1. Electrical ‘switch’ in brain’s capillary network monitors activity and controls blood flow

    March 29, 2017 by Ashley

    From the Larner College of Medicine at the University of Vermont press release:

    All it takes is the flip of a protein “switch” within the tiny wire-like capillaries of the brain to increase the blood flow that ensures optimal brain function. New research has uncovered that capillaries have the capacity to both sense brain activity and generate an electrical vasodilatory signal to evoke blood flow and direct nutrients to nourish hard-working neurons.

    These findings were reported online in Nature Neuroscience.

    When there is an increase in brain activity, there is an increase in blood flow, says Thomas Longden, Ph.D., assistant professor of pharmacology at the Larner College of Medicine at the University of Vermont and first author of the study. “The area of the brain covered by the capillaries — the smallest blood vessels in the body — vastly surpasses the area covered by arterioles. This ideally positions them for monitoring neuronal activity and controlling blood flow.”

    Understanding the mechanisms that precisely direct cerebrovascular blood flow to satisfy the brain’s ever-changing energy needs has, to date, eluded scientists. Neurons consume an enormous amount of the body’s energy supplies — about 20 percent — yet lack their own reserves, so are reliant on blood to deliver nutrients. Previously, capillaries were thought to be passive tubes and the arterioles were thought to be the source of action. Now, Longden and colleagues have discovered that capillaries actively control blood flow by acting like a series of wires, transmitting electrical signals to direct blood to the areas that need it most.

    To achieve this feat, the capillary sensory network relies on a protein (an ion channel) that detects increases in potassium during neuronal activity. Increased activity of this channel facilitates the flow of ions across the capillary membrane, thereby creating a small electrical current that generates a negative charge — a rapidly transmitted signal — that communicates the need for additional blood flow to the upstream arterioles, which then results in increased blood flow to the capillaries.

    The team’s study also determined that if the potassium level is too high, this mechanism can be disabled, which may contribute to blood flow disturbances in a broad range of brain disorders.

    “These findings open new avenues in the way we can investigate cerebral diseases with a vascular component,” says co-first author Fabrice Dabertrand, Ph.D., an assistant professor of pharmacology at the University of Vermont’s Larner College of Medicine. Cerebrovascular illnesses like Alzheimer’s disease, CADASIL, and other conditions that cause cognitive decline can, in part, be a consequence of neurons not receiving enough blood flow and therefore not getting sufficient nutrients.

    “If you’re hungry, you’re not able to do your best work; it may be the same for neurons,” says Dabertrand, who adds that the group’s next phase of research will focus on exploring potential pathological factors involved in disabling the capillary potassium-sensing mechanism.

    An image from the Vermont team’s research will be featured on the cover of the May 2017 issue of Nature Neuroscience.


  2. On the trail of Parkinson’s disease

    March 28, 2017 by Ashley

    From the University of Konstanz press release:

    In a complex series of experiments they examined what the effects were of changing a single amino acid in the protein. The physicochemists were able to prove how this tiny change disturbs the binding of alpha-synuclein to membranes. “We hope that the finding of this selectively defective membrane binding will help us to understand how Parkinson’s develops on a molecular level. Ultimately, this will facilitate the devising of therapeutic strategies,” outlines Julia Cattani, a doctoral student, who played a major role in the success of the research. The research results were revealed in the Journal of the American Chemical Society publication in its 16 March 2017 online edition; a print version is to follow.

    The human brain contains large quantities of the small alpha-synuclein protein. Its exact biological function is still unknown, yet it is closely linked to Parkinson’s disease; the protein “clumps together” in the nerve cells of Parkinson patients. Alpha-synuclein consists of a chain of 140 amino acids. In rare cases Parkinson’s disease is hereditary; where this occurs one of these 140 components has been replaced. Malte Drescher and his working group in the Department of Chemistry at the University of Konstanz have now found out the influence these selective changes in the protein sequence can have on the behaviour of alpha-synuclein. “We can show that the selective mutations disturb the membrane binding of alpha-synuclein on a local level,” explains Malte Drescher.

    To find out more about the influence of selective mutations, the Konstanz-based chemists Dr Marta Robotta and Julia Cattani applied tiny magnetic probe molecules to various places on the alpha-synuclein protein. With the help of electron paramagnetic resonance spectroscopy — a procedure similar in method to magnetic resonance imaging (MRI) used in the medical field — the researchers were able to measure the rotation of these nanomagnets. At every residue at which alpha-synuclein binds to a membrane, the rotation slows down. In this way they were able to find out precisely when and where a binding to the membranes takes place — and when it does not. In the case of the exchanged amino acids the physicochemists from Konstanz discovered a disturbance of the membrane binding of alpha-synuclein — an important clue for the molecular context of Parkinson’s disease.

    “We went to great lengths, performing over 200 spectroscopic experiments, the results of which we compared with our models by means of a specially developed simulation algorithm. The outcome certainly compensated our efforts,” says Julia Cattani. Project leader Malte Drescher believes that alongside the huge commitment of his staff, an important prerequisite for the success of the research was, above all, the environment of the Collaborative Research Centre (SFB) 969, “Chemical and biological principles of cellular proteostasis” which formed the basis for sponsoring the project: “By networking on an interdisciplinary level and discussing with colleagues we managed to solve the many problems we faced,” emphasises Malte Drescher.


  3. Study shows how brain combines subtle sensory signals to take notice

    by Ashley

    From the Brown University press release:

    A new study describes a key mechanism in the brain that allows animals to recognize and react when subtle sensory signals that might not seem important on their own occur simultaneously. Such “multisensory integration” (MSI) is a vital skill for young brains to develop, said the authors of the paper in eLife, because it shapes how effectively animals can make sense of their surroundings.

    For a mouse, that ability can make the difference between life and death. Neither a faint screech nor a tiny black speck in the sky might trigger any worry, but the two together strongly suggest a hawk is in the air. It matters in daily human life, too. An incoming call on a cell phone can be more noticeable when it is signaled visually and with sound, for example.

    “It’s really important to understand how all of our senses interact to give us a whole picture of the world,” said study lead author Torrey Truszkowski, a neuroscience doctoral student at Brown University. “If something is super salient in the visual system — a bright flash of light — you don’t need the multisensory mechanism. If there is only a small change in light levels, you might ignore it — but if in the same area of visual space you also have a piece of auditory information coming in, then you are more likely to notice that and decide if you need to do something about that.”

    To understand how that happens, Truszkowski and her team performed the new study in tadpoles. The juvenile frogs turn out to be a very convenient model of a developing MSI architecture that has a direct analog in the brains of mammals including humans.

    Neuroscientists call the key property the tadpoles modeled in this study, the ability of brain cells and circuits to sometimes respond strongly to faint signals, “inverse effectiveness.” Study senior author Carlos Aizenman, associate professor of neuroscience and member of the Brown Institute for Brain Science, said the new paper represents, “the first cellular-level explanation of inverse effectiveness, a property of MSI that allows the brain to selectively amplify weak sensory inputs from single sources and that represent multiple sensory modalities.”

    Tadpole trials

    To achieve that explanation at the level of cells and proteins, the researchers started with behavior. Tadpoles swimming in a laboratory dish will speed up — as if startled — when they detect a strong and sudden sensory stimulus, such as a pattern of stripes projected from beneath or a loud clicking sound. In their first experiment, the researchers measured changes in swimming speed when they provided strong stimuli, then weaker stimuli, and finally weaker stimuli in combination.

    What they found is that more subtle versions of the stimuli — for example, stripes with only 25 percent of maximum contrast — barely affected swim speed when presented alone. But when such subtle stripes were presented simultaneously with subtle clicks, they produced a startle response as great as when full-contrast stripes were projected on the dish.

    To understand how that works in the brain, the researchers conducted further experiments where they made measurements in a region called the optic tectum where tadpoles process sensory information. In mammals such as humans, the same function is performed by cells in the superior colliculus. The tadpole optic tectum sits right at the top of the brain. Given that fortuitous position and the animals’ transparent skin, scientists can easily observe the activity of cells and networks in living, behaving tadpoles using biochemistry to make different cells light up when they are active.

    In many individual cells and across networks in the optic tectum, the researchers found that neural activity barely budged when tadpoles saw, heard or felt a subtle stimulus individually, but it jumped tremendously when subtle stimuli were simultaneous. The “inverse effectiveness” apparent in the swim speed behavior had a clear correlate in the response of brain cells and networks that process the senses.

    The key question was how that inverse effectiveness works. The team had two molecular suspects in mind: a receptor for the neurotransmitter GABA or a specific type of glutamate receptor called NMDA. In experiments, they used chemicals to block receptors for either. They found the blocking GABA didn’t affect inverse effectiveness but that blocking NMDA made a significant difference.

    NMDA’s role makes sense because it is already known to matter in detecting coincidence, for instance when the spiny dendrites of a neuron receive simultaneous signals from other neurons. Truszkowski said the study shows that NMDA is crucial for inverse effectiveness in MSI, though it might not be the only receptor at work.

    Developing the senses

    The research is part of a larger study of multisensory integration in Aizenman’s lab. Last year, as part of the same investigation, the researchers found that developing tadpole brains refine their judgment of whether stimuli are truly simultaneous as they progressively change the balance of excitation and inhibition among neurons in the optic tectum.

    Aizenman’s lab seeks to understand how perception develops early in life, not only as a matter of basic science but also because it could provide insights into human disorders in which sensory processing develops abnormally, as in some forms of autism.

    The lab has an autism model in tadpoles. Truszkowski said an interesting next step could be to conduct these experiments with those tadpoles.


  4. Spiritual retreats change feel-good chemical systems in the brain

    by Ashley

    From the Thomas Jefferson University press release:

    More Americans than ever are turning to spiritual, meditative and religious retreats as a way to reset their daily life and enhance wellbeing. Now, researchers at The Marcus Institute of Integrative Health at Thomas Jefferson University show there are changes in the dopamine and serotonin systems in the brains of retreat participants. The team published their results in Religion, Brain & Behavior.

    “Since serotonin and dopamine are part of the reward and emotional systems of the brain, it helps us understand why these practices result in powerful, positive emotional experiences,” said Andrew Newberg, M.D., Director of Research in the Marcus Institute of Integrative Health. “Our study showed significant changes in dopamine and serotonin transporters after the seven-day retreat, which could help prime participants for the spiritual experiences that they reported.”

    The post-retreat scans revealed decreases in dopamine transporter (5-8 percent) and serotonin transporter (6.5 percent) binding, which could make more of the neurotransmitters available to the brain. This is associated with positive emotions and spiritual feelings. In particular, dopamine is responsible for mediating cognition, emotion and movement, while serotonin is involved in emotional regulation and mood.

    The study, funded by the Fetzer Institute, included 14 Christian participants ranging in age from 24 to 76. They attended an Ignatian retreat based on the spiritual exercises developed by St. Ignatius Loyola who founded the Jesuits. Following a morning mass, participants spent most of the day in silent contemplation, prayer and reflection and attended a daily meeting with a spiritual director for guidance and insights. After returning, study subjects also completed a number of surveys which showed marked improvements in their perceived physical health, tension and fatigue. They also reported increased feelings of self-transcendence which correlated to the change in dopamine binding.

    “In some ways, our study raises more questions than it answers,” said Dr. Newberg. “Our team is curious about which aspects of the retreat caused the changes in the neurotransmitter systems and if different retreats would produce different results. Hopefully, future studies can answer these questions.”


  5. Study tests the ‘three-hit’ theory of autism

    March 27, 2017 by Ashley

    From the Rockefeller University press release:

    Since the first case was documented in the United States in 1938, the causes of autism have remained elusive. Hundreds of genes, as well as environmental exposures, have been implicated in these brain disorders. Sex also seems to have something to do with it: About 80 percent of children diagnosed with an autism spectrum disorder are boys.

    This striking bias caught the attention of Rockefeller University’s Donald W. Pfaff. A neurobiologist who studies hormone effects and sex differences in the brain, Pfaff wondered if maleness might somehow amplify the genetic and environmental risk factors for the disease.

    In collaboration with colleagues specializing in child neurology and psychology, he has proposed a “three-hit” theory of autism, which suggests that a genetic predisposition in combination with early stress is more detrimental to boys than to girls, and more likely to produce the social avoidance that is a hallmark of autism disorders. Now, a team in his lab has found evidence in mice supporting this theory.

    “Together, these three hits — genes, environment, and sex — build on one another, such that their combined effect on behavior is much greater than the sum of the three individually,” says Pfaff, head of the Laboratory of Neurobiology and Behavior.

    A test run

    Pfaff and his colleagues formulated the three-hit theory based on studies of animals suggesting that the male hormone testosterone may sensitize the developing brain to stress in a way that can lead to social avoidance, a behavior characteristic of autism. Mice, like humans, are social animals, and in experiments, described in the Proceedings of the National Academy of Sciences, Pfaff’s team looked to see if male mice were more prone to problems with social responses than females when the other two risk factors were present.

    The theory and these experiments focus on the primary aspect of autism spectrum disorders, social problems, but there are others. In addition to social avoidance, autism is associated with difficulties in communication, as well as unusually restricted interests.

    To achieve a genetic hit, the team, led by Sara Schaafsma, a postdoc in the lab, used mice lacking a gene that is frequently mutated in people diagnosed with autism. To evoke stress in the as-yet unborn mice, the researchers prompted the immune systems of their pregnant mothers to react as though under attack from bacteria.

    Changes in brain and behavior

    The researchers later tested the social behavior of these mice in a series of experiments. The most compelling evidence for the three-hit theory came from a test of social recognition. Most of the animals, even those with two risk factors, showed signs of recognizing a once-unfamiliar mouse over multiple encounters. Only mice with all three hits — those that were male, were genetically predisposed to autism, and had experienced stress as embryos — seemed unable to recognize new acquaintances after encountering them multiple times.

    Next, the researchers looked for molecular changes within these rodents’ brains that might help to explain the differences in behavior. They found an increase in the expression of a gene that helps to kick off stress responses, in a brain region called the left hippocampus. With help from C. David Allis’s lab, they looked for chemical alterations in the packaging of DNA that might explain this uptick in gene activity. This effort revealed one particular chemical change in the nerve cell nucleus that encourages the expression of this stress-relevant gene.

    “Neurodevelopmental disorders, including autism, are often attributed to an interaction between genetic ‘nature’ and environmental ‘nurture.’ Our work indicates how male sex comes to be an important component of this dynamic, at least for one major aspect of autism,” Pfaff says. “By collecting a variety of evidence, we have begun to uncover one molecular mechanism, of many, by which these three hits alter sociability.”


  6. Researchers identify how inflammation spreads through the brain after injury

    March 26, 2017 by Ashley

    From the University of Maryland School of Medicine press release:

    Researchers have identified a new mechanism by which inflammation can spread throughout the brain after injury. This mechanism may explain the widespread and long-lasting inflammation that occurs after traumatic brain injury, and may play a role in other neurodegenerative diseases.

    The findings were published today in a study in the Journal of Neuroinflammation.

    This new understanding has the potential to transform how brain inflammation is understood, and, ultimately, how it is treated. The researchers showed that microparticles derived from brain inflammatory cells are markedly increased in both the brain and the blood following experimental traumatic brain injury (TBI). These microparticles carry pro-inflammatory factors that can activate normal immune cells, making them potentially toxic to brain neurons. Injecting such microparticles into the brains of uninjured animals creates progressive inflammation at both the injection site and eventually in more distant sites.

    Research has found that neuroinflammation often goes on for years after TBI, causing chronic brain damage. The researchers say that the microparticles may play a key role in this process.

    Chronic inflammation has been increasingly implicated in the progressive cell loss and neurological changes that occur after TBI. These inflammatory microparticles may be a key mechanism for chronic, progressive brain inflammation and may represent a new target for treating brain injury.

    The researchers on the paper include four University of Maryland School of Medicine researchers: Alan Faden, Stephen R. Thom, Bogdan A. Stoica, and David Loane.

    “These results potentially provide a new conceptual framework for understanding brain inflammation and its relationship to brain cell loss and neurological deficits after head injury, and may be relevant for other neurodegenerative disorders such as Alzheimer disease in which neuroinflammation may also play a role,” said Dr. Faden. “The idea that brain inflammation can trigger more inflammation at a distance through the release of microparticles may offer novel treatment targets for a number of important brain diseases.”

    The researchers studied mice, and found that in animals who had a traumatic brain injury, levels of microparticles in the blood were much higher. Because each kind of cell in the body has a distinct fingerprint, the researchers could track exactly where the microparticles came from. The microparticles they looked at in this study are released from cells known as microglia, immune cells that are common in the brain. After an injury, these cells often go into overdrive in an attempt to fix the injury. But this outsized response can change protective inflammatory responses to chronic destructive ones.

    The findings have important potential clinical implications. The researchers say that microparticles in the blood have the potential to be used as a biomarker — a way to determine how serious a brain injury may be. This could help guide treatment of the injuries, whose severity is often difficult to gauge.

    They also found that exposing the inflammatory microparticles to a compound called PEG-TB could neutralize them. This opens up the possibility of using that compound or others to treat TBI, and perhaps even other neurodegenerative diseases.


  7. Major research project provides new clues to schizophrenia

    by Ashley

    From the Karolinska Institutet press release:

    Researchers at Karolinska Institutet collaborating in the large-scale Karolinska Schizophrenia Project are taking an integrative approach to unravel the disease mechanisms of schizophrenia. In the very first results now presented in the scientific journal Molecular Psychiatry, the researchers show that patients with schizophrenia have lower levels of the vital neurotransmitter GABA as well as changes in the brain’s immune cells.

    Schizophrenia is one of the most disabling psychiatric diseases and affects approximately one per cent of the population. It commonly onsets in late adolescence and is often a life-long condition with symptoms such as delusions, hallucinations, and anxiety. The disease mechanisms are largely unknown, which has hampered the development of new drugs. The drugs currently available are designed to alleviate the symptoms, but are only partly successful, as only 20 per cent of the patients become symptom-free.

    The Karolinska Schizophrenia Project (KaSP) brings together researchers from a number of different scientific disciplines to build up a comprehensive picture of the disease mechanisms and to discover new targets for drug therapy. Patients with an acute first-episode psychosis are recruited and undergo extensive tests and investigations. Cognitive function, genetic variation, biochemical anomalies as well as brain structure and function are analysed using the latest techniques and then compared with healthy peers.

    The first results from the project are now presented in two studies published in the journal Molecular Psychiatry. One of the studies shows that patients with newly debuted schizophrenia have lower levels of the neurotransmitter GABA in their cerebrospinal fluid than healthy people and that the lower the concentration of GABA the more serious their symptoms are.

    GABA is involved in most brain functions and along with glutamate it accounts for almost 90 per cent of all signal transmission. While glutamate stimulates brain activity, GABA inhibits it, and the two neurotransmitters interact with each other.

    “Over the years, animal studies have suggested a link between decreased levels of GABA and schizophrenia,” says Professor Göran Engberg at Karolinska Institutet’s Department of Physiology and Pharmacology. “Our results are important because they clinically substantiate this hypothesis.”

    The other study used the imaging technique of positron emission tomography (PET) to show that patients with untreated schizophrenia have lower levels of TSPO (translocator protein), which is expressed on immune cells such as microglia and astrocytes.

    “Our interpretation of the results is an altered function of immune cells in the brain in early-stage schizophrenia,” says Senior lecturer Simon Cervenka at Karolinska Institutet’s Department of Clinical Neuroscience.

    The results of the two studies provide new clues to the pathological mechanisms of schizophrenia, but it is unclear if the changes are the cause or the result of the disease. Follow-up studies are now underway to examine what causes the anomalies and how these biological processes can be influenced to change the progression of the disease.

    KaSP is a collaboration between clinical and preclinical research groups at Karolinska Institutet and four psychiatric clinics under Stockholm County Council.


  8. Brain cells show teamwork in short-term memory

    March 23, 2017 by Ashley

    From the University of Western Ontario press release:

    Nerve cells in our brains work together in harmony to store and retrieve short-term memory, and are not solo artists as previously thought, Western-led brain research has determined.

    The research turns on its head decades of studies assuming that single neurons independently encode information in our working memories.

    “These findings suggest that even neurons we previously thought were ‘useless’ because they didn’t individually encode information have a purpose when working in concert with other neurons,” said researcher Julio Martinez-Trujillo, based at the Robarts Research Institute and the Brain and Mind Institute at Western University.

    “Knowing they work together helps us better understand the circuits in the brain that can either improve or hamper executive function. And that in turn may have implications for how we work though brain-health issues where short-term memory is a problem, including Alzheimer disease, schizophrenia, autism, depression and attention deficit disorder.”

    Working memory is the ability to learn, retain and retrieve bits of information we all need in the short term: items on a grocery list or driving directions, for example. Working memory deteriorates faster in people with dementia or other disorders of the brain and mind.

    In the past, researchers have believed this executive function was the job of single neurons acting independently from one another — the brain’s version of a crowd of people in a large room all singing different songs in different rhythms and different keys. An outsider trying to decipher any tune in all that white noise would have an extraordinarily difficult task.

    This research, however, suggests many in the neuron throng are singing from the same songbook, in essence creating chords to strengthen the collective voice of memory. With neural prosthetic technology — microchips that can “listen” to many neurons at the same time — researchers are able to find correlations between the activity of many nerve cells. “Using that same choir analogy, you can start perceiving some sounds that have a rhythm, a tune and chords that are related to each other: in sum, short-term memories,” said Martinez-Trujillo, who is also an associate professor at Western’s Schulich School of Medicine & Dentistry.

    And while the ramifications of this discovery are still being explored, “this gives us good material to work with as we move forward in brain research. It provides us with the necessary knowledge to find ways to manipulate brain circuits and improve short term memory in affected individuals,” Martinez-Trujillo said.

    “The microchip technology also allows us to extract signals from the brain in order to reverse-engineer brain circuitry and decode the information that is in the subject’s mind. In the near future, we could use this information to allow cognitive control of neural prosthetics in patients with ALS or severe cervical spinal cord injury,” said Adam Sachs, neurosurgeon and associate scientist at The Ottawa Hospital and assistant professor at the University of Ottawa Brain and Mind Research Institute.


  9. APA study suggests patients more likely to refuse drug therapy than psychotherapy for mental health

    by Ashley

    From the American Psychological Association press release:

    People seeking help for mental disorders are more likely to refuse or not complete the recommended treatment if it involves only psychotropic drugs, according to a review of research published by the American Psychological Association.

    Researchers conducted a meta-analysis of 186 studies of patients seeking help for mental health issues that examined whether they accepted the treatment that was recommended and if they did, whether they completed it. Fifty-seven of the studies, comprising 6,693 patients, had a component that reported refusal of treatment recommendations, and 182 of the studies, comprising 17,891 patients, had a component reporting premature termination of treatment.

    After diagnosis, patients in the studies were recommended to drug-only therapy (pharmacotherapy), talk therapy (psychotherapy) or a combination of the two.

    “We found that rates of treatment refusal were about two times greater for pharmacotherapy alone compared with psychotherapy alone, particularly for the treatment of social anxiety disorder, depressive disorders and panic disorder,” said lead researcher Joshua Swift, PhD, of Idaho State University. “Rates of premature termination of therapy were also higher for pharmacotherapy alone, compared with psychotherapy alone, particularly for anorexia/bulimia and depressive disorders.”

    The research was published in the APA journal Psychotherapy.

    Across all the studies, the average treatment refusal rate was 8.2 percent. Patients who were offered pharmacotherapy alone were 1.76 times more likely to refuse treatment than patients who were offered psychotherapy alone. Once in treatment, the average premature termination rate was 21.9 percent, with patients on drug-only regimens 1.2 times more likely to drop out early. There was no significant difference for refusal or dropout rates between pharmacotherapy alone and combination treatments, or between psychotherapy alone and combination treatments.

    While Swift said the findings overall were expected, the researchers were most surprised by how large the differences were for some disorders. For example, patients diagnosed with depressive disorders were 2.16 times more likely to refuse pharmacotherapy alone and patients with panic disorders were almost three times more likely to refuse pharmacotherapy alone.

    The findings are especially interesting because, as a result of easier access, recent trends show that a greater percentage of mental health patients in the U.S. are engaging in pharmacotherapy than psychotherapy, according to co-author Roger Greenberg, PhD, SUNY Upstate Medical University.

    Some experts have argued that psychotherapy should be the first treatment option for many mental health disorders. Those arguments have been largely based on good treatment outcomes for talk therapy with fewer side effects and lower relapse rates, said Greenberg. “Our findings support that argument, showing that clients are more likely to be willing to start and continue psychotherapy than pharmacotherapy.”

    Swift and Greenberg theorized that patients may be more willing to engage in psychotherapy because many individuals who experience mental health problems recognize that the source of their problems may not be entirely biological.

    “Patients often desire an opportunity to talk with and work through their problems with a caring individual who might be able to help them better face their emotional experiences,” said Greenberg. “Psychotropic medications may help a lot of people, and I think some do see them as a relatively easy and potentially quick fix, but I think others view their problems as more complex and worry that medications will only provide a temporary or surface level solution for the difficulties they are facing in their lives.”

    While the meta-analysis provides information on refusal and dropout rates, the studies did not report the patients’ reasons for their actions, Swift noted. Going forward, research designed to identify these reasons could lead to additional strategies to improve initiation and completion rates for both therapies, he said. It is also important to note that participants in the research studies initially indicated they were willing to be assigned to any therapy, and therefore may not be representative of all consumers of treatment.


  10. Sound waves boost older adults’ memory, deep sleep

    by Ashley

    From the Northwestern University press release:

    IF

    Gentle sound stimulation — such as the rush of a waterfall — synchronized to the rhythm of brain waves significantly enhanced deep sleep in older adults and improved their ability to recall words, reports a new Northwestern Medicine study.

    Deep sleep is critical for memory consolidation. But beginning in middle age, deep sleep decreases substantially, which scientists believe contributes to memory loss in aging.

    The sound stimulation significantly enhanced deep sleep in participants and their scores on a memory test.

    “This is an innovative, simple and safe non-medication approach that may help improve brain health,” said senior author Dr. Phyllis Zee, professor of neurology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine sleep specialist. “This is a potential tool for enhancing memory in older populations and attenuating normal age-related memory decline.”

    The study will be published March 8 in Frontiers in Human Neuroscience.

    In the study, 13 participants 60 and older received one night of acoustic stimulation and one night of sham stimulation. The sham stimulation procedure was identical to the acoustic one, but participants did not hear any noise during sleep. For both the sham and acoustic stimulation sessions, the individuals took a memory test at night and again the next morning. Recall ability after the sham stimulation generally improved on the morning test by a few percent. However, the average improvement was three times larger after pink-noise stimulation.

    The older adults were recruited from the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern.

    The degree of slow wave sleep enhancement was related to the degree of memory improvement, suggesting slow wave sleep remains important for memory, even in old age.

    Although the Northwestern scientists have not yet studied the effect of repeated nights of stimulation, this method could be a viable intervention for longer-term use in the home, Zee said.

    Previous research showed acoustic simulation played during deep sleep could improve memory consolidation in young people. But it has not been tested in older adults.

    The new study targeted older individuals — who have much more to gain memory-wise from enhanced deep sleep — and used a novel sound system that increased the effectiveness of the sound stimulation in older populations.

    The study used a new approach, which reads an individual’s brain waves in real time and locks in the gentle sound stimulation during a precise moment of neuron communication during deep sleep, which varies for each person.

    During deep sleep, each brain wave or oscillation slows to about one per second compared to 10 oscillations per second during wakefulness.

    Giovanni Santostasi, a study coauthor, developed an algorithm that delivers the sound during the rising portion of slow wave oscillations. This stimulation enhances synchronization of the neurons’ activity.

    After the sound stimulation, the older participants’ slow waves increased during sleep.

    Larger studies are needed to confirm the efficacy of this method and then “the idea is to be able to offer this for people to use at home,” said first author Nelly Papalambros, a Ph.D. student in neuroscience working in Zee’s lab. “We want to move this to long-term, at-home studies.”

    Northwestern scientists, under the direction of Dr. Roneil Malkani, assistant professor of neurology at Feinberg and a Northwestern Medicine sleep specialist, are currently testing the acoustic stimulation in overnight sleep studies in patients with memory complaints. The goal is to determine whether acoustic stimulation can enhance memory in adults with mild cognitive impairment.

    Previous studies conducted in individuals with mild cognitive impairment in collaboration with Ken Paller, professor of psychology at the Weinberg College of Arts and Sciences at Northwestern, have demonstrated a possible link between their sleep and their memory impairments.