ScienceDaily (July 24, 2009) — Though discoveries about Alzheimer's disease risk factors are often in the news, adults do not know about the relationship between Alzheimer's disease risk and heart health, nor that physical activity can be protective against dementia, according to new research reported at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD 2009) in Vienna.
An additional study reported at ICAD 2009 shows higher Alzheimer's risk in veterans with post-traumatic stress disorder (PTSD).
"Your brain plays a critical role in almost everything you do: thinking, feeling, remembering, working, and playing – even sleeping," said Maria Carrillo, PhD, Director of Medical & Scientific Relations at the Alzheimer's Association. "The good news is that we now know there's a lot you can do to help keep your brain healthier as you age. These steps might also reduce your risk of developing Alzheimer's disease or another dementia."
"There's a strong and credible association between heart health and brain health. If people learn about and do some simple lifestyle modifications, such as being more physically active and eating a brain healthy diet, it could have an enormous impact on our nation's public health and the cost of healthcare," Carrillo added.
Adults Show a Poor Understanding of Alzheimer's Link to Heart Health Risk Factors
Colleen E. Jackson, M.S., a doctoral student in Clinical Psychology at the University of Connecticut, and colleagues conducted an anonymous online survey of 690 adults to measure "dementia literacy," that is, their knowledge and beliefs that may assist in the recognition, management, or prevention of Alzheimer's.
Mean age of the population was 50 years, the range was 30-85 years; 76% of respondents were female. Ninety-four percent (94%) of participants were from the United States, with the remaining 6% from other English-speaking countries. The sample was relatively wealthy, with 18% of respondents making more than $200,000 per year at the peak of their careers, and well-educated, with 87% of respondents having completed at least 1-3 years of college.
The researchers found that 64% of study participants incorrectly indicated no association between Alzheimer's and obesity or high blood pressure. Sixty-six percent (66%) did not know that high stress is a risk factor for dementia, and 34% did not know that physical exercise is a protective factor.
On the positive side, nearly all study participants (94%) correctly indicated that Alzheimer's is not normal aging, and is not completely based on genetics.
"Our data suggest that American adults have limited knowledge and a poor understanding of factors that have been demonstrated to increase risk for Alzheimer's, such as obesity, high blood pressure, and other heart health risk factors," Jackson said. "They also didn't know much about protective factors against Alzheimer's, such as physical exercise, relative to the strength of the available research evidence."
"We need more education programs and opportunities, across all demographic groups, focusing on behaviors that modify your risk for developing Alzheimer's disease," Jackson added.
PTSD Linked to Nearly Double Dementia Risk in Veterans
Post-traumatic stress disorder (PTSD) is common among veterans returning from combat and there is some evidence that it may be associated with reduced cognitive function. However, no study has yet investigated if PTSD increases the risk of developing dementia.
To address this emerging issue, Kristine Yaffe, MD, Professor of Psychiatry, Neurology and Epidemiology and Associate Chair of Research for the Department of Psychiatry at the University of California, San Francisco, and Chief of Geriatric Psychiatry and Director of the Memory Disorders Clinic at the San Francisco VA Medical Center, and colleagues sought to determine if PTSD is associated with risk of developing dementia among older veterans in the U.S. receiving treatment in veterans' medical centers.
They studied 181,093 veterans aged 55 years and older without dementia (53,155 veterans diagnosed with PTSD and 127,938 veterans without PTSD) using data from the Department of Veterans Affairs National Patient Care Database. Mean baseline age of the veterans was 68.8 years and 97% were male. They followed the veterans from 2001 through 2007, including tracking whether they were diagnosed with Alzheimer's/dementia.
The researchers found that veterans with PTSD in the study developed new cases of dementia at a rate of 10.6% over the seven years of follow-up; those without PTSD had a rate of 6.6%. (Note: This is updated data from the researcher, which is why it differs from the attached abstract.) Even after adjusting for demographics, and medical and psychiatric comorbidities, PTSD patients in this study were still nearly twice as likely to develop incident dementia compared to veterans without PTSD (HR = 1.8, 95% CI 1.7-1.9). Results were similar when they excluded those with a history of traumatic brain injury, substance abuse or depression.
"It is critical to follow patients with PTSD, and evaluate them early for dementia," Yaffe said. "Further research is needed to fully understand what links these two important disorders. With that knowledge we may be able to find ways to reduce the increased risk of dementia associated with PTSD."
Friday, July 24, 2009
Monday, June 22, 2009
First Image of Memories Being Made
ScienceDaily (June 19, 2009) — The ability to learn and to establish new memories is essential to our daily existence and identity; enabling us to navigate through the world. A new study by researchers at the Montreal Neurological Institute and Hospital (The Neuro), McGill University and University of California, Los Angeles has captured an image for the first time of a mechanism, specifically protein translation, which underlies long-term memory formation.
The finding provides the first visual evidence that when a new memory is formed new proteins are made locally at the synapse - the connection between nerve cells - increasing the strength of the synaptic connection and reinforcing the memory. The study published in Science, is important for understanding how memory traces are created and the ability to monitor it in real time will allow a detailed understanding of how memories are formed.
When considering what might be going on in the brain at a molecular level two essential properties of memory need to be taken into account. First, because a lot of information needs to be maintained over a long time there has to be some degree of stability. Second, to allow for learning and adaptation the system also needs to be highly flexible. For this reason, research has focused on synapses which are the main site of exchange and storage in the brain. They form a vast but also constantly fluctuating network of connections whose ability to change and adapt, called synaptic plasticity, may be the fundamental basis of learning and memory. "But, if this network is constantly changing, the question is how do memories stay put, how are they formed? It has been known for some time that an important step in long-term memory formation is "translation", or the production, of new proteins locally at the synapse, strengthening the synaptic connection in the reinforcement of a memory, which until now has never been imaged," says Dr. Wayne Sossin, neuroscientist at The Neuro and co-investigator in the study. "Using a translational reporter, a fluorescent protein that can be easily detected and tracked, we directly visualized the increased local translation, or protein synthesis, during memory formation. Importantly, this translation was synapse-specific and it required activation of the post-synaptic cell, showing that this step required cooperation between the pre and post-synaptic compartments, the parts of the two neurons that meet at the synapse. Thus highly regulated local translation occurs at synapses during long-term plasticity and requires trans-synaptic signals."
Long-term memory and synaptic plasticity require changes in gene expression and yet can occur in a synapse-specific manner. This study provides evidence that a mechanism that mediates this gene expression during neuronal plasticity involves regulated translation of localized mRNA at stimulated synapses. These findings are instrumental in establishing the molecular processes involved in long-term memory formation and provide insight into diseases involving memory impairment.
This study was funded by the National Institutes of Health, the WM Keck Foundation and the Canadian Institutes of Health Research.
The finding provides the first visual evidence that when a new memory is formed new proteins are made locally at the synapse - the connection between nerve cells - increasing the strength of the synaptic connection and reinforcing the memory. The study published in Science, is important for understanding how memory traces are created and the ability to monitor it in real time will allow a detailed understanding of how memories are formed.
When considering what might be going on in the brain at a molecular level two essential properties of memory need to be taken into account. First, because a lot of information needs to be maintained over a long time there has to be some degree of stability. Second, to allow for learning and adaptation the system also needs to be highly flexible. For this reason, research has focused on synapses which are the main site of exchange and storage in the brain. They form a vast but also constantly fluctuating network of connections whose ability to change and adapt, called synaptic plasticity, may be the fundamental basis of learning and memory. "But, if this network is constantly changing, the question is how do memories stay put, how are they formed? It has been known for some time that an important step in long-term memory formation is "translation", or the production, of new proteins locally at the synapse, strengthening the synaptic connection in the reinforcement of a memory, which until now has never been imaged," says Dr. Wayne Sossin, neuroscientist at The Neuro and co-investigator in the study. "Using a translational reporter, a fluorescent protein that can be easily detected and tracked, we directly visualized the increased local translation, or protein synthesis, during memory formation. Importantly, this translation was synapse-specific and it required activation of the post-synaptic cell, showing that this step required cooperation between the pre and post-synaptic compartments, the parts of the two neurons that meet at the synapse. Thus highly regulated local translation occurs at synapses during long-term plasticity and requires trans-synaptic signals."
Long-term memory and synaptic plasticity require changes in gene expression and yet can occur in a synapse-specific manner. This study provides evidence that a mechanism that mediates this gene expression during neuronal plasticity involves regulated translation of localized mRNA at stimulated synapses. These findings are instrumental in establishing the molecular processes involved in long-term memory formation and provide insight into diseases involving memory impairment.
This study was funded by the National Institutes of Health, the WM Keck Foundation and the Canadian Institutes of Health Research.
CSF Fluid Shows Alzheimer's Disease Deterioration Much Earlier
ScienceDaily (June 19, 2009) — It is possible to determine which patients run a high risk of developing Alzheimer’s disease and the dementia associated with it, even in patients with minimal memory impairment. This has been shown by recent research at the Sahlgrenska Academy.
The results have just been published in the medical journal Lancet Neurology. "The earlier we can catch Alzheimer’s disease, the more we can do for the patient. The disease is one that progresses slowly, and the pharmaceuticals that are currently available are only able to alleviate the symptoms", says Kaj Blennow, professor at the Sahlgrenska Academy.
Several biomarkers have been identified in recent years. Biomarkers are proteins that can be detected in the cerebrospinal fluid and used to diagnose Alzheimer’s disease. It is now clear that the typical pattern of biomarkers known as the "CSF AD profile" can be seen in the cerebrospinal fluid of patients even with very mild memory deficiencies, before these can be detected by other tests.
"The patients who had the typical changes in biomarker profile of the cerebrospinal fluid had a risk of deterioration that was 27 times higher than the control group. We could also see that all patients with mild cognitive impairment who deteriorated and developed Alzheimer’s disease had these changes in the biomarker profile of their cerebrospinal fluid", says Kaj Blennow.
The scientists were also able to show a relationship between the profile of biomarkers and other typical signs of the disease, such as the presence of the gene APOE e4 and atrophy of the hippocampus, which is the part of the brain cortex that controls memory. "Our discovery that an analysis of biomarkers in the cerebrospinal fluid can reveal Alzheimer’s disease at a very early stage will have major significance if the new type of pharmaceutical that can directly slow the progression of the disease proves to have a clinical effect. It is important in this case to start treatment before the changes in the brain have become too severe", says Kaj Blennow. The research is part of a European research project known as DESCRIPA. Samples from 168 patients from seven countries are included in the study.
Alzheimer’s disease is one of the most widespread diseases in Sweden, with more than 100,000 people being affected. The disease is caused by harmful changes to the nerve cells in the brain, and it principally affects memory. The disease often leads to early death. Alzheimer’s disease not only causes untold suffering for patients and their families, it also gives rise to enormous costs for society.
The results have just been published in the medical journal Lancet Neurology. "The earlier we can catch Alzheimer’s disease, the more we can do for the patient. The disease is one that progresses slowly, and the pharmaceuticals that are currently available are only able to alleviate the symptoms", says Kaj Blennow, professor at the Sahlgrenska Academy.
Several biomarkers have been identified in recent years. Biomarkers are proteins that can be detected in the cerebrospinal fluid and used to diagnose Alzheimer’s disease. It is now clear that the typical pattern of biomarkers known as the "CSF AD profile" can be seen in the cerebrospinal fluid of patients even with very mild memory deficiencies, before these can be detected by other tests.
"The patients who had the typical changes in biomarker profile of the cerebrospinal fluid had a risk of deterioration that was 27 times higher than the control group. We could also see that all patients with mild cognitive impairment who deteriorated and developed Alzheimer’s disease had these changes in the biomarker profile of their cerebrospinal fluid", says Kaj Blennow.
The scientists were also able to show a relationship between the profile of biomarkers and other typical signs of the disease, such as the presence of the gene APOE e4 and atrophy of the hippocampus, which is the part of the brain cortex that controls memory. "Our discovery that an analysis of biomarkers in the cerebrospinal fluid can reveal Alzheimer’s disease at a very early stage will have major significance if the new type of pharmaceutical that can directly slow the progression of the disease proves to have a clinical effect. It is important in this case to start treatment before the changes in the brain have become too severe", says Kaj Blennow. The research is part of a European research project known as DESCRIPA. Samples from 168 patients from seven countries are included in the study.
Alzheimer’s disease is one of the most widespread diseases in Sweden, with more than 100,000 people being affected. The disease is caused by harmful changes to the nerve cells in the brain, and it principally affects memory. The disease often leads to early death. Alzheimer’s disease not only causes untold suffering for patients and their families, it also gives rise to enormous costs for society.
Saturday, June 6, 2009
Snoring Associated With Sleep Apnea May Impair Brain Function
ScienceDaily (June 4, 2009) — It has been linked to learning impairment, stroke and premature death. Now UNSW research has found that snoring associated with sleep apnea may impair brain function more than previously thought.
Sufferers of obstructive sleep apnea experience similar changes in brain biochemistry as people who have had a severe stroke or who are dying, the research shows.
A study by UNSW Brain Sciences, published this month in the Journal of Cerebral Blood Flow and Metabolism, is the first to analyse – in a second-by-second timeframe – what is happening in the brains of sufferers as they sleep. Previous studies have focused on recreating oxygen impairment in awake patients.
“It used to be thought that apneic snoring had absolutely no acute effects on brain function but this is plainly not true,” said lead author of the study, New South Global Professor Caroline Rae.
Sleep apnea affects as many as one in four middle-aged men, with around three percent going on to experience a severe form of the condition characterised by extended pauses in breathing, repetitive asphyxia and sleep fragmentation.
Children with enlarged tonsils and adenoids are also affected, raising concerns of long-term cognitive damage.
Professor Rae and collaborators from Sydney University’s Woolcock Institute used magnetic resonance spectroscopy to study the brains of 13 men with severe, untreated, obstructive sleep apnea. They found that even a moderate degree of oxygen desaturation during the patients’ sleep had significant effects on the brain’s bioenergetic status.
“The findings show that lack of oxygen while asleep may be far more detrimental than when awake, possibly because the normal compensatory mechanisms don't work as well when you are asleep,” Professor Rae, who is based at the Prince of Wales Medical Research Institute, said.
“This is happening in someone with sleep apnea acutely and continually when they are asleep. It’s a completely different biochemical mechanism from anything we’ve seen
before and is similar to what you see in somebody who has had a very severe stroke or is dying.”
The findings suggested societal perceptions of snoring needed to change, Professor Rae said.
“People look at people snoring and think it’s funny. That has to stop.”
Professor Rae said it was still unclear why the body responded to oxygen depletion in this way. It could be a form of ischemic preconditioning at work, much like in heart attack sufferers whose initial attack makes them more protected from subsequent attacks.
“The brain could be basically resetting its bioenergetics to make itself more resistant to lack of oxygen,” Professor Rae said. “It may be a compensatory mechanism to keep you alive, we just don’t know, but even if it is it’s not likely to be doing you much good.”
Sufferers of obstructive sleep apnea experience similar changes in brain biochemistry as people who have had a severe stroke or who are dying, the research shows.
A study by UNSW Brain Sciences, published this month in the Journal of Cerebral Blood Flow and Metabolism, is the first to analyse – in a second-by-second timeframe – what is happening in the brains of sufferers as they sleep. Previous studies have focused on recreating oxygen impairment in awake patients.
“It used to be thought that apneic snoring had absolutely no acute effects on brain function but this is plainly not true,” said lead author of the study, New South Global Professor Caroline Rae.
Sleep apnea affects as many as one in four middle-aged men, with around three percent going on to experience a severe form of the condition characterised by extended pauses in breathing, repetitive asphyxia and sleep fragmentation.
Children with enlarged tonsils and adenoids are also affected, raising concerns of long-term cognitive damage.
Professor Rae and collaborators from Sydney University’s Woolcock Institute used magnetic resonance spectroscopy to study the brains of 13 men with severe, untreated, obstructive sleep apnea. They found that even a moderate degree of oxygen desaturation during the patients’ sleep had significant effects on the brain’s bioenergetic status.
“The findings show that lack of oxygen while asleep may be far more detrimental than when awake, possibly because the normal compensatory mechanisms don't work as well when you are asleep,” Professor Rae, who is based at the Prince of Wales Medical Research Institute, said.
“This is happening in someone with sleep apnea acutely and continually when they are asleep. It’s a completely different biochemical mechanism from anything we’ve seen
before and is similar to what you see in somebody who has had a very severe stroke or is dying.”
The findings suggested societal perceptions of snoring needed to change, Professor Rae said.
“People look at people snoring and think it’s funny. That has to stop.”
Professor Rae said it was still unclear why the body responded to oxygen depletion in this way. It could be a form of ischemic preconditioning at work, much like in heart attack sufferers whose initial attack makes them more protected from subsequent attacks.
“The brain could be basically resetting its bioenergetics to make itself more resistant to lack of oxygen,” Professor Rae said. “It may be a compensatory mechanism to keep you alive, we just don’t know, but even if it is it’s not likely to be doing you much good.”
Discoveries Shed New LIght On How the Brain Processes What The Eye Sees
ScienceDaily (June 4, 2009) — Researchers at the Center for Molecular and Behavioral Neuroscience (CMBN) at Rutgers University in Newark have identified the need to develop a new framework for understanding “perceptual stability” and how we see the world with their discovery that visual input obtained during eye movements is being processed by the brain but blocked from awareness.
The process of seeing requires the eyes to move so light can hit the photoreceptors at the center of each retina, which then pass that information to the brain. If we were cognizant of the stimulus that passes before the eyes during the two to three times they move every second, however, vision would consist of a series of sensations of rapid motion rather than a stable perception of the world. To achieve perceptual stability, current theory has held that visual information gained during an eye movement is eliminated, as if cut off by a camera’s shutter, and removed from processing.
As published in Current Biology significant new research conducted by assistant professor Bart Krekelberg and post-doctoral researcher Tamara L. Watson now shows that theory of saccadic suppression is incorrect and what the brain is doing instead is processing information gained during eye movement but blocking it from being reported.
“Rather than completely suppressing inputs during eye movements, the brain is processing that as information it does not need to report back to awareness,” says Krekelberg.
The findings were obtained by making use of a visual illusion in which the presentation of a horizontal line makes a subsequent circle look like an ellipse. In Watson and Krekelberg’s study, the line was presented to research participants immediately before an eye movement. Under current theory, the line would be eliminated from visual processing and one would expect participants to report a subsequently presented circle to look like a circle. While the research participants did not recall seeing the line, the image they reported seeing was not a circle but rather an ellipse. In other words, the participants experienced the illusion, even though they were not aware of the line that causes the illusion.
“Although they did not recall seeing the line, the brain apparently did process the line,” says Watson. “What this shows is that perceptual stability is not accomplished by suppressing stimuli encountered during an eye movement, or removing them from processing, but rather that those signals are prevented from reaching awareness at a later stage of processing. Some suppression is also happening, but suppression is not enough to explain perceptual stability; it is not the whole story.”
One reason why the brain does not discard visual input during eye movements could be that it provides useful information about eye movements. “We speculate that the visual signals generated by eye movement may be important for determining how much and how fast the eye moved so the brain can maintain perceptual stability,” says Watson. “It may be that these signals are useful for improving perceptual stability as long as they do not enter into awareness.”
The findings also show that a new approach is needed to gain additional understanding into the cognitive and neural functions involved in visual processing and perceptual stability. Until now, research largely has focused on pinpointing those areas of the brain that show lower activity during an eye movement. “What we are seeing now is that things are much more complex than we suspected,” says Krekelberg. “We shouldn’t just be looking at areas of reduced activity in the brain during eye movement, but for areas that may change their processing to make use of the input that arises during eye movements.”
Providing a better understanding of those changes in processing could pave the way for earlier detection and more effective treatments for those who suffer from deficits associated with eye movements. For example, schizophrenic patients sometimes report a lack of perceptual stability. And while dyslexia traditionally has been interpreted as a deficit in language development, it also has been found to be associated with deficits in the control of eye movements.
The research was supported by a fellowship to Tamara Watson from the Human Frontiers Science Program and a scholarship to Bart Krekelberg from the Pew Charitable Trusts.
The process of seeing requires the eyes to move so light can hit the photoreceptors at the center of each retina, which then pass that information to the brain. If we were cognizant of the stimulus that passes before the eyes during the two to three times they move every second, however, vision would consist of a series of sensations of rapid motion rather than a stable perception of the world. To achieve perceptual stability, current theory has held that visual information gained during an eye movement is eliminated, as if cut off by a camera’s shutter, and removed from processing.
As published in Current Biology significant new research conducted by assistant professor Bart Krekelberg and post-doctoral researcher Tamara L. Watson now shows that theory of saccadic suppression is incorrect and what the brain is doing instead is processing information gained during eye movement but blocking it from being reported.
“Rather than completely suppressing inputs during eye movements, the brain is processing that as information it does not need to report back to awareness,” says Krekelberg.
The findings were obtained by making use of a visual illusion in which the presentation of a horizontal line makes a subsequent circle look like an ellipse. In Watson and Krekelberg’s study, the line was presented to research participants immediately before an eye movement. Under current theory, the line would be eliminated from visual processing and one would expect participants to report a subsequently presented circle to look like a circle. While the research participants did not recall seeing the line, the image they reported seeing was not a circle but rather an ellipse. In other words, the participants experienced the illusion, even though they were not aware of the line that causes the illusion.
“Although they did not recall seeing the line, the brain apparently did process the line,” says Watson. “What this shows is that perceptual stability is not accomplished by suppressing stimuli encountered during an eye movement, or removing them from processing, but rather that those signals are prevented from reaching awareness at a later stage of processing. Some suppression is also happening, but suppression is not enough to explain perceptual stability; it is not the whole story.”
One reason why the brain does not discard visual input during eye movements could be that it provides useful information about eye movements. “We speculate that the visual signals generated by eye movement may be important for determining how much and how fast the eye moved so the brain can maintain perceptual stability,” says Watson. “It may be that these signals are useful for improving perceptual stability as long as they do not enter into awareness.”
The findings also show that a new approach is needed to gain additional understanding into the cognitive and neural functions involved in visual processing and perceptual stability. Until now, research largely has focused on pinpointing those areas of the brain that show lower activity during an eye movement. “What we are seeing now is that things are much more complex than we suspected,” says Krekelberg. “We shouldn’t just be looking at areas of reduced activity in the brain during eye movement, but for areas that may change their processing to make use of the input that arises during eye movements.”
Providing a better understanding of those changes in processing could pave the way for earlier detection and more effective treatments for those who suffer from deficits associated with eye movements. For example, schizophrenic patients sometimes report a lack of perceptual stability. And while dyslexia traditionally has been interpreted as a deficit in language development, it also has been found to be associated with deficits in the control of eye movements.
The research was supported by a fellowship to Tamara Watson from the Human Frontiers Science Program and a scholarship to Bart Krekelberg from the Pew Charitable Trusts.
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