Today the U.S. Institute of Medicine released the following announcement:Contacts: Christine Stencel, Media Relations OfficerAlison Burnette, Media Relations AssistantOffice of News and Public Information202-334-2138; e-mail <news@nas.edu>Date: Dec. 4, 2008
FOR IMMEDIATE RELEASEMilitary Personnel With Traumatic Brain Injury at Risk for Serious Long-Term Health ProblemsMilitary personnel who suffer severe or moderate traumatic brain injury(TBI) face an increased risk for developing several long-term healthproblems, says a new report from the Institute of Medicine thatevaluates the evidence on long-term consequences of TBI.These conditions include Alzheimer's-like dementia, aggression, memoryloss, depression, and symptoms similar to those of Parkinson's disease.Even mild TBI is associated with some of these adverse consequences,noted the committee that wrote the report.In addition, the report notes that brain injuries sustained as a resultof exposure to the force of an explosion without a direct strike to thehead -- one of the most common perils for soldiers in Iraq andAfghanistan -- may be underdiagnosed due to the lack of research onblast injury. It calls for the U.S. Department of Defense and the U.S.Department of Veterans Affairs to step up clinical and animal studies ofblast-induced neurotrauma (BINT)."Explosive devices and other weaponry have become more powerful anddevastating throughout the wars in Iraq and Afghanistan, and we areseeing much higher rates of nonpenetrating traumatic brain injury andblast-induced injury among military personnel who have served in thesecountries than in earlier wars," said George W. Rutherford, professor ofepidemiology and preventive medicine and vice chair, department ofepidemiology and biostatistics, School of Medicine, University ofCalifornia, San Francisco, and chair of the committee that wrote thereport. "It is important to identify and understand any long-termhealth effects of these injuries so that wounded service members do notlose valuable time for therapy and rehabilitation."As of January, more than 5,500 military personnel have suffered TBIsduring the conflicts in Iraq and Afghanistan, according to DOD. Theprolific use of explosive weaponry in Iraq has made blast-relatedinjuries the signature wound of the war, with many service membershaving been exposed to multiple explosions.Although recent clinical findings and military experience have shownthat short-term and long-term neurologic deficits may result fromexposure to the energy of a blast without a direct blow to the head, theprevailing opinion among neurological professionals had been that blast-related impairments were rare because the skull adequately shields thebrain. The report recommends that VA and DOD support research on BINTand the development of a good animal model of BINT, which is currentlylacking. Without good research data, neurological and behavioralchanges in blast victims may be underestimated and undiagnosed, andthese individuals may not get timely needed treatment, the report notes.TBI can be mild, moderate, or severe. The committee's review of theresearch on TBI at all levels of severity determined that there issufficient evidence that brain injuries resulting from severe, skull-piercing wounds can cause unprovoked seizures and premature death.Seizures can also be caused by severe, nonpenetrating TBI as well asmore moderate brain injury.Studies link both moderate and severe TBI with other long-termconsequences, including increased risk for Alzheimer's-like dementia,symptoms similar to those of Parkinson's disease, and diminishedabilities to maintain social relationships. Other data links mild TBIto increased risk for PTSD among Gulf War veterans. The evidence inthese cases shows an association, but it is not sufficient to concludethat TBI causes these problems. Likewise, TBI at any level of severity-- even mild -- appears to be associated with increased risk foraggressive behavior, depression, and memory and concentration problems.TBI may be associated with certain other potential consequences, but theevidence is only suggestive of a link. For example, moderate and severeTBI may put individuals at greater risk for developing diabetesinsipidus and psychosis, but the evidence is limited. Some data suggestthat mild TBI accompanied by loss of consciousness is linked to thedevelopment of symptoms similar to Alzheimer's and Parkinson's diseaseas well as vision problems and seizures, but the data have significantshortcomings. Likewise, TBI at all levels of severity may be linked toreduced alcohol and drug use within the first few years following theinjury, but there is inadequate evidence to be certain.Due to insufficient evidence, it is not possible to say whether mild TBIcan result in neurocognitive deficits or loss of ability to functionsocially. Also, the evidence does not indicate whether mild TBI thatwas not accompanied by loss of consciousness could lead to thedevelopment of Alzheimer's-like dementia, or whether any TBI is linkedto mania, bipolar disorder, multiple sclerosis, or amyotrophic lateralsclerosis.To develop a fuller picture of the effects of TBI and blast injuries,the committee recommended that DOD conduct pre-deployment neurocognitivetests of all military personnel to establish a baseline for identifyingpost-injury consequences and that the VA include uninjured servicemembers and other comparison groups in the Traumatic Brain InjuryVeterans Health Registry which it is building.The study was sponsored by the U.S. Department of Veterans Affairs.Established in 1970 under the charter of the National Academy ofSciences, the Institute of Medicine provides independent, objective,evidence-based advice to policymakers, health professionals, the privatesector, and the public. The National Academy of Sciences, NationalAcademy of Engineering, Institute of Medicine, and National ResearchCouncil make up the National Academies. A committee roster follows.Copies of Gulf War and Health: Long-Term Consequences of TBI areavailable from the National Academies Press; tel. 202-334-3313 or1-800-624-6242 or on the Internet at http://www.nap.edu. Reporters mayobtain a copy from the Office of News and Public Information (contactslisted above).
Saturday, December 6, 2008
Alzheimer's Disease Biomarkers in Healthy Adults
New Study Identifies Link Between Alzheimer's Disease Biomarkers In Healthy Adults
ScienceDaily (Dec. 5, 2008) — A new study provides an insight into normal, physiological levels and association between proteins involved in development of Alzheimer's disease.
A group of scientists and physicians from the University of Washington and Puget Sound Veterans' Affairs Health Care System in Seattle, in collaboration with groups from the University of Pennsylvania and the University of California San Diego, performed a study in cognitively normal and generally healthy adults, from young to old (age range 21-88 years), of both genders, measuring levels of different brain-derived molecules associated with Alzheimer's disease.
Investigators determined that cerebrospinal fluid (CSF) levels of apolipoprotein E (apoE), one of the most important proteins involved in transfer of fatty substances between different brain cells, are highly correlated with the levels of proteins known to be involved in development of Alzheimer's disease, amyloid precursor protein (APP) and tau.
While many studies have previously shown that apoE gene is very important for Alzheimer's disease development, the connection between apoE protein and other relevant CSF markers in healthy adults was not known. Although this type of study cannot establish causal associations, the results strongly suggest that the CSF levels of apoE may explain a significant proportion of the levels of APP- and tau-related biological markers in the healthy human brain, indicating a strong physiological link between apoE, APP and tau. In other words, the study points to a possibility that modulation of the levels of apoE may affect the levels of APP and tau in the brain.
Furthermore, the study has shown that people who have a "beneficial" genetic form of apoE (so-called APOE2), which is associated with lower risk of Alzheimer's disease, have lower CSF levels of beta-amyloid peptide 42, a molecule implicated in development of Alzheimer's disease plaques. This finding may explain some of the basis for the known protective effects of the APOE2 observed in large population studies.
Dr. Simona Vuletic, Northwest Lipid Metabolism and Diabetes Research Laboratories, University of Washington School of Medicine, Seattle, commented, "Understanding the associations between these important molecules in the brain of cognitively normal, healthy people will help us develop better strategies not only for diagnosis, but possibly also better prevention and treatment for Alzheimer's disease. This study also provides baseline data and an opportunity to understand how these normal relationships change, leading to the disease."
Journal reference:
Simona Vuletic, Ge Li, Elaine R. Peskind, Hal Kennedy, Santica M. Marcovina, James B. Leverenz, Eric C. Petrie, Virginia M-Y. Lee, Douglas Galasko, Gerard D. Schellenberg, John J. Albers. Apolipoprotein E Highly Correlates with AßPP- and Tau-Related Markers in Human Cerebrospinal Fluid. Journal of Alzheimer's Disease, 15:3; November 2008
ScienceDaily (Dec. 5, 2008) — A new study provides an insight into normal, physiological levels and association between proteins involved in development of Alzheimer's disease.
A group of scientists and physicians from the University of Washington and Puget Sound Veterans' Affairs Health Care System in Seattle, in collaboration with groups from the University of Pennsylvania and the University of California San Diego, performed a study in cognitively normal and generally healthy adults, from young to old (age range 21-88 years), of both genders, measuring levels of different brain-derived molecules associated with Alzheimer's disease.
Investigators determined that cerebrospinal fluid (CSF) levels of apolipoprotein E (apoE), one of the most important proteins involved in transfer of fatty substances between different brain cells, are highly correlated with the levels of proteins known to be involved in development of Alzheimer's disease, amyloid precursor protein (APP) and tau.
While many studies have previously shown that apoE gene is very important for Alzheimer's disease development, the connection between apoE protein and other relevant CSF markers in healthy adults was not known. Although this type of study cannot establish causal associations, the results strongly suggest that the CSF levels of apoE may explain a significant proportion of the levels of APP- and tau-related biological markers in the healthy human brain, indicating a strong physiological link between apoE, APP and tau. In other words, the study points to a possibility that modulation of the levels of apoE may affect the levels of APP and tau in the brain.
Furthermore, the study has shown that people who have a "beneficial" genetic form of apoE (so-called APOE2), which is associated with lower risk of Alzheimer's disease, have lower CSF levels of beta-amyloid peptide 42, a molecule implicated in development of Alzheimer's disease plaques. This finding may explain some of the basis for the known protective effects of the APOE2 observed in large population studies.
Dr. Simona Vuletic, Northwest Lipid Metabolism and Diabetes Research Laboratories, University of Washington School of Medicine, Seattle, commented, "Understanding the associations between these important molecules in the brain of cognitively normal, healthy people will help us develop better strategies not only for diagnosis, but possibly also better prevention and treatment for Alzheimer's disease. This study also provides baseline data and an opportunity to understand how these normal relationships change, leading to the disease."
Journal reference:
Simona Vuletic, Ge Li, Elaine R. Peskind, Hal Kennedy, Santica M. Marcovina, James B. Leverenz, Eric C. Petrie, Virginia M-Y. Lee, Douglas Galasko, Gerard D. Schellenberg, John J. Albers. Apolipoprotein E Highly Correlates with AßPP- and Tau-Related Markers in Human Cerebrospinal Fluid. Journal of Alzheimer's Disease, 15:3; November 2008
Friday, November 28, 2008
Baffling Chronic Pain Linked to Weird Rewiring of Brain
Baffling Chronic Pain Linked To Weird Rewiring Of Brain
ScienceDaily (Nov. 27, 2008) — Scientists peered at the brains of people with a baffling chronic pain condition and discovered something surprising. Their brains looked like an inept cable guy had changed the hookups, rewiring the areas related to emotion, pain perception and the temperature of their skin.
The new finding by scientists at Northwestern University's Feinberg School of Medicine, begins to explain a mysterious condition that the medical community had doubted was real.
The people whose brains were examined have a chronic pain condition called complex region pain syndrome (CRPS.) It's a pernicious and nasty condition that usually begins with an injury causing significant damage to the hand or the foot. For the majority of people, the pain from the injury disappears once the limb is healed. But for 5 percent of the patients, the pain rages on long past the healing, sometimes for the rest of people's lives.
About 200,00 people in the U.S. have this condition.
In a hand injury, for example, the pain may radiate from the initial injury site and spread to the whole arm or even the entire body. People also experience changes in skin color to blue or red as well as skin temperature (hotter at first, then becoming colder as the condition turns chronic.) Their immune system also shifts into overdrive, indicated by a hike in blood immune markers.
The changes in the brain take place in the network of tiny, white "cables" that dispatch messages between the neurons. This is called the brain's white matter. Several years ago, Northwestern researchers discovered chronic pain caused the regions in the brain that contain the neurons -- called gray matter because of it looks gray -- to atrophy.
This is the first study to link pain with changes in the brain's white matter. It will be published November 26 in the journal Neuron.
"This is the first evidence of brain abnormality in these patients," said A. Vania Apkarian, professor of physiology at the Feinberg School and principal investigator of the study. " People didn't believe these patients. This is the first proof that there is a biological underpinning for the condition. Scientists have been trying to understand this baffling condition for a long time."
Apkarian said people with CRPS suffer intensely and have a high rate of suicide. "Physicians don't know what to do," he said. "We don't have the tools to take care of them."
The new findings provide anatomical targets for scientists, who can now look for potential pharmaceutical treatments to help these patients, Apkarian said. He doesn't know yet if chronic pain causes these changes in the brain or if CRPS patients' brains have pre-existing abnormalities that predispose them to this condition.
In the new study, the brains of 22 subjects with CRPS and 22 normal subjects were examined with an anatomical MRI and a diffusion tensor MRI, which enabled scientists to view the white matter. In addition to changes in white matter, the CRPS patients' brains showed an atrophy of neurons or gray matter similar to what has been previously shown in other types of chronic pain patients.
Apkarian said the white matter changes in patients' brains is related to the duration and intensity of their pain and their anxiety. It is likely that white matter reorganizes in other chronic pain conditions as well, but that has not yet been studied, he noted.
ScienceDaily (Nov. 27, 2008) — Scientists peered at the brains of people with a baffling chronic pain condition and discovered something surprising. Their brains looked like an inept cable guy had changed the hookups, rewiring the areas related to emotion, pain perception and the temperature of their skin.
The new finding by scientists at Northwestern University's Feinberg School of Medicine, begins to explain a mysterious condition that the medical community had doubted was real.
The people whose brains were examined have a chronic pain condition called complex region pain syndrome (CRPS.) It's a pernicious and nasty condition that usually begins with an injury causing significant damage to the hand or the foot. For the majority of people, the pain from the injury disappears once the limb is healed. But for 5 percent of the patients, the pain rages on long past the healing, sometimes for the rest of people's lives.
About 200,00 people in the U.S. have this condition.
In a hand injury, for example, the pain may radiate from the initial injury site and spread to the whole arm or even the entire body. People also experience changes in skin color to blue or red as well as skin temperature (hotter at first, then becoming colder as the condition turns chronic.) Their immune system also shifts into overdrive, indicated by a hike in blood immune markers.
The changes in the brain take place in the network of tiny, white "cables" that dispatch messages between the neurons. This is called the brain's white matter. Several years ago, Northwestern researchers discovered chronic pain caused the regions in the brain that contain the neurons -- called gray matter because of it looks gray -- to atrophy.
This is the first study to link pain with changes in the brain's white matter. It will be published November 26 in the journal Neuron.
"This is the first evidence of brain abnormality in these patients," said A. Vania Apkarian, professor of physiology at the Feinberg School and principal investigator of the study. " People didn't believe these patients. This is the first proof that there is a biological underpinning for the condition. Scientists have been trying to understand this baffling condition for a long time."
Apkarian said people with CRPS suffer intensely and have a high rate of suicide. "Physicians don't know what to do," he said. "We don't have the tools to take care of them."
The new findings provide anatomical targets for scientists, who can now look for potential pharmaceutical treatments to help these patients, Apkarian said. He doesn't know yet if chronic pain causes these changes in the brain or if CRPS patients' brains have pre-existing abnormalities that predispose them to this condition.
In the new study, the brains of 22 subjects with CRPS and 22 normal subjects were examined with an anatomical MRI and a diffusion tensor MRI, which enabled scientists to view the white matter. In addition to changes in white matter, the CRPS patients' brains showed an atrophy of neurons or gray matter similar to what has been previously shown in other types of chronic pain patients.
Apkarian said the white matter changes in patients' brains is related to the duration and intensity of their pain and their anxiety. It is likely that white matter reorganizes in other chronic pain conditions as well, but that has not yet been studied, he noted.
Wednesday, November 26, 2008
How Is Our Left Brain Different From Our Right?
ScienceDaily (Nov. 25, 2008) — Since the historical discovery of the speech center in the left cortex in 150 years ago, functional differences between left and right hemisphere have been well known; language is mainly handled by left hemisphere, while spatial recognition is more specialized to the right hemisphere. However, the structural differences of synapses underlying left-right difference of the brain remained unknown.
Japanese research team, led by Prof Ryuichi Shigemoto in National Institute for Physiological Sciences, Dr Yoshiaki Shinohara and his colleagues found that synaptic size and shape in the center of the spatial memory (i.e. hippocampus) were asymmetrical between synapses receiving input from the left and right hemisphere. Hajime Hirase in Brain Science Institute in RIKEN helped this study, and it was done under Japan Science Technorogy Agency support.
They investigated the electron microscopic structure of synapses in left and right hippocampus, and found synapses made by terminals from the right hippocampus are large, complex in shape, and rich in the GluR1 subunit of AMPA-type glutamate receptors. In contrast, synapses receiving input from the left hippocampus are small and rich in the NR2B subunit of NMDA receptors. That means, both synaptic structure and synaptic molecules differ between synapses with left and right inputs.
"Long-term potentiaon (LTP), that is known as the cellular mechanism of learning and memory, depends on the allocation of glutamate receptors in hippocampus.
According to our present finding, synapses receiving right input may be more suitable to initiate LTP. This finding may help understand how our left and right brains work differently", said Prof Shigemoto.
This report is published in Proceedings of National Academy of Sciences in the week of Nov 17, 2008.
Japanese research team, led by Prof Ryuichi Shigemoto in National Institute for Physiological Sciences, Dr Yoshiaki Shinohara and his colleagues found that synaptic size and shape in the center of the spatial memory (i.e. hippocampus) were asymmetrical between synapses receiving input from the left and right hemisphere. Hajime Hirase in Brain Science Institute in RIKEN helped this study, and it was done under Japan Science Technorogy Agency support.
They investigated the electron microscopic structure of synapses in left and right hippocampus, and found synapses made by terminals from the right hippocampus are large, complex in shape, and rich in the GluR1 subunit of AMPA-type glutamate receptors. In contrast, synapses receiving input from the left hippocampus are small and rich in the NR2B subunit of NMDA receptors. That means, both synaptic structure and synaptic molecules differ between synapses with left and right inputs.
"Long-term potentiaon (LTP), that is known as the cellular mechanism of learning and memory, depends on the allocation of glutamate receptors in hippocampus.
According to our present finding, synapses receiving right input may be more suitable to initiate LTP. This finding may help understand how our left and right brains work differently", said Prof Shigemoto.
This report is published in Proceedings of National Academy of Sciences in the week of Nov 17, 2008.
How To Know You're Having a Stroke; Most Stroke Pts Don't Think They're Having a Stroke; Time is Crucial
The Mayo Clinic released the following announcement:Do you know you're having a stroke?Symptom awareness can improve recoveryA Mayo Clinic study shows a majority of stroke patients don't thinkthey're having a stroke -- and as a result -- delay seeking treatmentuntil their condition worsens. The findings appear in the current issueof Emergency Medicine Journal at http://emj.bmj.com/.
Researchers studied 400 patients who were diagnosed at Mayo Clinic'semergency department with either acute ischemic stroke or a transientischemic attack (TIA), a temporary interruption of blood flow to part ofthe brain.Less than half of the patients -- 42 percent -- thought they were havinga stroke. In fact, most in the study did not go to the emergency roomwhen symptoms appeared. The median time from onset of symptoms toarrival at the hospital was over three and a half hours. Most said theythought the symptoms would simply go away. The delay in seeking medicalhelp was the same among men and women.When asked how they knew about stroke symptoms, nearly one-fifth saidthey thought a stroke always came on gradually. Just over half (51.9percent) said they thought that seeking medical care immediately wasimportant.Significance of the findings"Time is crucial in treating stroke," says Latha Stead, M.D., emergencymedicine specialist and lead author of the study. "Each individual'smedical background differs and affects recovery, but in general thesooner a patient experiencing a stroke reaches emergency care, the morelikely the stroke can be limited and the condition managed to preventfurther damage and improve recovery." The researchers say their findingsclearly indicate that better public
understanding of stroke symptomswill lead to a faster response and better outcomes.What you should knowStrokes can happen quickly or can occur over several hours, with thecondition continually worsening. The thrombus or clot that is causingthe stroke can frequently be dissolved or disintegrated so blood canagain flow to the brain. In such cases, immediate treatment can mean thedifference between a slight injury and a major disability. Interestinglyonly 20.8 percent of the participants knew about such treatment. By useof stents, medications and other technology, physicians can stop astroke from spreading and greatly limit damage. Stroke symptoms include:
* Sudden numbness, weakness, or paralysis of your face, arm or leg-- usually on one side of the body
* Sudden difficulty speaking or understanding speech (aphasia)
* Sudden blurred, double or decreased vision
* Sudden dizziness, loss of balance or loss of coordination
* A sudden, severe "bolt out of the blue" headache or an unusualheadache, which may be accompanied by a stiff neck, facial pain, painbetween your eyes, vomiting or altered consciousness
* Confusion or problems with memory, spatial orientation or perceptionIn such cases, a stroke gives no warning. But one possible sign of animpending stroke is a TIA.
The signs and symptoms of TIA are the same asfor a stroke, but they last for a shorter period -- several minutes to afew hours -- and then disappear, without leaving apparent permanenteffects. You may have more than one TIA, and the signs and symptoms maybe similar or different. A TIA indicates a serious risk that a full-blown stroke may follow
Researchers studied 400 patients who were diagnosed at Mayo Clinic'semergency department with either acute ischemic stroke or a transientischemic attack (TIA), a temporary interruption of blood flow to part ofthe brain.Less than half of the patients -- 42 percent -- thought they were havinga stroke. In fact, most in the study did not go to the emergency roomwhen symptoms appeared. The median time from onset of symptoms toarrival at the hospital was over three and a half hours. Most said theythought the symptoms would simply go away. The delay in seeking medicalhelp was the same among men and women.When asked how they knew about stroke symptoms, nearly one-fifth saidthey thought a stroke always came on gradually. Just over half (51.9percent) said they thought that seeking medical care immediately wasimportant.Significance of the findings"Time is crucial in treating stroke," says Latha Stead, M.D., emergencymedicine specialist and lead author of the study. "Each individual'smedical background differs and affects recovery, but in general thesooner a patient experiencing a stroke reaches emergency care, the morelikely the stroke can be limited and the condition managed to preventfurther damage and improve recovery." The researchers say their findingsclearly indicate that better public
understanding of stroke symptomswill lead to a faster response and better outcomes.What you should knowStrokes can happen quickly or can occur over several hours, with thecondition continually worsening. The thrombus or clot that is causingthe stroke can frequently be dissolved or disintegrated so blood canagain flow to the brain. In such cases, immediate treatment can mean thedifference between a slight injury and a major disability. Interestinglyonly 20.8 percent of the participants knew about such treatment. By useof stents, medications and other technology, physicians can stop astroke from spreading and greatly limit damage. Stroke symptoms include:
* Sudden numbness, weakness, or paralysis of your face, arm or leg-- usually on one side of the body
* Sudden difficulty speaking or understanding speech (aphasia)
* Sudden blurred, double or decreased vision
* Sudden dizziness, loss of balance or loss of coordination
* A sudden, severe "bolt out of the blue" headache or an unusualheadache, which may be accompanied by a stiff neck, facial pain, painbetween your eyes, vomiting or altered consciousness
* Confusion or problems with memory, spatial orientation or perceptionIn such cases, a stroke gives no warning. But one possible sign of animpending stroke is a TIA.
The signs and symptoms of TIA are the same asfor a stroke, but they last for a shorter period -- several minutes to afew hours -- and then disappear, without leaving apparent permanenteffects. You may have more than one TIA, and the signs and symptoms maybe similar or different. A TIA indicates a serious risk that a full-blown stroke may follow
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