1. Changes in brain regions may explain why some prefer order and certainty

    July 27, 2017 by Ashley

    From the University of California – Los Angeles press release:

    Why do some people prefer stable, predictable lives while others prefer frequent changes? Why do some people make rational decisions and others, impulsive and reckless ones? UCLA behavioral neuroscientists have identified changes in two brain regions that may hold answers to these questions.

    The research — reported by Alicia Izquierdo, UCLA associate professor of psychology and a member of UCLA’s Brain Research Institute, and her psychology graduate student, Alexandra Stolyarova — is published in the open-access online science journal eLife.

    The new experiments, which involved studying the orbitofrontal cortex and basolateral amygdala brain regions, assessed the ability of rats to work for rewards under both stable and variable conditions. Rats earned sugar pellets after choosing between two images displayed side by side. The animals made their selections by using their noses to touch a screen the size of an iPad. When a rat touched one image, it received a sugar pellet at a predictable time — generally 10 seconds later. When the rat touched the other image, it received a sugar pellet at a time that varied. This was the riskier option as the rats might have to wait as little as five seconds or as long as 15 seconds. The rats did this for a month at a time, as long as 45 minutes each day.

    The researchers discovered that the rats learned the task and were able to detect the fluctuations in wait times. When the rats experienced more variation in those wait times for their reward, the amount of the brain protein gephyrin in the basolateral amygdala region doubled, Izquierdo and Stolyarova reported.

    In some of the trials, the researchers made one option better than the other, with a shorter wait time. All rats were able to learn the pattern and make the better choice. They showed some evidence of learning on the first day and did better the second day and on subsequent days. In a group of rats without a functional basolateral amygdala, the rats learned more slowly about the changes, but caught up about two days later.

    Rats without a functional orbitofrontal cortex, however, did not learn at all, and instead treated each experience as a “reset” button, the researchers report. It is as if these rats did not have a record of the full range of possible outcomes. The important role for the orbitofrontal cortex surprised Izquierdo, who said there was more evidence that the basolateral amygdala would be important in conditions of uncertainty, and not as much for the orbitofrontal cortex.

    Stolyarova and Izquierdo are the first scientists to link gephyrin levels to the experience of reward. They report that when the rats experienced risk, the brain protein GluN1 also increased significantly in the basolateral amygdala.

    “I think the experience of uncertainty is making these changes occur in these brain regions,” Izquierdo said.

    All rats chose the risky option more often. The exception was the rats without a functional basolateral amygdala; those animals stayed risk-averse throughout the experiments.

    The orbitofrontal cortex and basolateral amygdala share anatomical connections, and both regions are involved in decision-making, earlier research has shown. The new research indicates this is especially so during changing or uncertain circumstances.

    Changes in these brain regions and brain proteins may help to explain a person’s preference for uncertain outcomes, Izquierdo said. Humans have individual differences in orbitofrontal cortex and basolateral amygdala function and in the expression of these proteins, she noted.

    For example, variations in the gephyrin gene have been linked to autism, and a feature of the disorder is a strong preference for order and certainty.

    In the future, Izquierdo said, precision medicine may be able to target any brain region to treat any disorder, including behavioral addictions such as gambling.

    People with obsessive-compulsive disorder also have a strong preference for order and certainty. Future research may answer whether the same brain changes occur in this disorder as well.


  2. Study suggests brain training has no effect on decision-making or cognitive function

    by Ashley

    From the Perelman School of Medicine at the University of Pennsylvania press release:

    During the last decade, commercial brain-training programs have risen in popularity, offering people the hope of improving their cognitive abilities through the routine performance of various “brain games” that tap cognitive functions such as memory, attention and cognitive flexibility.

    But a recent study at the University of Pennsylvania found that, not only did commercial brain training with Lumosity™ have no effect on decision-making, it also had no effect on cognitive function beyond practice effects on the training tasks.

    The findings were published in the Journal of Neuroscience.

    Seeking evidence for an intervention that could reduce the likelihood that people will engage in unhealthy behaviors such as smoking or overeating, a team of researchers at Penn, co-led by Joseph Kable, PhD, the Baird Term associate professor in the department of Psychology in the School of Arts & Sciences, and Caryn Lerman, PhD, the vice dean for Strategic Initiatives and the John H. Glick professor in Cancer Research in the Perelman School of Medicine, examined whether, through the claimed beneficial effect on cognitive function, commercial brain training regimes could reduce individuals’ propensity to make risky or impulsive choices.

    Lerman’s prior work had shown that engagement of brain circuits involved in self-control predicts whether people can refrain from smoking. This work provided the foundation for examining whether modulating these circuits through brain training could lead to behavior change.

    “Our motivation,” Kable said, “was that there are enough hints in the literature that cognitive training deserved a real, rigorous, full-scale test. Especially given the addiction angle, we’re looking for things that will help people make the changes in their lives that they want to make, one of which is being more future-oriented.”

    The researchers knew that people with stronger cognitive abilities tend to make less impulsive decisions on the kinds of tasks that Kable studies, which involve giving people choices between immediate smaller rewards and delayed larger rewards. They also knew that this behavior is likely mediated by a set of brain structures in the dorsolateral prefrontal area of the brain that have been associated with performance on the executive function tasks like the ones in the Lumosity™ battery.

    “The logic would be that if you can train cognitive abilities and change activity in these brain structures,” Kable said, “then that may change your likelihood of impulsive behavior.”

    The researchers recruited two groups, each with 64 healthy young adults. One group was asked to follow the Lumosity™ regimen, performing the executive function games for 30 minutes a day, five days a week for 10 weeks. The other group followed the same schedule but played online video games instead. Both groups were told that the study was investigating whether playing online video games improves cognition and changes one’s decision-making.

    The researchers had two assessments of decision-making that participants completed before and after the training regimen. To assess impulsive decision-making, the participants were asked to choose between smaller rewards now and larger rewards later. To assess risky decision-making, they were asked to choose between larger rewards at a lower probability versus smaller rewards at a higher probability.

    The researchers found that the training didn’t induce any changes in brain activity or decision-making during these tasks.

    The participants were also asked to complete a series of cognitive tests that were not part of the training to see if the program had any effect on their general cognitive abilities. While both groups showed improvement, the researchers found that commercial brain training didn’t lead to any more improvement than online video games. Furthermore, when they asked a no-contact group, which didn’t complete commercial brain training or video games, to complete the tests, the researchers found that the participants showed the same level of improvement as the first two groups, indicating that neither brain training nor online video games led to cognitive improvements beyond likely practice effects.

    Although the cognitive training by itself did not produce the desired benefits, initial findings from Lerman’s laboratory show that combining cognitive exercises with non-invasive brain stimulation enhances self-control over smoking behavior. This group is now conducting clinical trials to learn whether this combination approach can alter other risky behaviors such as unhealthy eating or improve attention and impulse control in persons with attention deficit hyperactivity disorder.

    “Habitual behaviors such as tobacco use and overeating,” said Mary Falcone, a senior research investigator at Penn and coauthor on the study, “contribute to preventable deaths from cancer, cardiovascular disease and other public health problems.”

    Lerman said, “As currently available behavioral and medical treatments for these habitual behaviors are ineffective for most people, there is a critical need to develop innovative approaches to behavior change. Changing the brain to change behavior is the approach that we are taking.”

    Kable hopes to use some of the data collected in this study to better understand both within-person differences in decision-making over time, why one person might be more patient at some times and more impulsive at others, and across-person differences, why some people tend to take the immediate reward and others tend to take the delayed reward.

    If they can better understand the neural basis for those differences, Kable said, it might provide some clues about what kinds of cognitive or neural interventions would be useful to try to intervene and push people to be less or more impulsive.

    Although, in this study, the researchers found that commercial cognitive training alone would not have an influence on one’s decision-making process or cognitive abilities, they believe that it was still an avenue worthy of rigorous investigation.

    “I think we’d all like to have better cognitive abilities,” Kable said. “And we all see ways in which the vagaries of where we grew up and what school we went to and who our parents were had these effects on learning at an early age. The notion that you could do something now that would remediate it was very exciting. I think it was just an idea that really needed to be tested.”

    This research was supported by grants R01-CA170297 and R35-CA197461 from the National Cancer Institute to Kable and Lerman through NCI’s Provocative Questions Initiative.


  3. Traumatic brain injury associated with dementia in working-age adults

    July 26, 2017 by Ashley

    From the University of Helsinki press release:

    According to a study encompassing the entire Finnish population, traumatic brain injury associated with an increased risk for dementia in working-age adults. Yet, no such relationship was found between traumatic brain injury and later onset of Parkinson’s disease or ALS.

    The researchers believe that these results may play a significant role for the rehabilitation and long-term monitoring of traumatic brain injury patients.

    Traumatic brain injuries (TBI) are among the top causes of death and disability, particularly among the young and middle aged. Approximately one in three that suffer from moderate-to-severe TBI die, and approximately half of the survivors will suffer from life-long disabilities.

    Degenerative brain diseases include memory disorders such as Alzheimer’s disease as well as Parkinson’s disease and amyotrophic lateral sclerosis (ALS). While the connection between TBI and degenerative brain diseases has been known, no comprehensive research data exist on the impact of TBI on degenerative brain diseases among adults of working age.

    Researchers from the University of Helsinki and the Helsinki University Hospital have now examined the relationship between TBI and degenerative brain diseases in a study encompassing the entire Finnish population. The study combined several nationwide registers to monitor more than 40,000 working-age adults, who survived the initial TBI, for ten years. Importantly, the persons´ level of education and socioeconomic status were accounted for.

    “It seems that the risk for developing dementia after TBI is the highest among middle-aged men. The more severe the TBI, the higher the risk for subsequent dementia. While previous studies have identified good education and high socioeconomic status as protective factors against dementia, we did not discover a similar effect among TBI survivors,” explains Rahul Raj, docent of experimental neurosurgery and one of the primary authors of the study.

    A significant discovery is that the risk of dementia among TBI survivors who have seemingly recovered well remains high for years after the injury. Raj points out that TBI patients may occasionally be incorrectly diagnosed with dementia due to the damage caused by the TBI itself, but such possible errors were considered in the study.

    “According to our results, it might be so that the TBI triggers a process that later leads to dementia.”

    “These results are significant for the rehabilitation and monitoring of TBI patients. Such a reliable study of the long-term impact of TBI has previously been impossible,” says Professor Jaakko Kaprio, a member of the research group.

    The WHO has predicted that TBI will become a leading cause of death and long-term illness during the next ten years. Already one per cent of the population in the United States suffers from a long-term disability caused by TBI. In western countries, the ageing of the population and age-related accidents increase the amount of TBIs, while in Asia, TBIs caused by traffic accidents are on the rise.

    Dementia is commonly seen as a problem of the elderly. However, the Finnish study shows that TBI may cause dementia to develop before old age, and that dementia caused by injuries are much more common than was thought.

    “It is a tragedy when an adult of working age develops dementia after recovering from a brain injury, not just for the patient and their families, but it also negatively impacts the whole society. In the future, it will be increasingly important to prevent TBIs and to develop rehabilitation and long-term monitoring for TBI patients,” says Docent Raj.


  4. Controlling memory by triggering specific brain waves during sleep

    July 25, 2017 by Ashley

    From the Institute for Basic Science press release:

    Have you ever tried to recall something just before going to sleep and then wake up with the memory fresh in your mind? While we absorb so much information during the day consciously or unconsciously, it is during shut eye that a lot of facts are dispatched to be filed away or fall into oblivion. A good quality sleep is the best way to feel mentally refreshed and memorize new information, but how is the brain working while we sleep? Could we improve such process to remember more, or maybe even use it to forget unwanted memories?

    Scientists at the Center for Cognition and Sociality, within the Institute for Basic Science (IBS), enhanced or reduced mouse memorization skills by modulating specific synchronized brain waves during deep sleep. This is the first study to show that manipulating sleep spindle oscillations at the right timing affects memory. The full description of the mouse experiments, conducted in collaboration with the University of Tüebingen, is published in the journal Neuron.

    The research team concentrated on a non-REM deep sleep phase that generally happens throughout the night, in alternation with the REM phase. It is called slow-wave sleep and it seems to be involved with memory formation, rather than dreaming.

    During slow-wave sleep, groups of neurons firing at the same time generate brain waves with triple rhythms: slow oscillations, spindles, and ripples. Slow oscillations originate from neurons in the cerebral cortex. Spindles come from a structure of the brain called thalamic reticular nucleus and spike around 7-15 per second. Finally, ripples are sharp and quick bursts of electrical energy, produced within the hippocampus, a brain component with an important role in spatial memory.

    “Often during the night a regular pattern is manifested, where a slow oscillation from the cortex is immediately followed by a thalamic spindle and while this happens, a hippocampal ripple appears in parallel. We believe that the correct timing of these three rhythms acts like a communication channel between different parts of the brains that facilitates memory consolidation,” explains Charles-Francois V. Latchoumane, first co-author of the study.

    The researchers focused on spindles because it was shown that the number of spindles is connected with memorization. It has been shown that the number of spindles increases following a day stuffed with learning and declines in the elderly, and in patients with schizophrenia. This is the first study to show that artificial thalamic spindles affect memory, if administered in sync with slow oscillations.

    In the experiment, mice were put in a special cage and given a mild electric shock after hearing a tonal noise. The day after, their memory was tested, by checking their fear reaction in response to either the same noise or the same cage. Latchoumane explains that this could be simplified and compared to the experience of hearing a fire alarm in a certain location, like a cafe. The incident would be followed by either another visit to the same cafe or the sound of the fire alarm in another cafe on the following day.

    At nighttime between the two days, scientists introduced artificial thalamic spindles in some of the mice using a light-based technique called optogenetics. The mice were divided into three groups. The first group received the light input just after the slow oscillations, so their spindle could form a triple rhythm (in phase): slow oscillation-spindle-ripples. In the second group the light stimulations were applied later “out of sync.” The third group was used as a control and did not receive any light stimulation.

    The day after, mice were placed in the same location and their movement was recorded. The mice of the first group were frozen in fear 40% of the time, even in absence of the noise. On the contrary, mice in the second and third groups only froze up to 20%. Instead, when the mice heard the same tone in a different location, remembered the tone and froze in fear up to 40% of the time, independently from the group they belonged to. The hippocampus is involved in spatial memories which might explain the difference.

    The opposite was also true: it was possible to make mice forget. By reducing the number of overnight spindles, the researchers could reduce the memory recall.

    The research team thinks that the thalamus is the coordinator of long-term memory consolidation, the process where recently acquired information is transferred from the hippocampus to the cortex to be filed away as long-term memory. The hippocampus is like a hub, where a lot of information comes in and has to be redirected to the correct destination within the brain, especially to the cortex. This study shows that the thalamus seems to mediate the information exchange between hippocampus and cortex. “We think that memorization during deep sleep has to do with time coordination. If the hippocampus tries to exchange information when the cortex neurons are not ready to receive it, the information could be wasted,” describes Latchoumane. “Slow oscillations might be the signal used by the cortex to flag that it is ready to accept information. Then, the thalamus would alert the hippocampus via the spindles.”

    It is possible to foresee that patients with memory deficiencies could benefit from translation of this research into humans. However, several points need to be clarified: can we manipulate single memories independently? Is the REM phase influencing the outcome? How is stored memory retrieved? While waiting for the next research outcomes on the science of sleep, sweet dreams… and sweet memories too.


  5. Study identifies gene that could play key role in depression

    by Ashley

    From the University of Maryland School of Medicine press release:

    Globally, depression affects more than 300 million people annually. Nearly 800,000 die from suicide every year — it is the second-leading cause of death among people between the ages of 15 to 29. Beyond that, depression destroys quality for life for tens of millions of patients and their families. Although environmental factors play a role in many cases of depression, genetics are also crucially important.

    Now, a new study by researchers at the University of Maryland School of Medicine (UM SOM) has pinpointed how one particular gene plays a central role — either protecting from stress or triggering a downward spiral, depending on its level of activity.

    The study, published in the Journal of Neuroscience, is the first to illuminate in detail how this particular gene, which is known as Slc6a15, works in a kind of neuron that plays a key role in depression. The study found the link in both animals and humans.

    “This study really shines a light on how levels of this gene in these neurons affects mood,” said the senior author of the study, Mary Kay Lobo, an assistant professor in the Department of Anatomy and Neurobiology. “It suggests that people with altered levels of this gene in certain brain regions may have a much higher risk for depression and other emotional disorders related to stress.”

    In 2006, Dr. Lobo and her colleagues found that the Slc6a15 gene was more common among specific neurons in the brain. They recently demonstrated that these neurons were important in depression. Since this gene was recently implicated in depression by other researchers, her lab decided to investigate its role in these specific neurons. In this latest study, she and her team focused on a part of the brain called the nucleus accumbens. This region plays a central role in the brain’s “reward circuit.” When you eat a delicious meal, have sex, drink alcohol, or have any other kind of enjoyable experience, neurons in the nucleus accumbens are activated, letting you know that the experience is pushing the proper buttons. In depression, any kind of enjoyment becomes difficult or impossible; this symptom is known as anhedonia, which in Latin means the inability to experience pleasure.

    The researchers focused on a subset of neurons in the nucleus accumbens called D2 neurons. These neurons respond to the neurotransmitter dopamine, which plays a central role in the reward circuit.

    They studied mice susceptible to depression; when subjected to social stress — exposure to larger, more aggressive mice — they tend to withdraw and exhibit behavior that indicates depression, such as social withdrawal and lack of interest in food that they normally enjoy. Dr. Lobo found that when these animals were subjected to chronic social stress, levels of the Slc6a15 gene in the D2 neurons of the nucleus accumbens was markedly reduced.

    The researchers also studied mice in which the gene had been reduced in D2 neurons. When those mice were subjected to stress, they also exhibited signs of depression. Conversely, when the researchers enhanced Slc6a15 levels in D2 neurons, the mice showed a resilient response to stress.

    Next, Dr. Lobo looked at the brains of humans who had a history of major depression and who had committed suicide. In the nucleus accumbens of these brains, the gene was reduced. This indicates that the link between gene and behavior extends from mice to humans.

    It is not clear exactly how Slc6a15 works in the brain. Dr. Lobo says it may work by altering neurotransmitter levels in the brain, a theory that has some evidence from other studies. She says her research could eventually lead to targeted therapies focused on Slc6a15 as a new way to treat depression.


  6. How plants grow like human brains

    by Ashley

    From the Salk Institute press release:

    Plants and brains are more alike than you might think: Salk scientists discovered that the mathematical rules governing how plants grow are similar to how brain cells sprout connections. The new work, published in Current Biology on July 6, 2017, and based on data from 3D laser scanning of plants, suggests there may be universal rules of logic governing branching growth across many biological systems.

    “Our project was motivated by the question of whether, despite all the diversity we see in plant forms, there is some form or structure they all share,” says Saket Navlakha, assistant professor in Salk’s Center for Integrative Biology and senior author of the paper. “We discovered that there is — and, surprisingly, the variation in how branches are distributed in space can be described mathematically by something called a Gaussian function, which is also known as a bell curve.”

    Being immobile, plants have to find creative strategies for adjusting their architecture to address environmental challenges, like being shaded by a neighbor. The diversity in plant forms, from towering redwoods to creeping thyme, is a visible sign of these strategies, but Navlakha wondered if there was some unseen organizing principle at work. To find out, his team used high-precision 3D scanning technology to measure the architecture of young plants over time and quantify their growth in ways that could be analyzed mathematically.

    “This collaboration arose from a conversation that Saket and I had shortly after his arrival at Salk,” says Professor and Director of the Plant Molecular and Cellular Biology Laboratory Joanne Chory, who, along with being the Howard H. and Maryam R. Newman Chair in Plant Biology, is also a Howard Hughes Medical Investigator and one of the paper’s coauthors. “We were able to fund our studies thanks to Salk’s innovation grant program and the Howard Hughes Medical Institute.”

    The team began with three agriculturally valuable crops: sorghum, tomato and tobacco. The researchers grew the plants from seeds under conditions the plants might experience naturally (shade, ambient light, high light, high heat and drought). Every few days for a month, first author Adam Conn scanned each plant to digitally capture its growth. In all, Conn scanned almost 600 plants.

    “We basically scanned the plants like you would scan a piece of paper,” says Conn, a Salk research assistant. “But in this case the technology is 3D and allows us to capture a complete form — the full architecture of how the plant grows and distributes branches in space.”

    Each plant’s digital representation is called a point cloud, a set of 3D coordinates in space that can be analyzed computationally. With the new data, the team built a statistical description of theoretically possible plant shapes by studying the plant’s branch density function. The branch density function depicts the likelihood of finding a branch at any point in the space surrounding a plant.

    This model revealed three properties of growth: separability, self-similarity and a Gaussian branch density function. Separability means that growth in one spatial direction is independent of growth in other directions. According to Navlakha, this property means that growth is very simple and modular, which may let plants be more resilient to changes in their environment. Self-similarity means that all the plants have the same underlying shape, even though some plants may be stretched a little more in one direction, or squeezed in another direction. In other words, plants don’t use different statistical rules to grow in shade than they do to grow in bright light. Lastly, the team found that, regardless of plant species or growth conditions, branch density data followed a Gaussian distribution that is truncated at the boundary of the plant. Basically, this says that branch growth is densest near the plant’s center and gets less dense farther out following a bell curve.

    The high level of evolutionary efficiency suggested by these properties is surprising. Even though it would be inefficient for plants to evolve different growth rules for every type of environmental condition, the researchers did not expect to find that plants would be so efficient as to develop only a single functional form. The properties they identified in this work may help researchers evaluate new strategies for genetically engineering crops.

    Previous work by one of the paper’s authors, Charles Stevens, a professor in Salk’s Molecular Neurobiology Laboratory, found the same three mathematical properties at work in brain neurons. “The similarity between neuronal arbors and plant shoots is quite striking, and it seems like there must be an underlying reason,” says Stevens. “Probably, they both need to cover a territory as completely as possible but in a very sparse way so they don’t interfere with each other.”

    The next challenge for the team is to identify what might be some of the mechanisms at the molecular level driving these changes. Navlakha adds, “We could see whether these principles deviate in other agricultural species and maybe use that knowledge in selecting plants to improve crop yields.”


  7. Learning with music can change brain structure

    July 24, 2017 by Ashley

    From the University of Edinburgh press release:

    Using musical cues to learn a physical task significantly develops an important part of the brain, according to a new study.

    People who practiced a basic movement task to music showed increased structural connectivity between the regions of the brain that process sound and control movement.

    The findings focus on white matter pathways — the wiring that enables brain cells to communicate with each other.

    The study could have positive implications for future research into rehabilitation for patients who have lost some degree of movement control.

    Thirty right-handed volunteers were divided into two groups and charged with learning a new task involving sequences of finger movements with the non-dominant, left hand. One group learned the task with musical cues, the other group without music.

    After four weeks of practice, both groups of volunteers performed equally well at learning the sequences, researchers at the University of Edinburgh found.

    Using MRI scans, it was found that the music group showed a significant increase in structural connectivity in the white matter tract that links auditory and motor regions on the right side of the brain. The non-music group showed no change.

    Researchers hope that future study with larger numbers of participants will examine whether music can help with special kinds of motor rehabilitation programmes, such as after a stroke.

    The interdisciplinary project brought together researchers from the University of Edinburgh’s Institute for Music in Human and Social Development, Clinical Research Imaging Centre, and Centre for Clinical Brain Sciences, and from Clinical Neuropsychology, Leiden University, The Netherlands.

    The results are published in the journal Brain & Cognition.

    Dr Katie Overy, who led the research team said: “The study suggests that music makes a key difference. We have long known that music encourages people to move. This study provides the first experimental evidence that adding musical cues to learning new motor task can lead to changes in white matter structure in the brain.”


  8. Sleep problems may be early sign of Alzheimer’s

    by Ashley

    From the American Academy of Neurology press release:

    Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer’s disease later in life than people who do not have sleep problems, according to a study published in the July 5, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. Researchers have found a link between sleep disturbances and biological markers for Alzheimer’s disease found in the spinal fluid.

    “Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison. “For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”

    Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.

    For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer’s disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.

    Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer’s disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.

    “It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending,” said Bendlin.

    While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.

    The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.

    “It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep,” said Bendlin. “More research is needed to further define the relationship between sleep and these biomarkers.”

    Bendlin added, “There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”

    One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.


  9. No link seen between traumatic brain injury and cognitive decline

    by Ashley

    From the Boston University Medical Center press release:

    Although much research has examined traumatic brain injury (TBI) as a possible risk factor for later life dementia from neurodegenerative diseases such as Alzheimer’s disease (AD), little is known regarding how TBI influences the rate of age-related cognitive change. A new study now shows that history of TBI (with loss of consciousness) does not appear to affect the rate of cognitive change over time for participants with normal cognition or even those with AD dementia.

    These findings appear in the Journal of Alzheimer’s Disease.

    More than 10 million individuals worldwide are affected annually by TBI, however the true prevalence is likely even greater given that a majority of TBIs are mild in severity and may not be recognized or reported. TBI is a major public health and socioeconomic concern resulting in $11.5 billion in direct medical costs and $64.8 billion in indirect costs to the U.S. health system in 2010 alone.

    According to the researchers the relationship between TBI and long-term cognitive trajectories remains poorly understood due to limitations of previous studies, including small sample sizes, short follow-up periods, biased samples, high attrition rates, limited or no reports of exposure to repetitive head impacts (such as those received through contact sports), and very brief cognitive test batteries.

    In an effort to examine this possible connection, researchers compared performance on cognitive tests over time for 706 participants (432 with normal cognition; 274 AD dementia) from the National Alzheimer’s Coordinating Center database. Normal and AD dementia participants with a history of TBI with loss of consciousness were matched to an equal number of demographically and clinically similar participants without a TBI history. The researchers also examined the possible role of genetics in the relationship between TBI and cognitive decline by studying a gene known to increase risk for AD dementia, the APOE ?4 gene.

    “Although we expected the rates of cognitive change to differ significantly between those with a history of TBI compared to those with no history of TBI, we found no significant difference between the groups, regardless of their APOE genotype,” explained corresponding author Robert Stern, PhD, Director of the Clinical Core of the Boston University Alzheimer’s Disease Center (BU ADC) and professor of neurology, neurosurgery and anatomy and neurobiology at Boston University School of Medicine.

    The study’s first author Yorghos Tripodis, PhD, Associate Director of the Data Management and Biostatistics Core of the BU ADC and associate professor of Biostatistics at Boston University School of Public Health, cautioned, “Our findings should still be interpreted cautiously due to the crude and limited assessment of TBI history available through the NACC database.” The researchers recommended that future studies should collect information on the number of past TBIs (including mild TBIs, as well as exposure to sub-concussive trauma through contact sports and other activities) along with time since TBI, which may play a significant role in cognitive change.


  10. Neuroscientists call for more comprehensive view of how brain forms memories

    July 23, 2017 by Ashley

    From the University of Chicago Medical Center press release:

    Neuroscientists from the University of Chicago argue that research on how memories form in the brain should consider activity of groups of brain cells working together, not just the connections between them.

    Memories are stored as “engrams,” or enduring physical or chemical changes to populations of neurons that are triggered by new information and experiences. Traditional thinking about how these engrams form centers on the ability of connections between neurons to strengthen or weaken over time based on what information they receive, or what’s known as “synaptic plasticity.” The new proposal, published this week in the journal Neuron, argues that while synaptic plasticity establishes the map of connectivity between individual neurons in an engram, it is not enough to account for all aspects of learning. A second process called “intrinsic plasticity,” or changes in the intensity of activity of neurons within an engram, plays an important role as well.

    “Synaptic plasticity does not fully account for the complexity of learning mechanisms that we are aware of right now,” said Christian Hansel, PhD, professor of neurobiology and senior author of the new paper. “There were elements missing, and with the introduction of intrinsic plasticity, all of a sudden you see a system that is more dynamic than we thought.”

    In recent studies using optogenetic tools, which enable scientists to control the activity of neurons with light, researchers have been able to monitor memory storage and retrieval from brain cells. Optogenetic tools give scientists a window to the activity of the brain as a whole, even in living animals. These new studies show how both individual neurons and groups, or ensembles, of neurons work together while memory and learning processes take place — often without requiring any changes to the connections between synapses.

    For instance, synaptic plasticity relies on repeated conditioning to develop stronger connections between cells, meaning that an animal has to experience something several times to learn and form a memory. But, of course, we also learn from single, brief experiences that don’t necessarily trigger changes in the synapses, meaning that another, faster learning process takes place.

    The authors point to several studies showing that intrinsic plasticity is a nearly instantaneous mechanism that likely has a lower threshold, or takes fewer experiences, to initiate. Thus, it might be more appropriate for fast learning resulting from single experiences, instead of the slow, adaptive process involved with synaptic plasticity.

    Theories about memory formation also don’t account for the relative strength of activity in neurons once connections between them have been established, the authors write. If you think of how memories are stored as working like the lights in a room, synaptic connections are the electrical wiring that determine how the lights are connected and what input (electricity) they receive. Changing how the lights are wired (i.e. the synaptic plasticity) obviously affects how they function, but so do the switches and light bulbs. Intrinsic plasticity is the ability to manipulate the intensity of the light without changing the wiring, like using dimmer switches or three-way bulbs. Both kinds of changes have an effect independently, but they work together to light the room.

    “They are two ideas that are very important to learning and memory and we bring them together in this paper,” said postdoctoral scholar Heather Titley, PhD, first author of the paper. “They’re not mutually exclusive.”

    The authors emphasize that this new line of thinking is just a starting point. More experiments should be designed, for instance, to tease out the relative effects of synaptic versus intrinsic plasticity on learning and memory. But given the evidence produced by new technology, they argue that it’s time to expand our thinking about how memories form.

    “People might argue whether this intrinsic plasticity is really something that plays a major role or not,” said Nicolas Brunel, professor of neurobiology and statistics, and another author of the paper. “But I don’t think people can argue that it doesn’t play any role, because there is an increasing amount of evidence that it does.”