Posts tagged brain function
Articles and news from the latest research reports.
Just 30 minutes of exercise has benefits for the brain
University of Adelaide neuroscientists have discovered that just one session of aerobic exercise is enough to spark positive changes in the brain that could lead to improved memory and coordination of motor skills.
A study conducted by researchers in the University’s Robinson Research Institute has found changes in the brain that were likely to make it more “plastic” after only 30 minutes of vigorous exercise.
The study involved a small group of healthy people aged in their late 20s to early 30s who rode exercise bikes. They were monitored for changes in the brain immediately after the exercise and again 15 minutes later.
"We saw positive changes in the brain straight away, and these improvements were sustained 15 minutes after the exercise had ended," says research leader Associate Professor Michael Ridding.
"Plasticity in the brain is important for learning, memory and motor skill coordination. The more ‘plastic’ the brain becomes, the more it’s able to reorganise itself, modifying the number and strength of connections between nerve cells and different brain areas."
Associate Professor Ridding says past research has shown that regular physical activity can have positive effects on brain function and plasticity, but it was unknown whether a stand-alone session of exercise would also have similar positive effects.
"We now have evidence suggesting that it does," he says. "This exercise-related change in the brain may, in part, explain why physical activity has a positive effect on memory and higher-level functions."
Associate Professor Ridding says there is now mounting evidence that engaging in aerobic exercise positively influences brain function in many ways - at cellular and molecular levels, as well as in the brain’s architecture.
"Although this was a small sample group, it helps us to better understand the overall picture of how exercise influences the brain," he says.
"We know that plasticity is also important for recovery from brain damage, so this opens up potential therapeutic avenues for patients.
"Further research will be required to see what the possible long-term benefits could be for patients as well as healthy people."
Genes exhibit different behaviours in different stages of development
The effect that genes have on our brain depends on our age. These are the findings of a group of researchers from the MedUni Vienna. It has been known for a number of years that particular genetic variations are of importance for the functioning of neural circuits in the brain. Just how these effects differ in the various stages of life has until recently not been fully understood. This international study has been able to demonstrate that genetic variations at different times in our lives can actually have opposite effects on the brain, which provides an explanation for the differences that clinicians observe in the psychiatric symptoms and response to medications of adolescents and adults.
The group of researchers from Vienna, in collaboration with international cooperation partners, has shown that the effect of a psychiatric risk gene on a resting state network in the forebrain depends greatly on the patient’s age.
The human forebrain is crucial for planning and action, which are closely interwoven with concentration, attention and memory functions. The nerve transmitter substance dopamine orchestrates the activity of neurons in the forebrain in order to ensure an ideal level of functioning. The amount of dopamine in the brain is not constant for life, however. Instead, it rises until adolescence and then falls by the time the individual reaches early adulthood to a much lower level. When the dopaminergic control function collapses, serious mental illnesses such as schizophrenia, depression or attention deficit / hyperactivity disorder (ADHD) can result that usually start around the period of transition to adulthood.
For a number of years, doctors have known that a risk gene involved in dopamine metabolism (COMT) can affect neuronal regulation of the forebrain in adults. Carriers of risk gene variants are more prone to dopaminergic mental illness.
The interaction of genes and stages of development
As part of the study, carried out at the MedUni Vienna’s University Department of Psychiatry and Psychotherapy (led by Siegfried Kasper), the study team used magnetic resonance imaging data from a large random sample of over 200 test subjects to analyse the complex interaction between stages of development and genetic variations in the COMT gene and how it affects the resting state network of the forebrain.
Some of the magnetic resonance scans were performed in Vienna (Centre of Excellent, High-Field MR, Department of MR Physics, Head: Ewald Moser) and some as part of an EU project (Institute of Psychiatry, London, Head: Gunther Schumann). Gene analyses (COMT Val158Met) were carried out in Vienna (Univ. Dept. of Laboratory Medicine, Harald Esterbauer and colleagues) or as part of the EU project.
"Our age has a crucial influence on the effects of psychiatric risk genes. A gene that has positive effects during puberty can be bad for us in adulthood," says study leader Lukas Pezawas, describing the results. In the study, adolescents exhibited contrary gene effects on the brain compared to adults.
The study highlights the dynamism of gene effects on brain function throughout the various stages of life such as adolescence or adulthood. “These results are important for understanding the onset of illness in conditions such as schizophrenia, depression or ADHD, which mostly occur at the threshold of adulthood. Our results also show that there are fundamental differences in the dopamine system between adolescents and adults, which we need to take into account in future treatments”, explains Pezawas.
(Source: meduniwien.ac.at)
New insight on why people with Down syndrome invariably develop Alzheimer’s disease
A new study by researchers at Sanford-Burnham Medical Research Institute reveals the process that leads to changes in the brains of individuals with Down syndrome—the same changes that cause dementia in Alzheimer’s patients. The findings, published in Cell Reports, have important implications for the development of treatments that can prevent damage in neuronal connectivity and brain function in Down syndrome and other neurodevelopmental and neurodegenerative conditions, including Alzheimer’s disease.
Down syndrome is characterized by an extra copy of chromosome 21 and is the most common chromosome abnormality in humans. It occurs in about one per 700 babies in the United States, and is associated with a mild to moderate intellectual disability. Down syndrome is also associated with an increased risk of developing Alzheimer’s disease. By the age of 40, nearly 100 percent of all individuals with Down syndrome develop the changes in the brain associated with Alzheimer’s disease, and approximately 25 percent of people with Down syndrome show signs of Alzheimer’s-type dementia by the age of 35, and 75 percent by age 65. As the life expectancy for people with Down syndrome has increased dramatically in recent years—from 25 in 1983 to 60 today—research aimed to understand the cause of conditions that affect their quality of life are essential.
"Our goal is to understand how the extra copy of chromosome 21 and its genes cause individuals with Down syndrome to have a greatly increased risk of developing dementia," said Huaxi Hu, Ph.D., professor in the Degenerative Diseases Program at Sanford-Burnham and senior author of the paper. "Our new study reveals how a protein called sorting nexin 27 (SNX27) regulates the generation of beta-amyloid—the main component of the detrimental amyloid plaques found in the brains of people with Down syndrome and Alzheimer’s. The findings are important because they explain how beta-amyloid levels are managed in these individuals."
Beta-Amyloid, Plaques and Dementia
Xu’s team found that SNX27 regulates beta-amyloid generation. Beta-amyloid is a sticky protein that’s toxic to neurons. The combination of beta-amyloid and dead neurons form clumps in the brain called plaques. Brain plaques are a pathological hallmark of Alzheimer’s disease and are implicated in the cause of the symptoms of dementia.
"We found that SNX27 reduces beta-amyloid generation through interactions with gamma-secretase—an enzyme that cleaves the beta-amyloid precursor protein to produce beta-amyloid," said Xin Wang, Ph.D., a postdoctoral fellow in Xu’s lab and first author of the publication. "When SNX27 interacts with gamma-secretase, the enzyme becomes disabled and cannot produce beta-amyloid. Lower levels of SNX27 lead to increased levels of functional gamma-secretase that in turn lead to increased levels of beta-amyloid."
SNX27’s Role in Brain Function
Previously, Xu and colleagues found that SNX27 deficient mice shared some characteristics with Down syndrome, and that humans with Down syndrome have significantly lower levels of SNX27. In the brain, SNX27 maintains certain receptors on the cell surface—receptors that are necessary for neurons to fire properly. When levels of SNX27 are reduced, neuron activity is impaired, causing problems with learning and memory. Importantly, the research team found that by adding new copies of the SNX27 gene to the brains of Down syndrome mice, they could repair the memory deficit in the mice.
The researchers went on to reveal how lower levels of SNX27 in Down syndrome are the result of an extra copy of an RNA molecule encoded by chromosome 21 called miRNA-155. miRNA-155 is a small piece of genetic material that doesn’t code for protein, but instead influences the production of SNX27.
With the current study, researchers can piece the entire process together—the extra copy of chromosome 21 causes elevated levels of miRNA-155 that in turn lead to reduced levels of SNX27. Reduced levels of SNX27 lead to an increase in the amount of active gamma-secretase causing an increase in the production of beta-amyloid and the plaques observed in affected individuals.
"We have defined a rather complex mechanism that explains how SNX27 levels indirectly lead to beta-amyloid," said Xu. "While there may be many factors that contribute to Alzheimer’s characteristics in Down syndrome, our study supports an approach of inhibiting gamma-secretase as a means to prevent the amyloid plaques in the brain found in Down syndrome and Alzheimer’s."
"Our next step is to develop and implement a screening test to identify molecules that can reduce the levels of miRNA-155 and hence restore the level of SNX27, and find molecules that can enhance the interaction between SNX27 and gamma-secretase. We are working with the Conrad Prebys Center for Chemical Genomics at Sanford-Burnham to achieve this," added Xu.
(Image caption: This image shows the brain’s default mode network, where memory and sensory information are stored. Credit: Marcus Raichle, Washington University)
What happens to your brain when your mind is at rest?
For many years, the focus of brain mapping was to examine changes in the brain that occur when people are attentively engaged in an activity. No one spent much time thinking about what happens to the brain when people are doing very little.
But Marcus Raichle, a professor of radiology, neurology, neurobiology and biomedical engineering at Washington University in St. Louis, has done just that. In the 1990s, he and his colleagues made a pivotal discovery by revealing how a specific area of the brain responds to down time.
"A great deal of meaningful activity is occurring in the brain when a person is sitting back and doing nothing at all," says Raichle, who has been funded by the National Science Foundation (NSF) Division of Behavioral and Cognitive Sciences in the Directorate for Social, Behavioral and Economic Sciences. "It turns out that when your mind is at rest, dispersed brain areas are chattering away to one another."
The results of these discoveries now are integral to studies of brain function in health and disease worldwide. In fact, Raichle and his colleagues have found that these areas of rest in the brain—the ones that ultimately became the focus of their work—often are among the first affected by Alzheimer’s disease, a finding that ultimately could help in early detection of this disorder and a much greater understanding of the nature of the disease itself.
For his pioneering research, Raichle this year was among those chosen to receive the prestigious Kavli Prize, awarded by The Norwegian Academy of Science and Letters. It consists of a cash award of $1 million, which he will share with two other Kavli recipients in the field of neuroscience.
His discovery was a near accident, actually what he calls “pure serendipity.” Raichle, like others in the field at the time, was involved in brain imaging, looking for increases in brain activity associated with different tasks, for example language response.
In order to conduct such tests, scientists first needed to establish a baseline for comparison purposes which typically complements the task under study by including all aspects of the task, other than just the one of interest.
"For example, a control task for reading words aloud might be simply viewing them passively," he says.
In the Raichle laboratory, they routinely required subjects to look at a blank screen. When comparing this simple baseline to the task state, Raichle noticed something.
"We didn’t specify that you clear your mind, we just asked subjects to rest quietly and don’t fall asleep," he recalls. "I don’t remember the day I bothered to look at what was happening in the brain when subjects moved from this simple resting state to engagement in an attention demanding task that might be more involved than simply increases in brain activity associated with the task.
"When I did so, I observed that while brain activity in some parts of the brain increased as expected, there were other areas that actually decreased their activity as if they had been more active in the ‘resting state,"’ he adds. "Because these decreases in brain activity were so dramatic and unexpected, I got into the habit of looking for them in all of our experiments. Their consistency both in terms of where they occurred and the frequency of their occurrence—that is, almost always—really got my attention. I wasn’t sure what was going on at first but it was just too consistent to not be real."
These observations ultimately produced ground-breaking work that led to the concept of a default mode of brain function, including the discovery of a unique fronto-parietal network in the brain. It has come to be known as the default mode network, whose regions are more active when the brain is not actively engaged in a novel, attention-demanding task.
"Basically we described a core system of the brain never seen before," he says. "This core system within the brain’s two great hemispheres increasingly appears to be playing a central role in how the brain organizes its ongoing activities"
The discovery of the brain’s default mode caused Raichle and his colleagues to reconsider the idea that the brain uses more energy when engaged in an attention-demanding task. Measurements of brain metabolism with PET (positron emission tomography) and data culled from the literature led them to conclude that the brain is a very expensive organ, accounting for about 20 percent of the body’s energy consumption in an adult human, yet accounting for only 2 percent of the body weight.
"The changes in activity associated with the performance of virtually any type of task add little to the overall cost of brain function," he continues. "This has initiated a paradigm shift in brain research that has moved increasingly to studies of the brain’s intrinsic activity, that is, its default mode of functioning."
Raichle, whose work on the role of this intrinsic brain activity on facets of consciousness was supported by NSF, is also known for his research in developing and using imaging techniques, such as positron emission tomography, to identify specific areas of the brain involved in seeing, hearing, reading, memory and emotion.
In addition, his team studied chemical receptors in the brain, the physiology of major depression and anxiety, and has evaluated patients at risk for stroke. Currently, he is completing research studying what happens to the brain under anesthesia.
"The brain is capable of so many things, even when you are not conscious," Raichle says. "If you are unconscious, the organization of the brain is maintained, but it is not the same as being awake."
Fixing a faulty molecular ‘transport hub’ could slow brain degeneration
University of Queensland researchers have gained new insights into how the body sorts and transports protein ‘cargo’ within our cells, in a finding that could eventually lead to treatments for neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
An international research team co-led by Dr Brett Collins from UQ’s Institute for Molecular Bioscience has revealed the structure of a molecular transport hub that sorts, directs and transports protein to correct destinations in the cell.
Dr Collins said protein cargoes that failed to reach the correct destinations in cells created ‘traffic jams’ that could affect neuronal activity and brain function.
“Having an understanding of how these proteins work together to sort and transport cargo could be the first step in developing drugs that reverse the effects of toxic protein accumulation in neurodegenerative disease,” he said.
Dr Collins has been studying how cargo is sorted, packaged, and trafficked within human cells for more than a decade.
He said that developing drugs that fix faulty proteins such as the transport hub was a relatively new and exciting approach to treatment.
“Traditionally, drugs are developed to try to block or inhibit the function of proteins in the body,” Dr Collins said.
“The problem with drugs that completely stop the function of a protein is that you often get harmful side-effects.”
Dr Collins said the promising finding provided new avenues to target multiple parts of the transport hub to enhance its function by stabilising the protein.
“If we can enhance or improve the function of this protein we could potentially slow down the brain degeneration that occurs in diseases such as Alzheimer’s and Parkinson’s,” he said.
(Source: uq.edu.au)
Scientists Identify the Signature of Aging in the Brain
How the brain ages is still largely an open question – in part because this organ is mostly insulated from direct contact with other systems in the body, including the blood and immune systems. In research that was recently published in Science, Weizmann Institute researchers Prof. Michal Schwartz of the Neurobiology Department and Dr. Ido Amit of Immunology Department found evidence of a unique “signature” that may be the “missing link” between cognitive decline and aging. The scientists believe that this discovery may lead, in the future, to treatments that can slow or reverse cognitive decline in older people.
(Image caption: Immunofluorescence microscope image of the choroid plexus. Epithelial cells are in green and chemokine proteins (CXCL10) are in red)
Until a decade ago, scientific dogma held that the blood-brain barrier prevents the blood-borne immune cells from attacking and destroying brain tissue. Yet in a long series of studies, Schwartz’s group had shown that the immune system actually plays an important role both in healing the brain after injury and in maintaining the brain’s normal functioning. They have found that this brain-immune interaction occurs across a barrier that is actually a unique interface within the brain’s territory.
This interface, known as the choroid plexus, is found in each of the brain’s four ventricles, and it separates the blood from the cerebrospinal fluid. Schwartz: “The choroid plexus acts as a ‘remote control’ for the immune system to affect brain activity. Biochemical ‘danger’ signals released from the brain are sensed through this interface; in turn, blood-borne immune cells assist by communicating with the choroid plexus. This cross-talk is important for preserving cognitive abilities and promoting the generation of new brain cells.”
This finding led Schwartz and her group to suggest that cognitive decline over the years may be connected not only to one’s “chronological age” but also to one’s “immunological age,” that is, changes in immune function over time might contribute to changes in brain function – not necessarily in step with the count of one’s years.
To test this theory, Schwartz and research students Kuti Baruch and Aleksandra Deczkowska teamed up with Amit and his research group in the Immunology Department. The researchers used next-generation sequencing technology to map changes in gene expression in 11 different organs, including the choroid plexus, in both young and aged mice, to identify and compare pathways involved in the aging process.
That is how they identified a strikingly unique “signature of aging” that exists solely in the choroid plexus – not in the other organs. They discovered that one of the main elements of this signature was interferon beta – a protein that the body normally produces to fight viral infection. This protein appears to have a negative effect on the brain: When the researchers injected an antibody that blocks interferon beta activity into the cerebrospinal fluid of the older mice, their cognitive abilities were restored, as was their ability to form new brain cells. The scientists were also able to identify this unique signature in elderly human brains. The scientists hope that this finding may, in the future, help prevent or reverse cognitive decline in old age, by finding ways to rejuvenate the “immunological age” of the brain.
(Source: wis-wander.weizmann.ac.il)
New EEG electrode set for fast and easy measurement of brain function abnormalities
A new, easy-to-use EEG electrode set for the measurement of the electrical activity of the brain was developed in a recent study completed at the University of Eastern Finland. The solutions developed in the PhD study of Pasi Lepola, MSc, make it possible to attach the electrode set on the patient quickly, resulting in reliable results without any special treatment of the skin. As EEG measurements in emergency care are often performed in challenging conditions, the design of the electrode set pays particular attention to the reduction of electromagnetic interference from external sources.
EEG measurements can be used to detect such abnormalities in the electrical activity of the brain that require immediate treatment. These abnormalities are often indications of severe brain damage, cerebral infarction, cerebral haemorrhage, poisoning, or unspecified disturbed levels of consciousness. One of the most serious brain function abnormalities is a prolonged epileptic seizure, status epilepticus, which is impossible to diagnose without an EEG measurement. In many cases, a rapidly performed EEG measurement and the start of a proper treatment significantly reduces the need for aftercare and rehabilitation. This, in turn, drastically improves the cost-effectiveness of the treatment chain.
Although the benefits of EEG measurements are indisputable, they remain underused in acute and emergency care. A significant reason for this is the fact that the electrode sets available on the markets are difficult to attach on the patient, and their use requires special skills and constant training. This new type of an electrode set is expected to provide solutions for making EEG measurements feasible at as an early stage as possible.
The EEG electrode set was produced using screen printing technology, in which silver ink was used to print the conductors and measurement electrodes on a flexible polyester film. The EEG electrode set consists of 16 hydrogel-coated electrodes which, unlike in the traditional method, are placed on the hair-free areas of the patient’s head, making it easy to attach. The new EEG electrode set significantly speeds up the measurement process because there is no need to scrape the patient’s skin or to use any separate gels. As the electrode set is flexible and solid, the electrodes get automatically placed in their correct places. Furthermore, there is no need to move the patient’s head when putting on the EEG electrode set, which is especially important in patients possibly suffering from a neck or skull injury. Due to the fact that the disposable electrode set is easy and fast to use, it is particularly well-suited to be used in emergency care, in ambulances and even in field conditions. Thanks to the materials used, the electrode set does not interfere with any magnetic resonance or computed tomography imaging the patient may undergo.
The performance of the electrode set was tested by using various electrical tests, on several volunteers, and in real patient cases. The results were compared to those obtained by traditional EEG methods.
The PhD study also focused on the use of screen printing technology solutions to protect electrodes against electromagnetic interference. The silver or graphite shielding layer printed to the outer edge of the electrode set was discovered to significantly reduce external interference on the EEG signal. This shielding layer can be easily and cost-efficiently introduced to all measurement electrodes produced with similar methods. Protecting the electrode with a shielding layer is beneficial when measuring weak signals in conditions that contain external interference.
(Source: uef.fi)
Single dose of antidepressant changes the brain
A single dose of antidepressant is enough to produce dramatic changes in the functional architecture of the human brain. Brain scans taken of people before and after an acute dose of a commonly prescribed SSRI (serotonin reuptake inhibitor) reveal changes in connectivity within three hours, say researchers who report their observations in the Cell Press journal Current Biology on September 18.
"We were not expecting the SSRI to have such a prominent effect on such a short timescale or for the resulting signal to encompass the entire brain," says Julia Sacher of the Max Planck Institute for Human Cognitive and Brain Sciences.
While SSRIs are among the most widely studied and prescribed form of antidepressants worldwide, it’s still not entirely clear how they work. The drugs are believed to change brain connectivity in important ways, but those effects had generally been thought to take place over a period of weeks, not hours.
The new findings show that changes begin to take place right away. Sacher says what they are seeing in medication-free individuals who had never taken antidepressants before may be an early marker of brain reorganization.
Study participants let their minds wander for about 15 minutes in a brain scanner that measures the oxygenation of blood flow in the brain. The researchers characterized three-dimensional images of each individual’s brain by measuring the number of connections between small blocks known as voxels (comparable to the pixels in an image) and the change in those connections with a single dose of escitalopram (trade name Lexapro).
Their whole-brain network analysis shows that one dose of the SSRI reduces the level of intrinsic connectivity in most parts of the brain. However, Sacher and her colleagues observed an increase in connectivity within two brain regions, specifically the cerebellum and thalamus.
The researchers say the new findings represent an essential first step toward clinical studies in patients suffering from depression. They also plan to compare the functional connectivity signature of brains in recovery and those of patients who fail to respond after weeks of SSRI treatment.
Understanding the differences between the brains of individuals who respond to SSRIs and those who don’t “could help to better predict who will benefit from this kind of antidepressant versus some other form of therapy,” Sacher says. “The hope that we have is that ultimately our work will help to guide better treatment decisions and tailor individualized therapy for patients suffering from depression.”
Network measures predict neuropsychological outcome after brain injury
Cognitive neuroscience research has shown that certain brain regions are associated with specific cognitive abilities, such as language, naming, and decision-making.
How and where these specific abilities are integrated in the brain to support complex cognition is still under investigation. However, researchers at the University of Iowa and Washington University in St. Louis, Missouri, believe that several hub regions may be especially important for the brain to function as an integrated network.
In research published online Sept. 15 in the Early Edition of the Proceedings of the National Academy of Sciences, scientists studied neurological patients with focal brain damage, and found that damage to six hub locations—identified in a model developed at Washington University using resting state fMRI, functional connectivity analyses, and graph theory—produced much greater cognitive impairment than damage to other locations.
Doctors have long observed that despite having similar locations or extent of brain injury, patients often present with wide-ranging degrees of impairment and exhibit different recovery trajectories. A better understanding of brain networks and hubs may improve the understanding of outcomes of brain injuries (for example, stroke, resection, or trauma) and help inform prognosis and rehabilitation efforts.
“We were able to identify a set of brain hubs and show that damage to those locations unexpectedly causes widespread cognitive impairments,” says David Warren, cognitive neuroscientist at the University of Iowa and lead study author. “We hope that this framework will help neurologists with diagnosis and prognosis, and neurosurgeons with surgical planning.”
Two contrasting views of brain hubs exist. One view focuses on the sheer number of connections between brain regions, with those regions showing the most connections considered hubs.
Warren and his colleagues contend that the number of connections a given region makes may not reflect the importance of a region to network function because it can be strongly influenced by network size. Instead, their framework defines hubs as brain regions that show correlated activity with multiple brain systems (rather than regions). The authors predicted that because hubs should be critical for brain function and complex cognition, damage to true hubs should produce widespread cognitive impairment.
This study evaluated long-term cognitive and behavioral data in 30 patients in the Iowa Neurological Patient Registry—19 with focal damage to one of the authors’ six target hub locations and 11 with damage to two control locations that fit the alternative hub definition.
On average, patients with lesions to target hubs had significant impairment in nine major cognitive domains—orientation/attention, perception, memory, language skills, motor performance, concept formation/reasoning, executive functions, emotional functions, and adaptive functions. In contrast, the group with lesions to control hubs was significantly impaired in just three of the nine domains (executive functions, emotional functions, and adaptive functions).
Additionally, the target group had significantly greater cognitive deficits than the control group in seven of nine domains (all except perception and emotional functions), again showing the widespread cognitive effects of target hub lesions.
“With a grant from the McDonnell Foundation, we’re planning to follow up by exploring the effects of damage to additional brain hubs, examining how damage to hubs alters brain activation, and studying neurosurgery patients prospectively before and after their surgeries,” says senior study author Daniel Tranel, professor of neurology in the UI Carver College of Medicine and psychology in the College of Liberal Arts and Sciences. “We think that this work could have a tremendous influence on clinical practice.”
(Source: now.uiowa.edu)
Brain damage caused by severe sleep apnea is reversible
A neuroimaging study is the first to show that white matter damage caused by severe obstructive sleep apnea can be reversed by continuous positive airway pressure therapy. The results underscore the importance of the “Stop the Snore” campaign of the National Healthy Sleep Awareness Project, a collaboration between the Centers for Disease Control and Prevention, American Academy of Sleep Medicine, Sleep Research Society and other partners.
Results show that participants with severe, untreated sleep apnea had a significant reduction in white matter fiber integrity in multiple brain areas. This brain damage was accompanied by impairments to cognition, mood and daytime alertness. Although three months of CPAP therapy produced only limited improvements to damaged brain structures, 12 months of CPAP therapy led to an almost complete reversal of white matter abnormalities. Treatment also produced significant improvements in nearly all cognitive tests, mood, alertness and quality of life.
“Structural neural injury of the brain of obstructive sleep apnea patients is reversible with effective treatment,” said principal investigator and lead author Vincenza Castronovo, PhD, clinical psychologist at the Sleep Disorders Center at San Raffaele Hospital and Vita-Salute San Raffaele University in Milano, Italy. “Treatment with CPAP, if patients are adherent to therapy, is effective for normalizing the brain structure.”
The study results are published in the September issue of the journal Sleep.
“Obstructive sleep apnea is a destructive disease that can ruin your health and increase your risk of death,” said American Academy of Sleep Medicine President Dr. Timothy Morgenthaler, a national spokesperson for the Healthy Sleep Project. “Treatment of sleep apnea can be life-changing and potentially life-saving.”
The “Stop the Snore” campaign was launched recently to encourage people to talk to a doctor about the warning signs for sleep apnea, which afflicts at least 25 million adults in the U.S. Sleep apnea warning signs include snoring and choking, gasping or silent breathing pauses during sleep. Pledge to stop the snore at www.stopsnoringpledge.org.
The study involved 17 men with severe, untreated obstructive sleep apnea who had an average age of 43 years. They were evaluated at baseline and after both three months and 12 months of treatment with CPAP therapy. At each time point they underwent a neuropsychological evaluation and a diffusion tensor imaging examination. DTI is a form of magnetic resonance imaging that measures the flow of water through brain tissue. Participants were compared with 15 age-matched, healthy controls who were evaluated only at baseline.
A previous study by Castronovo’s research team found similar damage to gray matter volume in multiple brain regions of people with severe sleep apnea. Improvements in gray matter volume appeared after three months of CPAP therapy. According to the authors, the two studies suggest that the white matter of the brain takes longer to respond to treatment than the gray matter.
“We are seeing a consistent message that the brain can improve with treatment,” said co-principal investigator Mark Aloia, PhD, Associate Professor of Medicine at National Jewish Health in Denver, Colorado, and Senior Director of Global Clinical Research for Philips Respironics, Inc. “We know that PAP therapy keeps people breathing at night; but demonstrating effects on secondary outcomes is critical, and brain function and structure are strong secondary outcomes.”