Employing a measure rarely used in sleep apnea studies, researchers at the UCLA School of Nursing have uncovered evidence of what may be damaging the brain in people with the sleep disorder — weaker brain blood flow.

(Image caption: This brain scan shows that the brain blood flow in a subject with obstructive sleep apnea (left) is markedly lower compared to a subject without the sleep disorder. Credit: UCLA)
In the study, published Aug. 28 in the peer-reviewed journal PLOS ONE, researchers measured blood flow in the brain using a non-invasive MRI procedure: the global blood volume and oxygen dependent (BOLD) signal. This method is usually used to observe brain activity. Because previous research showed that poor regulation of blood in the brain might be a problem for people with sleep apnea, the researchers used the whole-brain BOLD signal to look at blood flow in individuals with and without obstructive sleep apnea (OSA).
“We know there is injury to the brain from sleep apnea, and we also know that the heart has problems pumping blood to the body, and potentially also to the brain,” said Paul Macey, associate dean for Information Technology and Innovations at the UCLA School of Nursing and lead researcher for the study. “By using this method, we were able to show changes in the amount of oxygenated blood across the whole brain, which could be one cause of the damage we see in people with sleep apnea.”
Obstructive sleep apnea is a serious disorder that occurs when a person’s breathing is repeatedly interrupted during sleep, hundreds of times a night. Each time breathing stops, the oxygen level in the blood drops, which damages many cells in the body. If left untreated, it can lead to high blood pressure, stroke, heart failure, diabetes, depression and other serious health problems. Approximately 10 percent of adults struggle with obstructive sleep apnea, which is accompanied by symptoms of brain dysfunction, including extreme daytime sleepiness, depression and anxiety, and memory problems.
In this study, men and women — both with and without obstructive sleep apnea had their BOLD signals measured during three physical tasks while they were awake:
- The Valsalva maneuver: participants forcefully breathe out through a very small tube, which raises the pressure in the chest.
- A hand-grip challenge: participants squeeze hard with their hand.
- A cold pressor challenge: A participants’s right foot is put in icy water for a minute.
“When we looked at the results, we didn’t see much difference between the participants with and without OSA in the Valsalva maneuver,” said Macey. “But for the hand-grip and cold-pressor challenges, people with OSA saw a much weaker brain blood flow response.”
The researchers believe that the reason there were differences in the sleep apnea patients during the hand-grip and cold pressor challenge was because the signals from the nerves in the arms and legs had to be processed through the high brain areas controlling sensation and muscle movement, which was slower due to the brain injury. On the other hand, the changes from the Valsalva are mainly driven by blood pressure signaling in the chest, and do not need the sensory or muscle-controlling parts of the brain.
“This study brings us closer to understanding what causes the problems in the brain of people with sleep apnea,” concluded Macey.
The study also found the problem is greater in women with sleep apnea, which may explain the worse apnea-related outcomes in females than males. Studies recently published by the UCLA School of Nursing have shown that brain injury from sleep apnea is much worse in women than men.
The researchers are now looking at whether treatment for obstructive sleep apnea can reverse the damaging effects.
(Source: newsroom.ucla.edu)
Filed under sleep apnea blood flow brain activity neuroimaging neuroscience science
Device to help people with Parkinson’s disease communicate better now available
SpeechVive Inc. announced Wednesday (Sept. 10) the commercial launch of the SpeechVive device intended to help people with a soft voice due to Parkinson’s disease speak more loudly and communicate more effectively.
The device is now available to try as a demo through the National Parkinson’s Disease Foundation’s Centers of Excellence prior to purchasing. People who suffer from a soft voice due to Parkinson’s disease can make an appointment at any of these centers: the Muhammad Ali Parkinson Center at Barrow Neurological Institute in Phoenix; the University of Florida, Gainesville, Florida; University of North Carolina, Chapel Hill, North Carolina; Struthers Parkinson’s Center, Minneapolis, Minnesota; and Baylor College of Medicine, Waco, Texas.
"We are providing demo units and training at no cost to as many of the National Parkinson’s Centers of Excellence as are interested in offering SpeechVive in conjunction with or as an alternative to speech therapy," said Steve Mogensen, president and CEO of SpeechVive. "We also are offering the SpeechVive units and training to professionals at Veterans Administration Medical Centers across the country. The first VAMC to offer SpeechVive is in Cincinnati, Ohio."
The SpeechVive device also is available to try at the M.D. Steer Speech and Hearing Clinic at Purdue University in West Lafayette, Indiana.
The technology was developed over the past decade by Jessica Huber, associate professor in Purdue’s Department of Speech, Language and Hearing Sciences and licensed through the Purdue Office of Technology Commercialization. The focus of Huber’s research is the development and testing of behavioral treatments to improve communication and quality of life in older adults and people with degenerative motor diseases.
SpeechVive reduces the speech impairments associated with Parkinson’s disease, which cause people with the disease to speak in a hushed, whispery voice and to have mumbled speech. People with Parkinson’s disease are commonly affected in their ability to communicate effectively.
"The clinical data we have collected over the past four years demonstrates that SpeechVive is effective in 90 percent of the people using the device," Huber said. "I am proud of the improvements in communication and quality of life demonstrated in our clinical studies. I look forward to seeing the device on the market so that more people with Parkinson’s disease will have access to it."
More than 1.5 million people in the United States are diagnosed with Parkinson’s disease, and it is one of the most common degenerative neurological diseases. About 89 percent of those with the disease have voice-related change affecting how loudly they speak, and at least 45 percent have speech-related change affecting how clearly they speak.
Filed under parkinson's disease speech speechvive communication neuroscience science
Neuroscientists decode brain maps to discover how we take aim
Serena Williams won her third consecutive US Open title a few days ago, thanks to reasons including obvious ones like physical strength and endurance. But how much did her brain and its egocentric and allocentric functions help the American tennis star retain the cup?
Quite significantly, according to York University neuroscience researchers whose recent study shows that different regions of the brain help to visually locate objects relative to one’s own body (self-centred or egocentric) and those relative to external visual landmarks (world-centred or allocentric).
“The current study shows how the brain encodes allocentric and egocentric space in different ways during activities that involve manual aiming,” explains Distinguished Research Professor Doug Crawford, in the Department of Psychology. “Take tennis for example. Allocentric brain areas could help aim the ball toward the opponent’s weak side of play, whereas the egocentric areas would make sure your muscles return the serve in the right direction.”
The study finding will help healthcare providers to develop therapeutic treatment for patients with brain damage in these two areas, according to the neuroscientists at York Centre for Vision Research.
“As a neurologist, I am excited by the finding because it provides clues for doctors and therapists how they might design different therapeutic approaches,” says Ying Chen, lead researcher and PhD candidate in the School of Kinesiology and Health Science.
The study, Allocentric versus Egocentric Representation of Remembered Reach Targets in Human Cortex, published in the Journal of Neuroscience, was conducted using the state-of-the-art fMRI scanner at York U’s Sherman Health Science Research Centre. A dozen participants were tested using the scanner, which Chen modified to distinguish brain areas relating to these two functions.
The participants were given three different tasks to complete when viewing remembered visual targets: egocentric reach (remembering absolute target location), allocentric reach (remembering target location relative to a visual landmark) and a nonspatial control, colour report (reporting color of target).
When participants remembered egocentric targets’ locations, areas in the upper occipital lobe (at the back of the brain) encoded visual direction. In contrast, lower areas of the occipital and temporal lobes encoded object direction relative to other visual landmarks. In both cases, the parietal and frontal cortex (near the top of the brain) coded reach direction during the movement.
Filed under egocentric allocentric fMRI directional selectivity neuroscience science
(Image caption: Example axial sections of a three-dimensional MPF map (A) obtained from a 63-year old woman with SPMS disease course and results of brain tissue segmentation (B-D). Segmentation masks corresponding to white matter (WM) (B), gray matter (GM) (C), and lesi)
MRI Shows Gray Matter Myelin Loss Strongly Related to MS Disability
People with multiple sclerosis (MS) lose myelin in the gray matter of their brains and the loss is closely correlated with the severity of the disease, according to a new magnetic resonance imaging (MRI) study. Researchers said the findings could have important applications in clinical trials and treatment monitoring. The study appears online in the journal Radiology.
Loss of myelin, the fatty protective sheath around nerve fibers, is a characteristic of MS, an inflammatory disease of the central nervous system that can lead to a variety of serious neurological symptoms and disability. MS is typically considered a disease of the brain’s signal-conducting white matter, where myelin is most abundant, but myelin is also present in smaller amounts in gray matter, the brain’s information processing center that is made up primarily of nerve cell bodies. Though the myelin content in gray matter is small, it is still extremely important to proper function, as it enables protection of thin nerve fibers connecting neighboring areas of the brain cortex, according to Vasily L. Yarnykh, Ph.D., associate professor in the Department of Radiology at University of Washington in Seattle.
“The fact that MS patients lose myelin not only in white but also in gray matter has been proven by earlier post-mortem pathological studies,” he said. “However, the clinical significance of the myelin loss, or demyelination, in gray matter has not been established because of the absence of appropriate imaging methods.”
To learn more about associations between MS and demyelination in both white and gray matter, Dr. Yarnykh and colleagues used a refined MRI technique that provides information on the content of biological macromolecules – molecules present in tissues and composed of a large number of atoms, such as proteins, lipids and carbohydrates. The new method, known as macromolecular proton fraction (MPF) mapping, has been hampered in the past because of the length of time required for data collection, but improvements now allow much faster generation of whole-brain maps that reflect the macromolecular content in tissues.
“The method utilizes a standard MRI scanner and doesn’t require any special hardware—only some software modifications,” Dr. Yarnykh said. “MPF mapping allows quantitative assessment of microscopic demyelination in brain tissues that look normal on clinical images, and is the only existing method able to evaluate the myelin content in gray matter.”
The researchers looked at 30 MS patients, including 18 with relapsing-remitting MS (RRMS), the most common type of MS initially diagnosed, and 12 with the more advanced type of disease known as secondary progressive MS (SPMS). Fourteen healthy control participants were also included in the study. Each participant underwent MRI on a 3-Tesla imager, and the researchers reconstructed 3-D whole-brain MPF maps to look at normal-appearing white matter, gray matter and MS lesions. The researchers further compared the results of their imaging technique with clinical tests characterizing neurological dysfunction in MS patients.
The results showed that MPF was significantly lower in both white and gray matter in RRMS patients compared with healthy controls, and was also significantly reduced in both normal-appearing brain tissues and lesions of SPMS patients compared to RRMS patients with the largest relative decrease in gray matter. MPF in brain tissues of MS patients significantly correlated with clinical disability and the strongest associations were found for gray matter.
“The major finding of the study is that the loss of myelin in gray matter caused by MS in its relative amount is comparable to or even larger than that in white matter,” said Dr. Yarnykh. “Furthermore, gray matter demyelination is much more advanced in patients with secondary-progressive MS, and it is very strongly related to patients’ disability. As such, we believe that information about gray matter myelin damage in MS is of primary clinical relevance.”
The improved technique has potentially important applications for MS treatments targeted to protect and restore myelin.
“First, this method may provide an objective measure of the disease progression and treatment success in clinical trials,” Dr. Yarnykh said. “And second, assessment of both gray and white matter damage with this method may become an individual patient management tool in the future.”
Dr. Yarnykh and colleagues are currently conducting additional research on the new method with the support of the National Multiple Sclerosis Society and the National Institutes of Health.
“This study was done on the participants at a single point in time,” he said. “Now we want to compare MS patients with control participants to see how myelin content will evolve over time. We further plan to extend our method to the spinal cord imaging and test whether the combined assessment of demyelination in the brain and spinal cord could better explain disability progression as compared to brain demyelination alone.”
Filed under MS gray matter myelin sheath demyelination neuroimaging neuroscience science
Kessler Foundation scientists have shown that working memory may be an underlying mechanism of cognitive reserve in multiple sclerosis (MS). This finding informs the relationships between working memory, intellectual enrichment (the proxy measure for cognitive reserve) and long-term memory in this population. “Working memory mediates the relationship between intellectual enrichment and long-term memory in multiple sclerosis: An exploratory analysis of cognitive reserve” was published online ahead of print by the Journal of the International Neuropsychological Society on July 14. The authors are Joshua Sandry, PhD, and research scientist James F. Sumowski, PhD, of Neuropsychological & Neuroscience Research at Kessler Foundation. Dr. Sandry is a postdoctoral fellow funded by a grant from the National MS Society.

Cognitive symptoms, including deficits in long-term memory, are known to affect approximately half of individuals with MS. This study was conducted in 70 patients with MS, who were evaluated for intellectual enrichment, verbal long-term memory, and working memory capacity. “We found that working memory capacity explained the relationship between intellectual enrichment and long-term memory in this population,” said Dr Sandry. “This suggests that interventions targeted at working memory in people with MS may help build cognitive reserve to protect against decline in long-term memory.”
(Source: kesslerfoundation.org)
Filed under MS working memory LTM cognitive reserve cognitive decline neuroscience science
Association between sunshine and suicide examined in study
Lower rates of suicide are associated with more daily sunshine in the prior 14 to 60 days.
Light interacts with brain serotonin systems and possibly influences serotonin-related behaviors. Those behaviors, such as mood and impulsiveness, can play a role in suicide.
The authors examined the relationship between suicide and the duration of sunshine after mathematically removing seasonal variations in sunshine and suicide numbers. They analyzed data on 69,462 officially confirmed suicides in Austria between January 1970 and May 2010. Hours of sunshine per day were calculated from 86 representative meteorological stations.
There was a positive correlation between the number of suicides and hours of daily sunshine on the day of the suicide and up to 10 days before that seemed to facilitate suicide, while sunshine 14 to 60 days prior appeared to have a negative correlation and was associated with reduced suicides. The correlation between daily sunshine hours and suicide rates was seen largely among women, while negative correlations between the two were mainly found among men.
"Owing to the correlative nature of the data, it is impossible to directly attribute the increase in suicide to sunshine during the 10 days prior to the suicide event. … Further research is warranted to determine which patients with severe episodes of depression are more susceptible to the suicide-triggering effects of sunshine."
(Image: Shutterstock)
Filed under suicidal behavior suicide sunshine psychology neuroscience science
Can Your Blood Type Affect Your Memory?
People with blood type AB may be more likely to develop memory loss in later years than people with other blood types, according to a study published in the September 10, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.
AB is the least common blood type, found in about 4 percent of the U.S. population. The study found that people with AB blood were 82 percent more likely to develop the thinking and memory problems that can lead to dementia than people with other blood types. Previous studies have shown that people with type O blood have a lower risk of heart disease and stroke, factors that can increase the risk of memory loss and dementia.
The study was part of a larger study (the REasons for Geographic And Racial Differences in Stroke, or REGARDS Study) of more than 30,000 people followed for an average of 3.4 years. In those who had no memory or thinking problems at the beginning, the study identified 495 participants who developed thinking and memory problems, or cognitive impairment, during the study. They were compared to 587 people with no cognitive problems.
People with AB blood type made up 6 percent of the group who developed cognitive impairment, which is higher than the 4 percent found in the population.
“Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia,” said study author Mary Cushman, MD, MSc, of the University of Vermont College of Medicine in Burlington. “Blood type is also related to other vascular conditions like stroke, so the findings highlight the connections between vascular issues and brain health. More research is needed to confirm these results.”
Researchers also looked at blood levels of factor VIII, a protein that helps blood to clot. High levels of factor VIII are related to higher risk of cognitive impairment and dementia. People in this study with higher levels of factor VIII were 24 percent more likely to develop thinking and memory problems than people with lower levels of the protein. People with AB blood had a higher average level of factor VIII than people with other blood types.
(Image credit)
Filed under blood type memory memory loss dementia cognitive impairment neuroscience science
New Molecular Target is Key to Enhanced Brain Plasticity
As Alzheimer’s disease progresses, it kills brain cells mainly in the hippocampus and cortex, leading to impairments in “neuroplasticity,” the mechanism that affects learning, memory, and thinking. Targeting these areas of the brain, scientists hope to stop or slow the decline in brain plasticity, providing a novel way to treat Alzheimer’s. Groundbreaking new research has discovered a new way to preserve the flexibility and resilience of the brain.
The study, led by Tel Aviv University’s Prof. Illana Gozes and published in Molecular Psychiatry, reveals a nerve cell protective molecular target that is essential for brain plasticity. According to Prof. Gozes, “This discovery offers the world a new target for drug design and an understanding of mechanisms of cognitive enhancement.”
Prof. Gozes is the incumbent of the Lily and Avraham Gildor Chair for the Investigation of Growth Factors and director of the Adams Super Center for Brain Studies at the Sackler Faculty of Medicine and a member of TAU’s Sagol School of Neuroscience. Also contributing to the study were Dr. Saar Oz, Oxana Kapitansky, Yanina Ivashco-Pachima, Anna Malishkevich, Dr. Joel Hirsch, Dr. Rina Rosin-Arbersfeld, and their students, all from TAU. TAU staff scientists Dr. Eliezer Gildai and Dr. Leonid Mittelman provided the state-of-the-art molecular cloning and cellular protein imaging necessary for the study.
Building on past breakthroughs
The new finding is based on Prof. Gozes’ discovery of NAP, a snippet of a protein essential for brain formation (activity-dependent neuroprotective protein [ADNP]). As a result of this discovery, a drug candidate that showed efficacy in mild cognitive impairment patients, a precursor to Alzheimer’s disease, is being developed. NAP protects the brain by stabilizing microtubules — tiny cellular cylinders that provide “railways and scaffolding systems” to move biological material within cells and provide a cellular skeleton. Microtubules are of particular importance to nerve cells, which have long processes and would otherwise collapse. In neurodegenerative diseases like Alzheimer’s, the microtubule network falls apart, hindering cellular communication and cognitive function.
"Clinical studies have shown that Davunetide (NAP) protects memory in patients suffering from mild cognitive impairment preceding Alzheimer’s disease," said Prof. Gozes. "While the mechanism was understood in broad terms, the precise molecular target remained a mystery for years. Now, in light of our new research, we know why and we know how to proceed."
Stabilizing microtubules
The breakthrough was the discovery of the mechanism promoting microtubule growth at the tips of the tubes (“rails”). The researchers found that the NAP structure allows it to bind to the tip of the growing microtubule, the emerging “railway,” through specific microtubule end-binding proteins, which adhere to microtubules a bit like locomotors to provide for growth and forward movement, while the other end of the microtubule may to be disintegrating. These growing tips enlist regulatory proteins that are essential for providing plasticity at the nerve cell connection points, the synapses.
"We have now revealed that ADNP through its NAP motif binds the microtubule end binding proteins and enhances nerve cell plasticity, providing for brain resilience. We then discovered that NAP further enhances ADNP microtubule binding," said Prof. Gozes.
Researchers hope their discovery will help move Davunetide (NAP) and related compounds into further clinical trials, increasing the potential of future clinical use. Prof. Gozes is continuing to investigate microtubule end-binding proteins to better understand their protective properties in the brain.
Filed under alzheimer's disease plasticity ADNP microtubules nerve cells neuroscience science
Brain structure could predict risky behavior
Some people avoid risks at all costs, while others will put their wealth, health, and safety at risk without a thought. Researchers at Yale School of Medicine have found that the volume of the parietal cortex in the brain could predict where people fall on the risk-taking spectrum.
Led by Ifat Levy, assistant professor in comparative medicine and neurobiology at Yale School of Medicine, the team found that those with larger volume in a particular part of the parietal cortex were willing to take more risks than those with less volume in this part of the brain. The findings are published in the Sept. 10 issue of the Journal of Neuroscience.
Although several cognitive and personality traits are reflected in brain structure, there has been little research linking brain structure to economic preferences. Levy and her colleagues sought to examine this question in their study.
Study participants included young adult men and women from the northeastern United States. Participants made a series of choices between monetary lotteries that varied in their degree of risk, and the research team conducted standard anatomical MRI brain scans. The results were first obtained in a group of 28 participants, and then confirmed in a second, independent, group of 33 participants.
“Based on our findings, we could, in principle, use millions of existing medical brains scans to assess risk attitudes in populations,” said Levy. “It could also help us explain differences in risk attitudes based in part on structural brain differences.”
Levy cautions that the results do not speak to causality. “We don’t know if structural changes lead to behavioral changes or vice-versa,” she said.
Levy and her team had previously shown that risk aversion increases as people age, and we scientists also know that the cortex thins substantially with age. “It could be that this thinning explains the behavioral changes; we are now testing that possibility,” said Levy, who also notes that more studies in wider populations are needed.
Filed under risk-taking brain structure neuroimaging risky behavior neuroscience science
The same sex hormone that helps protect females from stroke may also reduce their risk of autism, scientists say.
In the first look at a potential role of the female sex hormone in autism, researchers at the Medical College of Georgia at Georgia Regents University have found expression of estrogen receptor beta – which enables estrogen’s potent brain protection – is significantly decreased in autistic brains. The receptor also plays a role in locomotion as well as behavior, including anxiety, depression, memory, and learning.

"If you ask any psychiatrist seeing patients with autistic behavior their most striking observation from the clinic, they will say there are more males compared to females," said Dr. Anilkumar Pillai, MCG neuroscientist and corresponding author of the study in Molecular Autism.
Estrogen is known to help protect premenopausal women from maladies such as stroke and impaired cognition. Exposure to high levels of the male hormone testosterone during early development has been linked to autism, which is five times more common in males than females.
The new findings of reduced expression of estrogen receptor beta as well as that of an enzyme that converts testosterone to estrogen could help explain the high testosterone levels in autistic individuals and higher autism rates in males, Pillai said.
It was the 5-to-1 male-to-female ratio along with the testosterone hypothesis that led Pillai and his colleagues to pursue whether estrogen might help explain the significant gender disparity and possibly point toward a new treatment.
"The testosterone hypothesis is already there, but nobody had investigated whether it had anything to do with the female hormone in the brain," Pillai said. "Estrogen is known to be neuroprotective, but nobody has looked at whether its function is impaired in the brain of individuals with autism. We found that the children with autism didn’t have sufficient estrogen receptor beta expression to mediate the protective benefits of estrogen."
Comparing the brains of 13 children with and 13 children without autism spectrum disorder, the researchers found a 35 percent decrease in estrogen receptor beta expression as well as a 38 percent reduction in the amount of aromatase, the enzyme that converts testosterone to estrogen.
Levels of estrogen receptor beta proteins, the active molecules that result from gene expression and enable functions like brain protection, were similarly low. There was no discernable change in expression levels of estrogen receptor alpha, which mediates sexual behavior.
The study focused on the brain’s prefrontal cortex, which is involved in social behavior and cognition. Brain tissue from both autistic and healthy subjects was obtained from the Eunice Kennedy Shriver National Institute of Child Health and Human Development Brain and Tissue Bank for Developmental Disorders at the University of Maryland. The children died at an average age of 11 from drowning, other accidents, or suicide. All the brain tissue was from male children except for one control.
While much work remains, estrogen receptor beta agonists, which are already known to improve brain plasticity and memory in animals, might one day help reverse autism’s behavioral deficits, such as reclusiveness and repetitive behavior, Pillai said.
The scientists already are moving to animal studies to see what happens when they reduce estrogen receptor beta expression in mice. They also plan to give an estrogen receptor beta agonist – which should increase receptor function – to a mouse with generalized inflammation and signs of autism to see if it mitigates those signs. Inflammation is a factor in many diseases of the brain and body, and estrogen receptor beta agonists already are in clinical trials for schizophrenia
Larger, follow-up studies should also include comparing expression of testosterone receptor levels in healthy and autistic children, Pillai said. MCG scientists also want to know more about why the reduced beta receptor expression occurs.
Studies published in the journal Molecular Psychiatry earlier this year by scientists at the University of Cambridge and Denmark’s Statens Serum Institute showed that male children who develop autism were exposed to higher levels of steroid hormones, including testosterone and progesterone, during development than their healthy peers.
The incidence of autism has increased about 30 percent in the past two years in the United States, to the current rate of about 1 in 68 children, according to the Centers for Disease Control and Prevention. Most children are diagnosed at about age 4, although the disorder can be diagnosed by about age 2, according to the CDC. Diagnosis is made through extensive behavioral and psychological testing.
(Source: eurekalert.org)
Filed under estrogen sex hormones autism ASD gene expression neuroscience science