Posts tagged neuroscience
Articles and news from the latest research reports.
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.”
Broken signals lead to neurodegeneration
Researchers from the RIKEN Brain Science Institute in Japan, in collaboration with Juntendo University and the Japan Science and Technology Agency, have discovered that a cell receptor widely involved in intracellular calcium signaling—the IP3R receptor—can be locked into a closed state by enzyme action, and that this locking may potentially play a role in the reduction of neuron signaling seen in neurodegenerative diseases such as Huntington’s and Alzheimer’s disease.
In the research published today in the Proceedings of the National Academy of Sciences, the scientists reported experiments in human cells and a mouse model of Huntington’s disease revealing that transglutaminase type 2—a protein cross-linking enzyme elevated in the cells of patients with neurodegenerative diseases—interacts with the IP3R receptor to lock it in a closed non-functional conformation preventing it from fulfilling its essential calcium-releasing role. They identified a specific amino acid site on the receptor, Gln2746, where the modification takes place, deepening our understanding of how receptors are locked and potentially opening the door to studies on other functional proteins that are also regulated by conformational changes.
The IP3R channel, which is located in the endoplasmic reticulum, a protein assembly and transport compartment, plays a crucial role in intracellular calcium signaling, and is involved in a wide range of cell functions including mitochondrial energy production and the regulation of autophagy, the process through which cells consume and degrade unused components to maintain a healthy balance of functional proteins. Although autophagy is normally a mechanism that sustains cell maintenance, it can also trigger a loss of cell function and has been associated with prominent diseases including Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease.
In this work, the scientists propose a general model under which abnormal IP3R-mediated calcium signaling caused by the action of transglutaminase type 2 leads to cellular dysfunction and subsequently to the emergence of progressive brain dysfunction. Transglutaminase 2 activation is commonly associated with inflammation and stress, and its action on the IP3R channel might provide an explanation for the initiation and progression steps common to different neurodegenerative diseases.
According to Katsuhiko Mikoshiba, who led the study, “We think that the mechanism we identified in this study could provide us with a more general model of other diseases both of the brain and other parts of the body, where transglutaminase type 2 is upregulated. We hope that this insight could eventually lead to the development of new drug therapies for a number of neurodegenerative diseases that place a high burden on patients and society.”
Researchers Identify New Rare Neuromuscular Disease
An international team of researchers has identified a new inherited neuromuscular disorder. The rare condition is the result of a genetic mutation that interferes with the communication between nerves and muscles, resulting in impaired muscle control.
The new disease was diagnosed in two families – one in the U.S. and the other in Great Britain – and afflicts multiple generations. The discovery was published in the American Journal of Human Genetics.
“This discovery gives us new insight into the mechanisms of diseases that are caused by a breakdown in neuromuscular signal transmission,” said David Herrmann, M.B.B.Ch., a professor in the Department of Neurology at the University of Rochester School of Medicine and Dentistry and co-lead author of the study. “It is our hope that these findings will help identify new targets for therapies that can eventually be used to treat these diseases.”
The focus of the research is the neuromuscular junction, the point at which the axon fibers that extend from peripheral nerves meet the muscle cells. The chemical signals that pass across the junction are essential for motor function.
There are a number of disorders – both acquired and inherited – that interfere with the communication that occurs at the neuromuscular junction. For example, in Lambert-Eaton myasthenic syndrome, which is most commonly triggered by certain cancers, the body’s own immune system attacks the neuromuscular junction, interrupting signal transmission. These diseases, which are rare, result in muscle weakness and fatigue, primarily in the limbs.
While the families in the study had at one point been diagnosed with other neuromuscular conditions, the researchers identified them as unique, due to their particular motor abnormalities, including problems resembling Lambert-Eaton, and because the disease was passed from one generation to the next.
The researchers compiled a genetic profile of the family members. Specifically, they analyzed the section of DNA code responsible for creating proteins using a technique called whole exome sequencing.
They discovered that the two different families had mutations in the code that creates the protein synaptotagmin 2 (SYT2). Scientists have long understood the function of this protein, but it had never before been associated with a disease in humans.
SYT2 is present at the pre-synaptic terminal, the end of the nerve cell that sits at the neuromuscular junction and helps the cells sense fluctuations in calcium levels. Calcium plays an important role in the electrical function of cells and, in the case of the neuromuscular junction, helps dictate the release of acetylcholine, a chemical responsible for passing communication between the nerve and muscle cells.
In the two families, the mutation disrupted the ability of the nerve cells to sense the changes in calcium levels that would normally trigger the release of acetylcholine. As a result, communication was disrupted and muscle control was impaired.
The authors have used the mutation in SYT2 to create a fruit fly (drosophila) model of the disease. Fruit flies are an important research tool and the study of their neurobiology has contributed greatly to our understanding of neurological development and diseases and the researchers see this as a first step to the development of potential new therapies to treat the condition.
(Source: urmc.rochester.edu)
Control your environment through brain commands
Many patients with amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s Disease) and other neurodegenerative conditions live every day with a frustrating inability to do small, everyday tasks, such as turning on the lights, changing the volume on the TV, or even communicating with their friends and loved ones.
Today, a first-ever proof of concept demonstrates how wearable technology and consumer products can be brought together with digital innovations to let a person with no mobility control their environment using brain commands, via a custom-built tablet application and wearable display interface.
This proof of concept demonstrates the potential to improve the quality of life for ALS patients – or any person with limited muscle and speech function – by giving them the ability to interact, communicate and issue commands without moving their body or using their voice.
Socioeconomic status and structural brain development
Recent advances in neuroimaging methods have made accessible new ways of disentangling the complex interplay between genetic and environmental factors that influence structural brain development. In recent years, research investigating associations between socioeconomic status (SES) and brain development have found significant links between SES and changes in brain structure, especially in areas related to memory, executive control, and emotion. This review focuses on studies examining links between structural brain development and SES disparities of the magnitude typically found in developing countries. We highlight how highly correlated measures of SES are differentially related to structural changes within the brain.
Cockatoos pick up tool use and manufacture through social learning
Two years ago, we brought you the story of Figaro, a Goffin’s cockatoo that lived at a research center in Vienna. These birds don’t use tools in the wild—Figaro’s minders even argue that the cockatoo’s curved beak makes tool use rather difficult for them.
But Figaro’s environment, which features lots of wired mesh, apparently drove him to some novel behaviors. He was observed splitting off splinters from wooden material, and the bird used them to retrieve objects (generally food or toys) that were on the wrong side of the wire. Figaro was making tools.
Chimps Outplay Humans in Brain Games
We humans assume we are the smartest of all creations. In a world with over 8.7 million species, only we have the ability to understand the inner workings of our body while also unraveling the mysteries of the universe. We are the geniuses, the philosophers, the artists, the poets and savants. We amuse at a dog playing ball, a dolphin jumping rings, or a monkey imitating man because we think of these as remarkable acts for animals that, we presume, aren’t smart as us. But what is smart? Is it just about having ideas, or being good at language and math?
Scientists have shown, time and again, that many animals have an extraordinary intellect. Unlike an average human brain that can barely recall a vivid scene from the last hour, chimps have a photographic memory and can memorize patterns they see in the blink of an eye. Sea lions and elephants can remember faces from decades ago. Animals also have a unique sense perception. Sniffer dogs can detect the first signs of colon cancer by the scents of patients, while doctors flounder in early diagnosis. So the point is animals are smart too. But that’s not the upsetting realization. What happens when, for just once, a chimp or a dog challenges man to one of their feats? Well, for one, a precarious face-off – like the one Matt Reeves conceived in the Planet of the Apes – would seem a tad less unlikely than we thought.
In a recent study by psychologists Colin Camerer and Tetsuro Matsuzawa, chimps and humans played a strategy game – and unexpectedly, the chimps outplayed the humans.
(Image: Shutterstock)
Neuroscience: Where is the brain in the Human Brain Project?
Launched in October 2013, the Human Brain Project (HBP) was sold by charismatic neurobiologist Henry Markram as a bold new path towards understanding the brain, treating neurological diseases and building information technology. It is one of two ‘flagship’ proposals funded by the European Commission’s Future and Emerging Technologies programme (see go.nature.com/icotmi). Selected after a multiyear competition, the project seemed like an exciting opportunity to bring together neuroscience and IT to generate practical applications for health and medicine (see go.nature.com/2eocv8).
Contrary to public assumptions that the HBP would generate knowledge about how the brain works, the project is turning into an expensive database-management project with a hunt for new computing architectures. In recent months, the HBP executive board revealed plans to drastically reduce its experimental and cognitive neuroscience arm, provoking wrath in the European neuroscience community.
The crisis culminated with an open letter from neuroscientists (including one of us, G.L.) to the European Commission on 7 July 2014 (see www.neurofuture.eu), which has now gathered more than 750 signatures. Many signatories are scientists in experimental and theoretical fields, and the list includes former HBP participants. The letter incorporates a pledge of non-participation in a planned call for ‘partnering projects’ that must raise about half of the HBP’s total funding. This pledge could seriously lower the quality of the project’s final output and leave the planned databases empty.
With the initial funding, or ‘ramp-up’, phase now in full swing, the European Commission is currently evaluating the HBP directors’ plan for the larger second part of the project. This offers an opportunity to introduce reforms and reconciliation. Here, we offer our analysis of how the HBP project strayed off course and how it might be steered back.
Status and the Brain
Social hierarchy is a fact of life for many animals. Navigating social hierarchy requires understanding one’s own status relative to others and behaving accordingly, while achieving higher status may call upon cunning and strategic thinking. The neural mechanisms mediating social status have become increasingly well understood in invertebrates and model organisms like fish and mice but until recently have remained more opaque in humans and other primates. In a new study in this issue, Noonan and colleagues explore the neural correlates of social rank in macaques. Using both structural and functional brain imaging, they found neural changes associated with individual monkeys’ social status, including alterations in the amygdala, hypothalamus, and brainstem—areas previously implicated in dominance-related behavior in other vertebrates. A separate but related network in the temporal and prefrontal cortex appears to mediate more cognitive aspects of strategic social behavior. These findings begin to delineate the neural circuits that enable us to navigate our own social worlds. A major remaining challenge is identifying how these networks contribute functionally to our social lives, which may open new avenues for developing innovative treatments for social disorders.
Scientists Find Possible Neurobiological Basis for Tradeoff Between Honesty, Self-Interest
What’s the price on your integrity? Tell the truth; everyone has a tipping point. We all want to be honest, but at some point, we’ll lie if the benefit is great enough. Now, scientists have confirmed the area of the brain in which we make that decision.
The result was published online this week in Nature Neuroscience.
(Source: newswise.com)