface of how plaque deposition impacts astrocyte function," he adds. "One key question will be how increased astrocyte signaling impacts neuronal function, and another will be whether astrocyte activity limits or intensifies plaque deposition."
Brian Bacskai, PhD, of MGH-MIND, senior author of the Science report, says, "This study not only provides insight into the role of astrocytic networks in the brain, it also suggests new opportunities to manipulate these networks to treat or prevent Alzheimer's disease as well as other neurological disorders. Further studies of pharmacological compounds that interact with astrocytes may someday lead to potential new therapies"
Kuchibhotla is a Harvard University doctoral candidate in Biophysics, working in Bacskai's laboratory. Additional co-authors of the paper are Carli Lattarulo and Bradley Hyman, MD, PhD, both of MGH MIND. The study was supported by grants from the National Institutes of Health.
Saturday, February 28, 2009
Friday, February 27, 2009
New Research In Alzheimer's Puzzle
ScienceDaily (Feb. 27, 2009) — Yale researchers have filled in a missing gap on the molecular road map of Alzheimer's disease.
In the Feb. 26 issue of the journal Nature, the Yale team reports that cellular prion proteins trigger the process by which amyloid-beta peptides block brain function in Alzheimer's patients.
"It has been a black box," said Stephen M. Strittmatter, senior author of the study and the Vincent Coates Professor of Neurology and director of Cellular Neuroscience, Neurodegeneration and Repair at the Yale School of Medicine. "We have known that amyloid-beta is bad for the brain, but we have not known exactly how amyloid-beta does bad things to neurons."
After an extensive gene expression analysis, the first step in amyloid-beta damage appears to involve cellular prion proteins. These proteins are normally harmless and exist within all cells, but on rare occasions they change shape and cause notorious prion diseases such as Creutzfeldt- Jacob disease, or its well-known variant, mad cow disease.
When the Yale team searched hundreds of thousands of candidates for potential disease-mediating receptors for the specific amyloid-beta form known to play a role in the development of Alzheimer's disease, the most likely candidate was cellular prion proteins. It seems that amyloid-beta peptides latch onto these cellular prion proteins and precipitate the damage in brain cells.
"They start the cascade that make neurons sick" said Strittmatter, a member of the Kavli Institute for Neuroscience.
Since these cellular prion proteins act at an early stage of disease development, the receptors make a promising target for new Alzheimer's therapies, Strittmatter said.
The study does not suggest that the conversion of cellular prion proteins to an infectious agent occurs in Alzheimer's disease, Strittmatter noted. However, the Nature paper does suggest that the role of usually harmless cellular prion proteins in common neurodegenerative diseases should be studied more rigorously, he said.
Other members of the Yale team included Juha Lauren, David A. Gimbel, Haakon B. Nygaard, and John W. Gilbert.
This work was supported by research grants from the Falk Medical Research Trust and the National Institutes of Health.
Adapted from materials provided by Yale University.
In the Feb. 26 issue of the journal Nature, the Yale team reports that cellular prion proteins trigger the process by which amyloid-beta peptides block brain function in Alzheimer's patients.
"It has been a black box," said Stephen M. Strittmatter, senior author of the study and the Vincent Coates Professor of Neurology and director of Cellular Neuroscience, Neurodegeneration and Repair at the Yale School of Medicine. "We have known that amyloid-beta is bad for the brain, but we have not known exactly how amyloid-beta does bad things to neurons."
After an extensive gene expression analysis, the first step in amyloid-beta damage appears to involve cellular prion proteins. These proteins are normally harmless and exist within all cells, but on rare occasions they change shape and cause notorious prion diseases such as Creutzfeldt- Jacob disease, or its well-known variant, mad cow disease.
When the Yale team searched hundreds of thousands of candidates for potential disease-mediating receptors for the specific amyloid-beta form known to play a role in the development of Alzheimer's disease, the most likely candidate was cellular prion proteins. It seems that amyloid-beta peptides latch onto these cellular prion proteins and precipitate the damage in brain cells.
"They start the cascade that make neurons sick" said Strittmatter, a member of the Kavli Institute for Neuroscience.
Since these cellular prion proteins act at an early stage of disease development, the receptors make a promising target for new Alzheimer's therapies, Strittmatter said.
The study does not suggest that the conversion of cellular prion proteins to an infectious agent occurs in Alzheimer's disease, Strittmatter noted. However, the Nature paper does suggest that the role of usually harmless cellular prion proteins in common neurodegenerative diseases should be studied more rigorously, he said.
Other members of the Yale team included Juha Lauren, David A. Gimbel, Haakon B. Nygaard, and John W. Gilbert.
This work was supported by research grants from the Falk Medical Research Trust and the National Institutes of Health.
Adapted from materials provided by Yale University.
Tuesday, February 24, 2009
How We Keep Visual Details In Short-Term Memory
ScienceDaily (Feb. 23, 2009) — Working memory (also known as short term memory) is our ability to keep a small amount of information active in our mind. This is useful for information we need to know on-the-fly, such as a phone number or the few items we need to pick up from the grocery store. We hang on to the information for a brief period of time, just long enough to make a phone call or get through the checkout line, and then we forget it forever.
People voluntarily pick what information they store in short-term memory. Now, using functional magnetic resonance imaging (fMRI), researchers can see just what information people are holding in memory based only on patterns of activity in the brain.
Psychologists from the University of Oregon and the University of California, San Diego, reported their findings in the February issue of Psychological Science. By analyzing blood-flow activity, they were able to identify the specific color or orientation of an object that was intentionally stored by the observer.
The experiments, in which subjects viewed a stimulus for one second and held a specific aspect of the object in mind after the stimulus disappeared, were conducted in the UO's Robert and Beverly Lewis Center for Neuroimaging. In 10-second delays after each exposure, researchers recorded brain activity during memory selection and storage processing in the visual cortex, a brain region that they hypothesized would support the maintenance of visual details in short-term memory.
"Another interesting thing was that if subjects were remembering orientation, then that pattern of activity during the delay period had no information about color, even though they were staring at a colored-oriented stimulus," said Edward Awh, a UO professor of psychology. "Likewise, if they chose to remember color we were able to decode which color they remembered, but orientation information was completely missing."
Researchers used machine-learning algorithms to examine spatial patterns of activation in the early visual cortex that are associated with remembering different stimuli, said John T. Serences, professor of psychology at UC-San Diego. "This algorithm," he said, "can then be used to predict exactly what someone is remembering based on these activation patterns."
Increases in blood flow, as seen with fMRI, are measured in voxels -- small units displayed in a 3-D grid. Different vectors of the grid, corresponding to neurons, respond as subjects view and store their chosen memories. Based on patterns of activity in an individual's visual cortex, located at the rear of the brain, researchers can pinpoint what is being stored and where, Awh said.
The study is similar to one published this month in Nature and led by Vanderbilt University neuroscientist Frank Tong and colleagues, who were able to predict with 80-percent-plus accuracy which patterns individuals held in memory 11 seconds after seeing a stimulus.
"Their paper makes a very similar point to ours," Awh said, "though they did not vary which 'dimension' of the stimulus people chose to remember, and they did not compare the pattern of activity during sensory processing and during memory. They showed that they could look at brain activity to classify which orientation was being stored in memory."
What Awh and colleagues found was that the sensory area of the brain had a pattern of activity that represented only an individual's intentionally stored aspect of the stimulus. This voluntary control in memory selection, Awh said, falls in line with previous research, including that done by Awh and co-author Edward K. Vogel, also of the UO, that there is limited capacity for what can be stored at one time.
People choose what is important and relevant to them, Awh said.
"Basically, our study shows that information about the precise feature a person is remembering is represented in the visual cortex," Serences said, "This is important because it demonstrates that people recruit the same neural machinery during memory as they do when they see a stimulus."
That demonstration, Awh said, supports the sensory recruitment hypothesis, which suggests the same parts of the brain are involved in perception of a stimulus and memory storage.
A fourth co-author with Awh, Serences and Vogel was Edward F. Ester, a UO doctoral student. Serences was with the University of California, Irvine, when the project began. The research was primarily funded by a grant from the National Institutes of Health to Awh, and by support from the UO's Robert and Beverly Lewis Center for Neuroimaging
People voluntarily pick what information they store in short-term memory. Now, using functional magnetic resonance imaging (fMRI), researchers can see just what information people are holding in memory based only on patterns of activity in the brain.
Psychologists from the University of Oregon and the University of California, San Diego, reported their findings in the February issue of Psychological Science. By analyzing blood-flow activity, they were able to identify the specific color or orientation of an object that was intentionally stored by the observer.
The experiments, in which subjects viewed a stimulus for one second and held a specific aspect of the object in mind after the stimulus disappeared, were conducted in the UO's Robert and Beverly Lewis Center for Neuroimaging. In 10-second delays after each exposure, researchers recorded brain activity during memory selection and storage processing in the visual cortex, a brain region that they hypothesized would support the maintenance of visual details in short-term memory.
"Another interesting thing was that if subjects were remembering orientation, then that pattern of activity during the delay period had no information about color, even though they were staring at a colored-oriented stimulus," said Edward Awh, a UO professor of psychology. "Likewise, if they chose to remember color we were able to decode which color they remembered, but orientation information was completely missing."
Researchers used machine-learning algorithms to examine spatial patterns of activation in the early visual cortex that are associated with remembering different stimuli, said John T. Serences, professor of psychology at UC-San Diego. "This algorithm," he said, "can then be used to predict exactly what someone is remembering based on these activation patterns."
Increases in blood flow, as seen with fMRI, are measured in voxels -- small units displayed in a 3-D grid. Different vectors of the grid, corresponding to neurons, respond as subjects view and store their chosen memories. Based on patterns of activity in an individual's visual cortex, located at the rear of the brain, researchers can pinpoint what is being stored and where, Awh said.
The study is similar to one published this month in Nature and led by Vanderbilt University neuroscientist Frank Tong and colleagues, who were able to predict with 80-percent-plus accuracy which patterns individuals held in memory 11 seconds after seeing a stimulus.
"Their paper makes a very similar point to ours," Awh said, "though they did not vary which 'dimension' of the stimulus people chose to remember, and they did not compare the pattern of activity during sensory processing and during memory. They showed that they could look at brain activity to classify which orientation was being stored in memory."
What Awh and colleagues found was that the sensory area of the brain had a pattern of activity that represented only an individual's intentionally stored aspect of the stimulus. This voluntary control in memory selection, Awh said, falls in line with previous research, including that done by Awh and co-author Edward K. Vogel, also of the UO, that there is limited capacity for what can be stored at one time.
People choose what is important and relevant to them, Awh said.
"Basically, our study shows that information about the precise feature a person is remembering is represented in the visual cortex," Serences said, "This is important because it demonstrates that people recruit the same neural machinery during memory as they do when they see a stimulus."
That demonstration, Awh said, supports the sensory recruitment hypothesis, which suggests the same parts of the brain are involved in perception of a stimulus and memory storage.
A fourth co-author with Awh, Serences and Vogel was Edward F. Ester, a UO doctoral student. Serences was with the University of California, Irvine, when the project began. The research was primarily funded by a grant from the National Institutes of Health to Awh, and by support from the UO's Robert and Beverly Lewis Center for Neuroimaging
Saturday, February 21, 2009
Revolutionary New Model For Alzheimer's Disease
ScienceDaily (Feb. 20, 2009) — A study from the Buck Institute for Age Research offers a revolutionary new model for Alzheimer’s disease (AD), a devastating neurodegenerative disorder which afflicts 24 million people worldwide.
In an effort to unravel the normal function of a protein implicated in AD, scientists in California and France have discovered a naturally occurring protein that provides a new therapeutic target for the disease.
The finding upsets the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain – this research points to the condition as a disorder involving an imbalance in signaling between neurons. The study appears online in the Nature publication Cell Death and Differentiation.
One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) which are concentrated at the points where neurons connect. Even though the sticky amyloid plaques which have been viewed as a hallmark sign of AD result from APP, it seems unlikely that APP exists simply to cause Alzheimer’s disease.
In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced.
These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections -- both by binding to APP and activating normal cell programs. Not only did the netrin-1 binding to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.
“I think we’re going to see an explosion in the next five years involving the dissection of these signaling pathways whose imbalance leads to Alzheimer’s disease,” said Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research. “We now believe that APP is part of a ‘plasticity module’ that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance.”
“We believe that Alzheimer’s disease is somewhat analogous to cancer, which results from an imbalance between the normal processes that support cell survival and those that cause cell turnover,” said Patrick Mehlen, PhD, Director of the Apoptosis, Cancer and Development CNRS Laboratory at the University of Lyon and co-senior author of the study.
“Our hope is that this research will lead to therapeutics that will be used to address this imbalance much earlier in the disease process.”
Research is underway to develop a drug based on the findings. The Buck Institute and the CNRS in Lyon are partnering with Neurobiological Technologies Inc., to bring the discovery from the laboratory to clinical trials.
Other researchers involved in the study include first author Filipe Calheiros Lourenço, of the University of Lyon, along with co-workers Joanna Fombonne, Véronique Corset and Fabien Llambi; Verónica Galvan of the Buck Institute, and Ulrike Müller of the University of Heidelberg. The work was supported by the Agence Nationale de la Recherche, the CNRS (Centre Nationale de la Recherche Scientifique), the National Institutes of Health, the Joseph Drown Foundation, the John Douglas French Foundation, and the Alzheimer’s Association
In an effort to unravel the normal function of a protein implicated in AD, scientists in California and France have discovered a naturally occurring protein that provides a new therapeutic target for the disease.
The finding upsets the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain – this research points to the condition as a disorder involving an imbalance in signaling between neurons. The study appears online in the Nature publication Cell Death and Differentiation.
One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) which are concentrated at the points where neurons connect. Even though the sticky amyloid plaques which have been viewed as a hallmark sign of AD result from APP, it seems unlikely that APP exists simply to cause Alzheimer’s disease.
In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced.
These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections -- both by binding to APP and activating normal cell programs. Not only did the netrin-1 binding to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.
“I think we’re going to see an explosion in the next five years involving the dissection of these signaling pathways whose imbalance leads to Alzheimer’s disease,” said Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research. “We now believe that APP is part of a ‘plasticity module’ that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance.”
“We believe that Alzheimer’s disease is somewhat analogous to cancer, which results from an imbalance between the normal processes that support cell survival and those that cause cell turnover,” said Patrick Mehlen, PhD, Director of the Apoptosis, Cancer and Development CNRS Laboratory at the University of Lyon and co-senior author of the study.
“Our hope is that this research will lead to therapeutics that will be used to address this imbalance much earlier in the disease process.”
Research is underway to develop a drug based on the findings. The Buck Institute and the CNRS in Lyon are partnering with Neurobiological Technologies Inc., to bring the discovery from the laboratory to clinical trials.
Other researchers involved in the study include first author Filipe Calheiros Lourenço, of the University of Lyon, along with co-workers Joanna Fombonne, Véronique Corset and Fabien Llambi; Verónica Galvan of the Buck Institute, and Ulrike Müller of the University of Heidelberg. The work was supported by the Agence Nationale de la Recherche, the CNRS (Centre Nationale de la Recherche Scientifique), the National Institutes of Health, the Joseph Drown Foundation, the John Douglas French Foundation, and the Alzheimer’s Association
Thursday, February 19, 2009
Can Exercising Your Brain Prevent Memory Loss?
ScienceDaily (Feb. 18, 2009) — Participating in certain mental activities, like reading magazines or crafting in middle age or later in life, may delay or prevent memory loss, according to a study released February 17 that will be presented at the American Academy of Neurology's 61st Annual Meeting in Seattle, April 25 to May 2, 2009.
The study involved 197 people between the ages of 70 and 89 with mild cognitive impairment, or diagnosed memory loss, and 1,124 people that age with no memory problems. Both groups answered questions about their daily activities within the past year and in middle age, when they were between 50 to 65 years old.
The study found that during later years, reading books, playing games, participating in computer activities and doing craft activities such as pottery or quilting led to a 30 to 50 percent decrease in the risk of developing memory loss compared to people who did not do those activities. People who watched television for less than seven hours a day in later years were 50 percent less likely to develop memory loss than people who watched for more than seven hours a day.
People who participated in social activities and read magazines during middle age were about 40 percent less likely to develop memory loss than those who did not do those activities.
"This study is exciting because it demonstrates that aging does not need to be a passive process. By simply engaging in cognitive exercise, you can protect against future memory loss," said study author Yonas Geda, MD, MSc, a neuropsychiatrist at Mayo Clinic in Rochester, MN, and a member of the American Academy of Neurology. "Of course, the challenge with this type of research is that we are relying on past memories of the participants, therefore, we need to confirm these findings with additional research."
The study was supported by the National Institutes of Health, Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program and the Robert Wood Johnson Foundation.
The study involved 197 people between the ages of 70 and 89 with mild cognitive impairment, or diagnosed memory loss, and 1,124 people that age with no memory problems. Both groups answered questions about their daily activities within the past year and in middle age, when they were between 50 to 65 years old.
The study found that during later years, reading books, playing games, participating in computer activities and doing craft activities such as pottery or quilting led to a 30 to 50 percent decrease in the risk of developing memory loss compared to people who did not do those activities. People who watched television for less than seven hours a day in later years were 50 percent less likely to develop memory loss than people who watched for more than seven hours a day.
People who participated in social activities and read magazines during middle age were about 40 percent less likely to develop memory loss than those who did not do those activities.
"This study is exciting because it demonstrates that aging does not need to be a passive process. By simply engaging in cognitive exercise, you can protect against future memory loss," said study author Yonas Geda, MD, MSc, a neuropsychiatrist at Mayo Clinic in Rochester, MN, and a member of the American Academy of Neurology. "Of course, the challenge with this type of research is that we are relying on past memories of the participants, therefore, we need to confirm these findings with additional research."
The study was supported by the National Institutes of Health, Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program and the Robert Wood Johnson Foundation.
Wednesday, February 18, 2009
Maintaining Balance And Listening At The Same Time May Become More Difficult For Older Adults
ScienceDaily (Feb. 17, 2009) — Listening to a conversation or audio book while walking or exercising sounds simple enough for most people, but it may become more difficult for people in their upper 70s and above, according to new research from the University of Pittsburgh Medical Center.
Supported by the National Institute on Deafness and Other Communication Disorders, one of the National Institutes of Health, the scientists are presenting their findings at the 2009 Midwinter Meeting of the Association for Research in Otolaryngology in Baltimore.
Researchers evaluated how well three groups of adults -- healthy young (ages 24-27), old (ages 65-71), and "old-old" (ages 76-82 years) -- were able to conduct a listening exercise while their visual and balance systems were kept busy. Seated in swivel chairs that were either upright or at a 30-degree tilt, the volunteers performed two listening-related tasks while motionless or spinning in darkness or in light. In one task, they listened to a high- or low-pitch tone and pressed a button in their right or left hand depending on the pitch.
In the second task, volunteers listened to tones in their right or left ears and pressed the corresponding button.
The researchers found that, in general, all age groups reacted more slowly to the audio cues when spinning than when motionless. However, this was especially true for people in the oldest age group. They also found that stimulation of the ear's gravity-sensing organs – through the 30-degree tilt of the chair -- was especially powerful in slowing down a person's auditory reaction time. Again, this effect was most pronounced for people in the oldest age group.
The National Institute on Aging also supported this research.
Supported by the National Institute on Deafness and Other Communication Disorders, one of the National Institutes of Health, the scientists are presenting their findings at the 2009 Midwinter Meeting of the Association for Research in Otolaryngology in Baltimore.
Researchers evaluated how well three groups of adults -- healthy young (ages 24-27), old (ages 65-71), and "old-old" (ages 76-82 years) -- were able to conduct a listening exercise while their visual and balance systems were kept busy. Seated in swivel chairs that were either upright or at a 30-degree tilt, the volunteers performed two listening-related tasks while motionless or spinning in darkness or in light. In one task, they listened to a high- or low-pitch tone and pressed a button in their right or left hand depending on the pitch.
In the second task, volunteers listened to tones in their right or left ears and pressed the corresponding button.
The researchers found that, in general, all age groups reacted more slowly to the audio cues when spinning than when motionless. However, this was especially true for people in the oldest age group. They also found that stimulation of the ear's gravity-sensing organs – through the 30-degree tilt of the chair -- was especially powerful in slowing down a person's auditory reaction time. Again, this effect was most pronounced for people in the oldest age group.
The National Institute on Aging also supported this research.
Loneliness Affects How the Brain Operates
ScienceDaily (Feb. 17, 2009) — Social isolation affects how people behave as well as how their brains operate, a study at the University of Chicago shows.
The research, presented February 15 at a symposium, "Social Emotion and the Brain," at the annual meeting of the American Association for the Advancement of Science, is the first to use fMRI scans to study the connections between perceived social isolation (or loneliness) and activity in the brain. Combining fMRI scans with data relevant to social behavior is part of an emerging field examining brain mechanisms—an approach to psychology being pioneered at the University of Chicago.
Researchers found that the ventral striatum—a region of the brain associated with rewards—is much more activated in non-lonely people than in the lonely when they view pictures of people in pleasant settings. In contrast, the temporoparietal junction—a region associated with taking the perspective of another person—is much less activated among lonely than in the non-lonely when viewing pictures of people in unpleasant settings.
"Given their feelings of social isolation, lonely individuals may be left to find relative comfort in nonsocial rewards," said John Cacioppo, the Tiffany and Margaret Blake Professor in Psychology at the University. He spoke at the briefing along with Jean Decety, the Irving B. Harris Professor in Psychology and Psychiatry at the University.
The ventral striatum, which is critical to learning, is a key portion of the brain and is activated through primary rewards such as food and secondary rewards such as money. Social rewards and feelings of love also may activate the region.
Cacioppo, one of the nation's leading scholars on loneliness, has shown that loneliness undermines health and can be as detrimental as smoking. About one in five Americans experience loneliness, he said. Decety is one of the nation's leading researchers to use fMRI scans to explore empathy.
They were among five co-authors of a paper, "In the Eye of the Beholder: Individual Differences in Perceived Social Isolation Predict Regional Brain Activation to Social Stimuli," published in the current issue of the Journal of Cognitive Neuroscience.
In the study, 23 female undergraduates were tested to determine their level of loneliness. While in an fMRI scanner, the subjects were shown unpleasant pictures and human conflict as well as pleasant things such as money and happy people.
The subjects who rated as lonely were least likely to have strong activity in their ventral striata when shown pictures of people enjoying themselves.
Although loneliness may be influence brain activity, the research also suggests that activity in the ventral striatum may prompt feelings of loneliness, Decety said. "The study raises the intriguing possibility that loneliness may result from reduced reward-related activity in the ventral striatum in response to social rewards."
In addition to differing responses in the ventral striatum, the subjects also recorded differing responses in parts of the brain that indicated loneliness played a role in how their brain operates.
Joining Decety and Cacioppo in writing the Journal of Cognitive Science paper were Catherine Norris, Assistant Professor of Psychology at Dartmouth College; George Monteleone, a graduate student at the University of Chicago; and Howard Nusbaum, Chair of Psychology at the University of Chicago.
Decety and Cacioppo discussed the new field of brain mechanism in a paper in the current issue of Perspectives on Psychological Science. The new field extends the work of Charles Darwin, who "regarded the brain as a product of evolution and the science of psychology as concerned with these foundations," they wrote.
By studying brain mechanisms, researchers hope to gain new insights by examining mental activities surrounding consciousness, perception and thought through an understanding of how columns of neurons stacked next to each other form elementary circuits to function as a unit, they wrote.
New visualization tools such as three-dimensional imaging will help scholars develop a new way of studying psychology, they said.
"Psychological science in the 21st century can, and should, become not only the science of overt behavior, and not only the science of the mind, but also the science of the brain," they concluded.
The research, presented February 15 at a symposium, "Social Emotion and the Brain," at the annual meeting of the American Association for the Advancement of Science, is the first to use fMRI scans to study the connections between perceived social isolation (or loneliness) and activity in the brain. Combining fMRI scans with data relevant to social behavior is part of an emerging field examining brain mechanisms—an approach to psychology being pioneered at the University of Chicago.
Researchers found that the ventral striatum—a region of the brain associated with rewards—is much more activated in non-lonely people than in the lonely when they view pictures of people in pleasant settings. In contrast, the temporoparietal junction—a region associated with taking the perspective of another person—is much less activated among lonely than in the non-lonely when viewing pictures of people in unpleasant settings.
"Given their feelings of social isolation, lonely individuals may be left to find relative comfort in nonsocial rewards," said John Cacioppo, the Tiffany and Margaret Blake Professor in Psychology at the University. He spoke at the briefing along with Jean Decety, the Irving B. Harris Professor in Psychology and Psychiatry at the University.
The ventral striatum, which is critical to learning, is a key portion of the brain and is activated through primary rewards such as food and secondary rewards such as money. Social rewards and feelings of love also may activate the region.
Cacioppo, one of the nation's leading scholars on loneliness, has shown that loneliness undermines health and can be as detrimental as smoking. About one in five Americans experience loneliness, he said. Decety is one of the nation's leading researchers to use fMRI scans to explore empathy.
They were among five co-authors of a paper, "In the Eye of the Beholder: Individual Differences in Perceived Social Isolation Predict Regional Brain Activation to Social Stimuli," published in the current issue of the Journal of Cognitive Neuroscience.
In the study, 23 female undergraduates were tested to determine their level of loneliness. While in an fMRI scanner, the subjects were shown unpleasant pictures and human conflict as well as pleasant things such as money and happy people.
The subjects who rated as lonely were least likely to have strong activity in their ventral striata when shown pictures of people enjoying themselves.
Although loneliness may be influence brain activity, the research also suggests that activity in the ventral striatum may prompt feelings of loneliness, Decety said. "The study raises the intriguing possibility that loneliness may result from reduced reward-related activity in the ventral striatum in response to social rewards."
In addition to differing responses in the ventral striatum, the subjects also recorded differing responses in parts of the brain that indicated loneliness played a role in how their brain operates.
Joining Decety and Cacioppo in writing the Journal of Cognitive Science paper were Catherine Norris, Assistant Professor of Psychology at Dartmouth College; George Monteleone, a graduate student at the University of Chicago; and Howard Nusbaum, Chair of Psychology at the University of Chicago.
Decety and Cacioppo discussed the new field of brain mechanism in a paper in the current issue of Perspectives on Psychological Science. The new field extends the work of Charles Darwin, who "regarded the brain as a product of evolution and the science of psychology as concerned with these foundations," they wrote.
By studying brain mechanisms, researchers hope to gain new insights by examining mental activities surrounding consciousness, perception and thought through an understanding of how columns of neurons stacked next to each other form elementary circuits to function as a unit, they wrote.
New visualization tools such as three-dimensional imaging will help scholars develop a new way of studying psychology, they said.
"Psychological science in the 21st century can, and should, become not only the science of overt behavior, and not only the science of the mind, but also the science of the brain," they concluded.
Thursday, February 12, 2009
Improving Brain Processing Speed Helps Memory
ScienceDaily (Feb. 11, 2009) — Mayo Clinic researchers found that healthy, older adults who participated in a computer-based training program to improve the speed and accuracy of brain processing showed twice the improvement in certain aspects of memory, compared to a control group.
"What's unique in this study is that brain-processing activities seemed to help aspects of memory that were not directly exercised by the program -- a new finding in memory research," says Glenn Smith, Ph.D., Mayo Clinic neuropsychologist and lead researcher on the study.
The research, a controlled, multisite, double-blind study, will be published in the April issue of the Journal of the American Geriatrics Society. A copy is available online Feb. 9, 2009.
For an hour a day, five days a week for eight weeks, study participants worked on computer-based activities in their homes. The participants, from Minnesota and California, were age 65 or older. No one had a diagnosis of cognitive impairment, such as early Alzheimer's disease.
The control group, with 245 adults, watched educational videos on art, history and literature topics. They completed quizzes on the content.
The experimental therapy group, with 242 adults, completed six auditory exercises designed to help the brain improve the speed and accuracy of processing. For example, participants were asked to distinguish between high- and low-pitched sounds. To start, the sounds were slow and distinct. Gradually, the speed increased and separation disappeared.
"The sounds go faster and faster, until it ends up sounding almost like a click," says Dr. Smith. The difficulty increases only as participants master each step with 85 percent accuracy. Other exercises, such as matching or distinguishing between similar-sounding words, for example, pop and pot, also were part of the skill building.
The commercially available program was developed by Posit Science, San Francisco company that financed the research. Mayo Clinic researchers do not have financial ties to this business.
At the end of eight weeks, researchers used a standardized tool to measure participants' memory changes. Called the Repeatable Battery for the Assessment of Neuropsychological Status, it includes tasks such as repeating words or numbers after hearing them once.
"We found that the improvement in these skills was significantly greater in the experimental group -- about double," says Dr. Smith.
Participants in the experimental group self-reported memory improvement, too, indicating the change was noticeable in day-to-day tasks.
While the study results are statistically significant, Dr. Smith says it is important to understand the extent of the memory boost. Collectively, the experimental group's memory function increased about 4 percent over the baseline measured at the study's onset. The control group's overall memory gain was about 2 percent.
But, Dr. Smith says, because participants were in generally good health, the results don't offer insights on preventing Alzheimer's or other forms of dementia.
Results indicate that aging adults may be able to make better-informed decisions about ways to improve memory. "Brain processing speed slows as we age," says Dr. Smith. "The study indicates that choosing a memory-enhancing approach that focuses on improving brain processing speed and accuracy, rather than memory retention, may be helpful."
There's no harm in trying other approaches -- mnemonics, workshops or even doing crosswords or playing piano, he says, but there's little evidence these methods sustain benefits in memory.
Other researchers involved in this study include: Patricia Housen, Ph.D., and Elizabeth Zelinski, Ph.D., both with Leonard Davis School of Gerontology, University of Southern California, Los Angeles; Kristine Yaffe, M.D., University of California, San Francisco; Ronald Ruff, Ph.D., Stanford University, Stanford, Calif.; Robert Kennison, Ph.D., California State University, Los Angeles; and Henry Mahncke, Ph.D., Posit Science Corporation, San Francisco. His affiliation with this company is noted in the journal article.
"What's unique in this study is that brain-processing activities seemed to help aspects of memory that were not directly exercised by the program -- a new finding in memory research," says Glenn Smith, Ph.D., Mayo Clinic neuropsychologist and lead researcher on the study.
The research, a controlled, multisite, double-blind study, will be published in the April issue of the Journal of the American Geriatrics Society. A copy is available online Feb. 9, 2009.
For an hour a day, five days a week for eight weeks, study participants worked on computer-based activities in their homes. The participants, from Minnesota and California, were age 65 or older. No one had a diagnosis of cognitive impairment, such as early Alzheimer's disease.
The control group, with 245 adults, watched educational videos on art, history and literature topics. They completed quizzes on the content.
The experimental therapy group, with 242 adults, completed six auditory exercises designed to help the brain improve the speed and accuracy of processing. For example, participants were asked to distinguish between high- and low-pitched sounds. To start, the sounds were slow and distinct. Gradually, the speed increased and separation disappeared.
"The sounds go faster and faster, until it ends up sounding almost like a click," says Dr. Smith. The difficulty increases only as participants master each step with 85 percent accuracy. Other exercises, such as matching or distinguishing between similar-sounding words, for example, pop and pot, also were part of the skill building.
The commercially available program was developed by Posit Science, San Francisco company that financed the research. Mayo Clinic researchers do not have financial ties to this business.
At the end of eight weeks, researchers used a standardized tool to measure participants' memory changes. Called the Repeatable Battery for the Assessment of Neuropsychological Status, it includes tasks such as repeating words or numbers after hearing them once.
"We found that the improvement in these skills was significantly greater in the experimental group -- about double," says Dr. Smith.
Participants in the experimental group self-reported memory improvement, too, indicating the change was noticeable in day-to-day tasks.
While the study results are statistically significant, Dr. Smith says it is important to understand the extent of the memory boost. Collectively, the experimental group's memory function increased about 4 percent over the baseline measured at the study's onset. The control group's overall memory gain was about 2 percent.
But, Dr. Smith says, because participants were in generally good health, the results don't offer insights on preventing Alzheimer's or other forms of dementia.
Results indicate that aging adults may be able to make better-informed decisions about ways to improve memory. "Brain processing speed slows as we age," says Dr. Smith. "The study indicates that choosing a memory-enhancing approach that focuses on improving brain processing speed and accuracy, rather than memory retention, may be helpful."
There's no harm in trying other approaches -- mnemonics, workshops or even doing crosswords or playing piano, he says, but there's little evidence these methods sustain benefits in memory.
Other researchers involved in this study include: Patricia Housen, Ph.D., and Elizabeth Zelinski, Ph.D., both with Leonard Davis School of Gerontology, University of Southern California, Los Angeles; Kristine Yaffe, M.D., University of California, San Francisco; Ronald Ruff, Ph.D., Stanford University, Stanford, Calif.; Robert Kennison, Ph.D., California State University, Los Angeles; and Henry Mahncke, Ph.D., Posit Science Corporation, San Francisco. His affiliation with this company is noted in the journal article.
Monday, February 9, 2009
Education May Not Affect How Fast You Will Lose Your Memory
ScienceDaily (Feb. 6, 2009) — While a higher level of education may help lower the risk of Alzheimer's disease, new research shows that once educated people start to become forgetful, a higher level of education does not appear to protect against how fast they will lose their memory.
The research is published in the February 3, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.
In the study, scientists tested the thinking skills of 6,500 people with an average age of 72 from the Chicago area with different levels of education. The education level of people in the study ranged from eight years of school or fewer to 16 or more years of schooling. Interviews and tests about memory and thinking functions were given every three years for an average of 6.5 years.
At the beginning of the study, those with more education had better memory and thinking skills than those with less education. However, education was not related to how rapidly these skills declined during the course of the study.
The study found that results remained the same regardless of other factors related to education such as occupation and race and the effects of practice with the tests.
"This is an interesting and important finding because scientists have long debated whether aging and memory loss tend to have a lesser affect on highly educated people. While education is associated with the memory's ability to function at a higher level, we found no link between higher education and how fast the memory loses that ability," says study author Robert S. Wilson, PhD, with the Alzheimer's Disease Center at Rush University Medical Center in Chicago.
The study was supported by the National Institute on Aging and by the National Institute of Environmental Health Sciences.
The research is published in the February 3, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.
In the study, scientists tested the thinking skills of 6,500 people with an average age of 72 from the Chicago area with different levels of education. The education level of people in the study ranged from eight years of school or fewer to 16 or more years of schooling. Interviews and tests about memory and thinking functions were given every three years for an average of 6.5 years.
At the beginning of the study, those with more education had better memory and thinking skills than those with less education. However, education was not related to how rapidly these skills declined during the course of the study.
The study found that results remained the same regardless of other factors related to education such as occupation and race and the effects of practice with the tests.
"This is an interesting and important finding because scientists have long debated whether aging and memory loss tend to have a lesser affect on highly educated people. While education is associated with the memory's ability to function at a higher level, we found no link between higher education and how fast the memory loses that ability," says study author Robert S. Wilson, PhD, with the Alzheimer's Disease Center at Rush University Medical Center in Chicago.
The study was supported by the National Institute on Aging and by the National Institute of Environmental Health Sciences.
Heart Failure Linked To Cognitive Impairment
ScienceDaily (Feb. 7, 2009) — Nearly half of patients with heart failure (HF) have problems with memory and other aspects of cognitive functioning, reports a new study published in the February issue of Journal of Cardiac Failure.
Memory problems and other cognitive deficits may be an important factor to consider in planning medical care for patients with HF, according to the new study, led by Mary Jane Sauvé, D.N.Sc., R.N., of the University of California, Davis.
The researchers administered tests of cognitive (intellectual) function to 50 patients with HF and 50 people without HF, matched for age and estimated intelligence. Most of the patients had mild to moderate HF. Overall, patients with HF scored lower than controls on 14 of 19 cognitive tests. Forty-six percent of the HF patients were rated as having mild to severe cognitive impairment, compared to a 16 percent rate of mild impairment in controls.
Memory problems, especially short-term memory, were the most common type of cognitive deficit.
With adjustment for other factors, the risk of cognitive impairment was more than four times higher in the HF group. The rate, types, and severity of cognitive impairment in this group of patients living with HF were similar to those seen in patients with end-stage HF awaiting heart transplantation.
Changes in cognitive function have long been recognized in patients with heart disease. Although past reports have noticed an increased rate of cognitive impairment among people with HF, this has been assumed to reflect the age-related risk of cognitive decline.
These findings may have important implications for the care of patients with HF, Dr. Sauvé and colleagues believe. For example, "Care instructions and medication or dietary changes need to be written and given verbally because of patient difficulties with information requiring attention, learning, and memory functions."
"This is a very important article dealing with a neglected area of research," commented Barry M. Massie, M.D., Editor-in-Chief of the Journal of Cardiac Failure. "The authors have performed a well-designed study assessing heart failure patients for cognitive impairment, which was significant in a substantial proportion of patients. Furthermore, it was closely related to the severity of symptoms or left ventricular dysfunction. Clinicians should be aware of this problem, as it has the potential to interfere with optimal patient management."
Memory problems and other cognitive deficits may be an important factor to consider in planning medical care for patients with HF, according to the new study, led by Mary Jane Sauvé, D.N.Sc., R.N., of the University of California, Davis.
The researchers administered tests of cognitive (intellectual) function to 50 patients with HF and 50 people without HF, matched for age and estimated intelligence. Most of the patients had mild to moderate HF. Overall, patients with HF scored lower than controls on 14 of 19 cognitive tests. Forty-six percent of the HF patients were rated as having mild to severe cognitive impairment, compared to a 16 percent rate of mild impairment in controls.
Memory problems, especially short-term memory, were the most common type of cognitive deficit.
With adjustment for other factors, the risk of cognitive impairment was more than four times higher in the HF group. The rate, types, and severity of cognitive impairment in this group of patients living with HF were similar to those seen in patients with end-stage HF awaiting heart transplantation.
Changes in cognitive function have long been recognized in patients with heart disease. Although past reports have noticed an increased rate of cognitive impairment among people with HF, this has been assumed to reflect the age-related risk of cognitive decline.
These findings may have important implications for the care of patients with HF, Dr. Sauvé and colleagues believe. For example, "Care instructions and medication or dietary changes need to be written and given verbally because of patient difficulties with information requiring attention, learning, and memory functions."
"This is a very important article dealing with a neglected area of research," commented Barry M. Massie, M.D., Editor-in-Chief of the Journal of Cardiac Failure. "The authors have performed a well-designed study assessing heart failure patients for cognitive impairment, which was significant in a substantial proportion of patients. Furthermore, it was closely related to the severity of symptoms or left ventricular dysfunction. Clinicians should be aware of this problem, as it has the potential to interfere with optimal patient management."
Monday, February 2, 2009
Imaging Studies Illustrate How Memories Change Over Time In The Brain
ScienceDaily (Jan. 31, 2009) — A new brain imaging study illustrates what happens to memories as time goes by. The study, in the January 28 issue of The Journal of Neuroscience, shows that distinct brain structures are involved in recalling recent and older events.
Ffindings support earlier studies of memory-impaired patients with damage limited to the hippocampus. These patients show deficits in learning new information and in recalling events that occurred just prior to their injuries. However, they are able to recall older events, which are thought to involve other regions of the brain, particularly the cortex.
"It has long been known that older memories are more resistant to hippocampal damage than newer memories, and this was thought to reflect the fact that the hippocampus becomes less involved in remembering as a memory gets older," said Russell Poldrack, PhD, an expert on the cognitive and neural mechanisms of memory at the University of California, Los Angeles, who was not involved in the study. "However, there has been a recent debate over whether the hippocampus ever really stops being involved, even for older memories," Poldrack said.
To address this debate, Christine Smith, PhD, and Larry Squire, PhD, at the University of California, San Diego and the San Diego VA Medical Center, imaged study participants as they answered 160 questions about news events that occurred over the past 30 years. The hippocampus and related brain structures were most active when recalling recent events. Hippocampal activity gradually declined as participants recalled events that were 1-12 years old and remained low when they recalled events that were 13-30 years old.
In contrast, Smith and Squire found the opposite pattern of activity in frontal, temporal, and parietal cortices. In these brain regions — which are located at the surface of the brain — activity increased with the age of the news event recalled. "Our findings support the idea that these cortical regions are the ultimate repositories for long-term memory," Smith said. The researchers found that brain activity was unrelated to the richness of memories or to the recollection of personal events related to the tested news events.
"This is the best evidence to date supporting a long-held view about how memories become permanent," said Howard Eichenbaum, PhD, an expert on memory at Boston University who was unaffiliated with the study.
The research was supported by the U.S. Department of Veterans Affairs, National Institute of Mental Health, the Metropolitan Life Foundation, and the National Institute on Aging
Ffindings support earlier studies of memory-impaired patients with damage limited to the hippocampus. These patients show deficits in learning new information and in recalling events that occurred just prior to their injuries. However, they are able to recall older events, which are thought to involve other regions of the brain, particularly the cortex.
"It has long been known that older memories are more resistant to hippocampal damage than newer memories, and this was thought to reflect the fact that the hippocampus becomes less involved in remembering as a memory gets older," said Russell Poldrack, PhD, an expert on the cognitive and neural mechanisms of memory at the University of California, Los Angeles, who was not involved in the study. "However, there has been a recent debate over whether the hippocampus ever really stops being involved, even for older memories," Poldrack said.
To address this debate, Christine Smith, PhD, and Larry Squire, PhD, at the University of California, San Diego and the San Diego VA Medical Center, imaged study participants as they answered 160 questions about news events that occurred over the past 30 years. The hippocampus and related brain structures were most active when recalling recent events. Hippocampal activity gradually declined as participants recalled events that were 1-12 years old and remained low when they recalled events that were 13-30 years old.
In contrast, Smith and Squire found the opposite pattern of activity in frontal, temporal, and parietal cortices. In these brain regions — which are located at the surface of the brain — activity increased with the age of the news event recalled. "Our findings support the idea that these cortical regions are the ultimate repositories for long-term memory," Smith said. The researchers found that brain activity was unrelated to the richness of memories or to the recollection of personal events related to the tested news events.
"This is the best evidence to date supporting a long-held view about how memories become permanent," said Howard Eichenbaum, PhD, an expert on memory at Boston University who was unaffiliated with the study.
The research was supported by the U.S. Department of Veterans Affairs, National Institute of Mental Health, the Metropolitan Life Foundation, and the National Institute on Aging
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