Neuroscience
Month
Delirium is widespread among older people but often goes ignored and untreated, according to new research by US and UK researchers including the University of East Anglia.
Published in the September issue of the Journal of Hospital Medicine, the findings show that delirium - or acute confusion – is common among older adults in hospitals and nursing homes. It has a negative impact on cognition and independence, significantly increases the risk of developing dementia, and triples the likelihood of death. Yet this common, acute condition is frequently either undiagnosed or accepted as inevitable.
Led by the Regenstrief Institute and Indiana University, the research team reviewed 45 years of research encompassing 585 studies. They found that one in three cases of delirium were preventable and are calling for delirium to be identified and treated early to prevent poor long-term prognosis.
“As a geriatric psychiatrist I have seen that around 50 per cent or people with dementia in hospital develop delirium,” said co-author Dr Chris Fox, of Norwich Medical School at the University of East Anglia.
“This is because in addition to having dementia, they have multiple risk factors that can predispose and precipitate delirium – including serious illnesses and pre-existing cognitive impairment. In addition, hospital staff commonly label the signs as dementia related and do not pick up the delirium.”
“We need to develop better mechanisms for diagnosing delirium so that prompt treatment regimes can be initiated.”
In general patient groups, more than 60 per cent of delirium cases are not recognised or treated, and significant numbers of elderly patients leave hospital with ongoing delirium which has been missed.
The authors, led by Dr Babar Khan of the Regenstrief Institute and Indiana University School of Medicine, said that delirium could be prevented by eliminating restraints, treating depression, ensuring that patients have access to glasses and hearing aids, and prescribing classes of antipsychotics that do not negatively affect the aging brain. They also noted the need for a more sensitive screening tool for delirium, especially when administered by a non-expert.
“Delirium is extremely common among older adults in intensive care units and is not uncommon in other hospital units and in nursing homes, but too often it is ignored or accepted as inevitable,” said Dr Khan. “Delirium significantly increases risk of developing dementia and triples likelihood of death. It cannot be ignored.”
Co-author Dr Malaz Boustani, of the Regenstrief Institute, Indiana University School of Medicine and Wishard Healthy Aging Brain Center, said: “Having delirium prolongs the length of a hospital stay, increases the risk of post-hospitalization transfer to a nursing home, increases the risk of death and may lead to permanent brain damage.”
Contrary to the prevailing theories that music and language are cognitively separate or that music is a byproduct of language, theorists at Rice University’s Shepherd School of Music and the University of Maryland, College Park (UMCP) advocate that music underlies the ability to acquire language.
“Spoken language is a special type of music,” said Anthony Brandt, co-author of a theory paper published online this month in the journal Frontiers in Cognitive Auditory Neuroscience. “Language is typically viewed as fundamental to human intelligence, and music is often treated as being dependent on or derived from language. But from a developmental perspective, we argue that music comes first and language arises from music.”
Brandt, associate professor of composition and theory at the Shepherd School, co-authored the paper with Shepherd School graduate student Molly Gebrian and L. Robert Slevc, UMCP assistant professor of psychology and director of the Language and Music Cognition Lab.
“Infants listen first to sounds of language and only later to its meaning,” Brandt said. He noted that newborns’ extensive abilities in different aspects of speech perception depend on the discrimination of the sounds of language – “the most musical aspects of speech.”
The paper cites various studies that show what the newborn brain is capable of, such as the ability to distinguish the phonemes, or basic distinctive units of speech sound, and such attributes as pitch, rhythm and timbre.
The authors define music as “creative play with sound.” They said the term “music” implies an attention to the acoustic features of sound irrespective of any referential function. As adults, people focus primarily on the meaning of speech. But babies begin by hearing language as “an intentional and often repetitive vocal performance,” Brandt said. “They listen to it not only for its emotional content but also for its rhythmic and phonemic patterns and consistencies. The meaning of words comes later.”
Brandt and his co-authors challenge the prevailing view that music cognition matures more slowly than language cognition and is more difficult. “We show that music and language develop along similar time lines,” he said.
Infants initially don’t distinguish well between their native language and all the languages of the world, Brandt said. Throughout the first year of life, they gradually hone in on their native language. Similarly, infants initially don’t distinguish well between their native musical traditions and those of other cultures; they start to hone in on their own musical culture at the same time that they hone in on their native language, he said.
The paper explores many connections between listening to speech and music. For example, recognizing the sound of different consonants requires rapid processing in the temporal lobe of the brain. Similarly, recognizing the timbre of different instruments requires temporal processing at the same speed — a feature of musical hearing that has often been overlooked, Brandt said.
“You can’t distinguish between a piano and a trumpet if you can’t process what you’re hearing at the same speed that you listen for the difference between ‘ba’ and ‘da,’” he said. “In this and many other ways, listening to music and speech overlap.” The authors argue that from a musical perspective, speech is a concert of phonemes and syllables.
“While music and language may be cognitively and neurally distinct in adults, we suggest that language is simply a subset of music from a child’s view,” Brandt said. “We conclude that music merits a central place in our understanding of human development.”
Brandt said more research on this topic might lead to a better understanding of why music therapy is helpful for people with reading and speech disorders. People with dyslexia often have problems with the performance of musical rhythm. “A lot of people with language deficits also have musical deficits,” Brandt said.
More research could also shed light on rehabilitation for people who have suffered a stroke. “Music helps them reacquire language, because that may be how they acquired language in the first place,” Brandt said.
Misfolded proteins can cause various neurodegenerative diseases such as spinocerebellar ataxias (SCAs) or Huntington’s disease, which are characterized by a progressive loss of neurons in the brain. Researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany, together with their colleagues of the Université Paris Diderot, Paris, France, have now identified 21 proteins that specifically bind to a protein called ataxin-1. Twelve of these proteins enhance the misfolding of ataxin-1 and thus promote the formation of harmful protein aggregate structures, whereas nine of them prevent the misfolding (PLoS Genetics).
Proteins only function properly when the chains of amino acids, from which they are built, fold correctly. Misfolded proteins can be toxic for the cells and assemble into insoluble aggregates together with other proteins. Ataxin-1, the protein that the researchers have now investigated, is very prone to misfolding due to inherited gene defects that cause neurodegenerative diseases. The reason for this is that the amino acid glutamine is repeated in the amino acid chain of ataxin-1 very often - the more glutamine, the more toxic the protein. Approximately 40 repeats of glutamine are considered to be toxic for the cells.
Now, Dr. Spyros Petrakis, Dr. Miguel Andrade, Professor Erich Wanker and colleagues have identified 21 proteins that mainly interact with ataxin-1 and influence its folding or misfolding. Twelve of these proteins enhance the toxicity of ataxin-1 for the nerve cells, whereas nine of the identified proteins reduce its toxicity.
Furthermore, the researchers detected a common feature in the structure of those proteins that enhances toxicity and aggregation. It is a special structure scientists call “coiled-coil-domain” because it resembles a double twisted spiral or helix. Apparently this structure promotes aggregation, because proteins that interact with ataxin-1 and have this domain enhance the toxic effect of mutated ataxin-1. As the researchers said, this structure could be a potential target for therapy: “A careful analysis of the molecular details could help to discover drugs that suppress toxic processes.”
Scientists at Washington University School of Medicine in St. Louis have taken one of the first detailed looks into how Alzheimer’s disease disrupts coordination among several of the brain’s networks. The results, reported in The Journal of Neuroscience, include some of the earliest assessments of Alzheimer’s effects on networks that are active when the brain is at rest.
“Until now, most research into Alzheimer’s effects on brain networks has either focused on the networks that become active during a mental task, or the default mode network, the primary network that activates when a person is daydreaming or letting the mind wander,” says senior author Beau Ances, MD, assistant professor of neurology. “There are, however, a number of additional networks besides the default mode network that become active when the brain is idling and could tell us important things about Alzheimer’s effects.”
Ances and his colleagues analyzed brain scans of 559 subjects. Some of these subjects were cognitively normal, while others were in the early stages of very mild to mild Alzheimer’s disease. Scientists found that all of the networks they studied eventually became impaired during the initial stages of Alzheimer’s.
“Communications within and between networks are disrupted, but it doesn’t happen all at once,” Ances says. “There’s even one network that has a momentary surge of improved connections before it starts dropping again. That’s the salience network, which helps you determine what in your environment you need to pay attention to.”
Other networks studied by the researchers included:
Scientists also examined Alzheimer’s effects on a brain networking property known as anti-correlations. Researchers identify networks by determining which brain areas frequently become active at the same time, but anti-correlated networks are noteworthy for the way their activities fluctuate: when one network is active, the other network is quiet. This ability to switch back-and-forth between networks is significantly diminished in participants with mild to moderate Alzheimer’s disease.
The default mode network, previously identified as one of the first networks to be impaired by Alzheimer’s, is a partner in two of the three pairs of anti-correlated networks scientist studied.
“While we can’t prove this yet, one hypothesis is that as things go wrong in the processing of information in the default mode network, that mishandled data is passed on to other networks, where it creates additional problems,” Ances says.
It’s not practical to use these network breakdowns to clinically diagnose Alzheimer’s disease, Ances notes, but they may help track the development of the disease and aid efforts to better understand its spread through the brain.
Ances plans to look at other markers for Alzheimer’s disease in the same subjects, such as levels in the cerebrospinal fluid of amyloid beta, a major component of Alzheimer’s plaques.
MRI brain scans no longer just show the various regions of brain activity; nowadays the networks in the brain can now be imaged with ever greater precision. This will make functional MRI (fMRI) increasingly powerful in the coming years, leading to tools that can be used in cognitive neuroscience. This is the claim made by Prof. David Norris in his inaugural lecture as Professor of Neuroimaging at the University of Twente on 13 September.
During the twenty years since the invention of fMRI (functional Magnetic Resonance Imaging) developments have come thick and fast, from initially identifying active brain regions to more complex analysis of the connections and hubs in the brain. In his inaugural lecture Norris describes how this has been achieved thanks to not only a growing understanding of the underlying biophysics but also rapid technological developments: scanners with larger magnetic fields, better image-processing techniques and algorithms. His aim is to go beyond merely localizing which parts of the brain are active. The challenge is to answer two questions: How are the various regions interconnected, structurally and functionally? What do the networks in our brains look like?
Faster and more powerful
Back in the 19th century scientists observed increased blood flow in brain regions that are functionally active. fMRI enables the change in oxygen content to be seen. Haemoglobin, the substance that transports oxygen in the blood, can take the form of oxyhaemoglobin (when it is still combined with oxygen) and deoxyhaemoglobin (when the oxygen has been released), each of which has different magnetic properties. One of the complicating factors when interpreting the scans is that various physiological mechanisms are at work simultaneously, causing the deoxyhaemoglobin level to rise and fall. One of the remedies to increase accuracy, Norris explains, has been to increase the magnetic field strength: there are now MRI scanners operating at 7 Tesla. At the same time the speed at which laminae can be imaged has gone up by leaps and bounds: the entire brain can be scanned in three seconds with a precision of 1 millimetre.
Hubs
The functional connections between parts of the brain can be registered by means of blood flow, but MRI also enables the structural and anatomical connections to be seen. This involves measuring the movement of water molecules caused by the ‘white matter’ in nerve fibres. This technology is known as diffusion-weighted imaging (DWI). Combining these technologies provides a wealth of fresh information on the networks in the brain and the places where many connections come together, the ‘hubs’. Not only have ‘known networks’ thus been proven, so have networks that neuroscience posits as plausible but that have never been measured.
Image showing the distribution of connector hubs on the surface of a flattened brain. The top two figures show the medial views of each hemisphere, the bottom two show the external views.
CMI
The new Centre for Medical Imaging that is to come to the University of Twente campus will soon provide extensive facilities for collaborating in the field of fMRI, says Norris, who is also on the staff of the Donders Institute in Nijmegen.
Inflammation is the hallmark of many human diseases, from infection to neurodegeneration. The chemical balance within a tissue is disturbed, resulting in the accumulation of reactive oxygen species (ROS) such as hydrogen peroxide, which can cause oxidative stress and associated toxic effects.
Although some ROS are important in cell signaling and the body’s defense mechanisms, these chemicals also contribute to and are indicators of many diseases, including cardiovascular dysfunction. A non-invasive way of detecting measurable, low levels of hydrogen peroxide and other ROS would provide a viable way to detect inflammation. Such a method would also provide a way to selectively deliver drugs to their targets.
Adah Almutairi, PhD, associate professor at the Skaggs School of Pharmacy and Pharmaceutical Sciences, the Department of NanoEngineering, and the Materials Science and Engineering Program at the University of California, San Diego, and colleagues have developed the first degradable polymer that is extremely sensitive to low but biologically relevant concentrations of hydrogen peroxide.
Their work is currently published in the online issue of the Journal of the American Chemical Society.
These polymeric capsules, or nanoparticles, are taken up by macrophages and neutrophils – immune system cells that rush to the site of inflammation. The nanoparticles then release their contents when they degrade in the presence of hydrogen peroxide produced by these cells.
“This is the first example of a biocompatible way to respond to oxidative stress and inflammation,” said Almutairi, director of the UC San Diego Laboratory of Bioresponsive Materials. “Because the capsules are tailored to biodegrade and release their cargo when encountering hydrogen peroxide, they may allow for targeted drug delivery to diseased tissue.”
Almutairi is looking to test this method in a model of atherosclerosis. “Cardiologists have long needed a non-invasive method to determine which patients are vulnerable to a heart attack caused by ruptured plaque in the arteries before the attack,” she said. “Since the most dangerous of plaques is inflamed, our system could provide a safe way to detect and treat this disease.”
Researchers from the Centre for Addiction and Mental Health (CAMH) have identified a new role of a chemical involved in controlling the genes underlying memory and learning.
"The brain is a plastic tissue, and we know that learning and memory require various genes to be expressed,” says CAMH Senior Scientist Dr. Art Petronis, who is a senior author on the new study. “Our research has identified how the chemical 5-hmC may be involved in the epigenetic processes allowing this plasticity.” Dr. Petronis is head of the Krembil Family Epigenetics Laboratory in CAMH’s Campbell Family Mental Health Research Institute.
5-hmC is an epigenetic modification of DNA, and was discovered in humans and mice in 2009. DNA modifications are chemical changes to DNA. They flag genes to be turned “on” - signalling the genome to make a protein - or turned “off.” As the overwhelming majority of cells in an individual contain the same genetic code, this pattern of flags is what allows a neuron to use the same genome as a blood or liver cell, but create a completely different and specialized cellular environment.
The research, published online in Nature Structural & Molecular Biology, sheds light on the role of 5-hmC. Intriguingly, it is more abundant in the brain than in other tissues in the body, for reasons not clear to date.
The CAMH team of scientists examined DNA from a variety of tissues, including the mouse and human brain, and looked at where 5-hmC was found in the genome. They detected that 5-hmC had a unique distribution in the brain: it was highly enriched in genes related to the synapse, the dynamic tips of brain cells. Growth and change in the synapse allow different brain cells to “wire” together, which allows learning and memory.
"This enrichment of 5-hmC in synapse-related genes suggests a role for this epigenetic modification in learning and memory," says Dr. Petronis.
The team further showed that 5-hmC had a special distribution even within the gene. The code for one gene can be edited and “spliced” to create several different proteins. Dr. Petronis found that 5-hmC is located at “splice junctions,” the points where the gene is cut before splicing.
"5-hmC may signal the cell’s splicing machinery to generate the diverse proteins that, in turn, give rise to the unprecedented complexity of the brain," he says.
The research team is continuing to investigate the role of 5-hmC in more detail, and to determine whether 5-hmC function is different in people with bipolar disorder and schizophrenia compared to people without these diagnoses.
This research was funded by the U.S National Institutes of Health, the Canadian Institutes of Health Research, and the Tapscott Chair in Schizophrenia Studies at the University of Toronto.
The Centre for Addiction and Mental Health (CAMH) is Canada’s largest mental health and addiction teaching hospital, as well as one of the world’s leading research centres in the area of addiction and mental health. CAMH combines clinical care, research, education, policy development and health promotion to help transform the lives of people affected by mental health and addiction issues.
An enzyme that could represent a powerful new tool for combating Alzheimer’s disease has been discovered by researchers at Mayo Clinic in Florida. The enzyme — known as BACE2 — destroys beta-amyloid, a toxic protein fragment that litters the brains of patients who have the disease. The findings were published online Sept. 17 in the science journal Molecular Neurodegeneration.
Alzheimer’s disease is the most common memory disorder. It affects more that 5.5 million people in the United States. Despite the disorder’s enormous financial and personal toll, effective treatments have not yet been found.
The Mayo research team, led by Malcolm A. Leissring, Ph.D., a neuroscientist at Mayo Clinic in Florida, made the discovery by testing hundreds of enzymes for the ability to lower beta-amyloid levels. BACE2 was found to lower beta-amyloid more effectively than all other enzymes tested. The discovery is interesting because BACE2 is closely related to another enzyme, known as BACE1, involved in producing beta-amyloid.
“Despite their close similarity, the two enzymes have completely opposite effects on beta-amyloid — BACE1 giveth, while BACE2 taketh away,” Dr. Leissring says.
Beta-amyloid is a fragment of a larger protein, known as APP, and is produced by enzymes that cut APP at two places. BACE1 is the enzyme responsible for making the first cut that generates beta-amyloid. The research showed that BACE2 cuts beta-amyloid into smaller pieces, thereby destroying it, instead. Although other enzymes are known to break down beta-amyloid, BACE2 is particularly efficient at this function, the study found.
Previous work had shown that BACE2 can also lower beta-amyloid levels by a second mechanism: by cutting APP at a different spot from BACE1. BACE2 cuts in the middle of the beta-amyloid portion, which prevents beta-amyloid production.
“The fact that BACE2 can lower beta-amyloid by two distinct mechanisms makes this enzyme an especially attractive candidate for gene therapy to treat Alzheimer’s disease,” says first author Samer Abdul-Hay, Ph.D., a neuroscientist at Mayo Clinic in Florida.
The discovery suggests that impairments in BACE2 might increase the risk of Alzheimer’s disease. This is important because certain drugs in clinical use — for example, antiviral drugs used to treat human immunodeficiency virus (HIV) — work by inhibiting enzymes similar to BACE2.
Although BACE2 can lower beta-amyloid by two distinct mechanisms, only the newly discovered mechanism — beta-amyloid destruction — is likely relevant to the disease, the researchers note. This is because the second mechanism, which involves BACE2 cutting APP, does not occur in the brain. The researchers have obtained a grant from the National Institutes of Health to study whether blocking beta-amyloid destruction by BACE2 can increase the risk for Alzheimer’s disease in a mouse model of the disease.
One small change to the DNA sequence can cause more weighty changes to the human body, according to a new study released today. The discovery comes thanks to a worldwide consortium of researchers that includes Professor and Chair of Quantitative Genetics at The University of Queensland (UQ), Peter Visscher, from the Queensland Brain Institute (QBI) and Diamantina Institute (DI) at UQ.
He and his team have found a single change in genetic sequence at the gene FTO had a significant effect on the variability of body mass index (BMI). BMI is a commonly used measure of obesity. It measures someone’s weight adjusted for his or her height.
Professor Visscher said that the genetic change, called a single nucleotide polymorphism (SNP), was the replacement of one nucleotide – the units that make up our DNA – with another. “They are the most abundant type of variation in the human genome,” he said. “SNPs occur normally throughout our DNA and most have no effect on our health, however, we’ve found one that does have a small but significant effect on variation in BMI.”
After analysing data from almost 170,000 people, he and his team established that those with a sequence variant in the FTO gene not only weighed more on average, but the measured weights varied more than in the group without the variant. The variability of BMI within the group with two copies of the variant was, in fact, 7 per cent larger than the group without the variant.
Professor Visscher said this equated to around half a kilogram difference in the standard deviation of weight. “So as a group, people with two copies of the weight increasing variant are a few kilograms heavier and vary more,” he said. Genetic differences in variability of specific traits have been seen in many plant and animal species but specific genes or mechanisms to explain the phenomenon had not been identified.
Professor Visscher’s study is the first to look systematically at genetic effects on variation of a complex trait in humans using a very large sample size. “The study is important because it demonstrates that genes can be found that affect trait variability. “This is a first step towards understanding how genes control variation,” Professor Visscher said.
This study is also the first to offer researchers an indirect method to measure genotype by environment interactions without having a measure of specific environmental factors. “If a gene interacts with specific environmental factors then this can be observed with our method,” Professor Visscher said.
“For example, if the effect of a gene on weight is smaller in people who physically exercise than in people who do not, then this will lead to less variation among people with two copies of the weight decreasing variant.
“In our study we did not measure specific environmental effects such as physical exercise so we can’t say for sure whether our results are due to a genotype-environment interaction.”
This is the second study Professor Visscher has published in the prestigious journal Nature this year. Earlier this year he identified that genetic differences also affect how intelligence changes across a lifetime. The work also suggested these changes in intelligence were largely influenced by environmental factors.
The rare disorder Wolfram syndrome is caused by mutations in a single gene, but its effects on the body are far reaching. The disease leads to diabetes, hearing and vision loss, nerve cell damage that causes motor difficulties, and early death.
Now, researchers at Washington University School of Medicine in St. Louis, the Joslin Diabetes Center in Boston and the Novartis Institutes for BioMedical Research report that they have identified a mechanism related to mutations in the WFS1 gene that affects insulin-secreting beta cells. The finding will aid in the understanding of Wolfram syndrome and also may be important in the treatment of milder forms of diabetes and other disorders.
The study is published online in the journal Nature Cell Biology
“We found something we didn’t expect,” says researcher Fumihiko Urano, MD, PhD, associate professor of medicine in Washington University’s Division of Endocrinology, Metabolism and Lipid Research. “The study showed that the WFS1 gene is crucial to producing a key molecule involved in controlling the metabolic activities of individual cells.” That molecule is called cyclic AMP (cyclic adenosine monophosphate).
Insulin-secreting beta cells in the pancreas (above) cannot make enough cyclic AMP in patients with Wolfram syndrome. As a result, the pancreas produces and secretes less insulin, and the cells eventually die.
In insulin-secreting beta cells in the pancreas, for example, cyclic AMP rises in response to high blood sugar, causing those cells to produce and secrete insulin.
“I would compare cyclic AMP to money,” Urano says. “You can’t just take something you make to the store and use it to buy food. First, you have to convert it into money. Then, you use the money to buy food. In the body, external signals stimulate a cell to make cyclic AMP, and then the cyclic AMP, like money, can ‘buy’ insulin or whatever else may be needed.”
The reason patients with Wolfram syndrome experience so many problems, he says, is because mutations in the WFS1 gene interfere with cyclic AMP production in beta cells in the pancreas.
“In patients with Wolfram syndrome, there is no available WFS1 protein, and that protein is key in cyclic AMP production,” he explains. “Then, because levels of cyclic AMP are low in insulin-secreting beta cells, those cells produce and secrete less insulin. And in nerve cells, less cyclic AMP can lead to nerve cell dysfunction and death.”
By finding that cyclic AMP production is affected by mutations in the WFS1 gene, researchers now have a potential target for understanding and treating Wolfram syndrome.
“I don’t know whether we can find a way to control cyclic AMP production in specific tissues,” he says. “But if that’s possible, it could help a great deal.”
Meanwhile, although Wolfram syndrome is rare, affecting about 1 in 500,000 people, Urano says the findings also may be important to more common disorders.
“It’s likely this mechanism is related to diseases such as type 2 diabetes,” he says. “If a complete absence of the WFS1 protein causes Wolfram syndrome, perhaps a partial impairment leads to something milder, like diabetes.”
Hear the word “party” and memories of your 8th birthday sleepover or the big bash you attended last New Year’s may come rushing to mind. But it’s exactly these kinds of memories, embedded in a specific place and time, that people with depression have difficulty recalling.
Research has shown that people who suffer from, or are at risk of, depression have difficulty tapping into specific memories from their own past, an impairment that affects their ability to solve problems and leads them to focus on feelings of distress.
In a study forthcoming in Clinical Psychological Science, a new journal of the Association for Psychological Science, psychological scientists Hamid Neshat-Doost of the University of Isfahan, Iran, Laura Jobson of the University of East Anglia, Tim Dalgleish of the Cognition and Brain Sciences Unit, Medical Research Council, Cambridge and colleagues investigated whether a particular training program, Memory Specificity Training, might improve people’s memory for past events and ameliorate their symptoms of depression.
In Iran, the researchers recruited 23 adolescent Afghani refugees who had lost their fathers in the war in Afghanistan and who showed symptoms of depression. Twelve of the adolescents were randomly assigned to participate in the memory training program and 11 were randomly assigned to a control group that received no training.
All of the adolescents completed a memory test in which they saw 18 positive, neutral, and negative words in Persian and were asked to recall a specific memory related to each word. Their responses were categorized as either a specific or a non-specific type of memory. They also completed questionnaires design to measure symptoms of depression and anxiety symptoms.
For five weeks, the adolescents assigned to the training attended a weekly 80-minute group session, in which they learned about different types of memory and memory recall, and practiced recalling specific memories after being given positive, neutral, and negative keywords.
At the end of the five weeks, both the training group and the control group were given the same memory test that they were given at the beginning of the study. And they took the memory test again as part of a follow-up visit two months later.
The adolescents who participated in the training were able to provide more specific memories after the training than those who did not receive intervention. They also showed fewer symptoms of depression than the control group at the two month follow-up. The researchers found that the relationship between participant group (training or control) and their symptoms of depression at follow-up could be accounted for by changes in specific memory recall over time.
These findings are promising because they suggest that a standalone training program that focuses on specific memory recall can actually improve depression symptoms.
Based on the results of this study, Jobson, Dalgleish, and colleagues conclude that, for individuals suffering from depression, “including a brief training component that targets memory recall as an adjunct to cognitive behavioral therapy or prior therapy may have beneficial effects on memory recall and mood.”
What makes a person altruistic? Philosophers throughout the ages often pondered the question but failed to get concrete answers. New research from the University of Zurich in Switzerland shows that the answer may lie in our brains, or more accurately, that the volume of a small brain region can influences one’s predisposition for altruistic behaviour. The results, presented in the journal Neuron, indicate that individuals who behave more altruistically than others have more grey matter at the junction between the parietal and temporal lobe. This shows for the very first time that there is a connection between brain anatomy, brain activity and altruistic behaviour.
Contary to past studies that showed that social categories like gender, income or education cannot fully explain differences in altruistic behaviour, recent research in the area of neuroscience have demonstrated that differences in brain structure might be linked to differences in personality traits and abilities. Now, for the first time, a team of researchers from the University of Zurich, headed by Ernst Fehr, the director of the Department of Economics, demonstrates that there is a connection between brain anatomy and altruistic behaviour.
For their study, the researchers asked volunteers to divide money between themselves and someone else who was anonymous. The participants always had the option of sacrificing a certain portion of the money for the benefit of the other person. The monetary sacrifice was considered to be altruistic because it helped someone else at one’s own expense. The researchers found major differences in this respect: some participants were almost never willing to sacrifice money to benefit others while others behaved very altruistically.
Previous studies showed that the place where the parietal and temporal lobes meet is linked to the ability to put oneself in someone else’s shoes in order to understand their thoughts and feelings, an ability the researchers considered closely related to altruism.
So the team hypothesised that individual differences in this part of the brain might be linked to differences in altruistic behaviour. And, according to Yosuke Morishima, a postdoctoral researcher at the Department of Economics at the University of Zurich, they were right: ‘People who behaved more altruistically also had a higher proportion of grey matter at the junction between the parietal and temporal lobes.’
The researchers also discovered that the subjects displayed marked differences in brain activity while they were deciding how to split up the money. In the case of selfish people, the small brain region behind the ear is already active when the cost of altruistic behaviour is very low. In altruistic people, however, this brain region only becomes more active when the cost is very high. The brain region is activated especially strongly when people reach the limits of their willingness to behave altruistically. The reason, the researchers suspect, is that this is when there is the greatest need to overcome man’s natural self-centeredness by activating this brain region.
Said Dr Fehr: ‘These are exciting results for us. However, one should not jump to the conclusion that altruistic behaviour is determined by biological factors alone.’
It appears that the volume of grey matter can also be influenced by social processes. According to Dr Fehr, the findings therefore raise the question as to whether it is possible to promote the development of brain regions that are important for altruistic behaviour through training or social norms.
People who bear the genetic mutation for Huntington’s disease learn faster than healthy people. The more pronounced the mutation was, the more quickly they learned. This is reported by researchers from the Ruhr-Universität Bochum and from Dortmund in the journal Current Biology. The team has thus demonstrated for the first time that neurodegenerative diseases can go hand in hand with increased learning efficiency. “It is possible that the same mechanisms that lead to the degenerative changes in the central nervous system also cause the considerably better learning efficiency” says Dr. Christian Beste, head of the Emmy Noether Junior Research Group “Neuronal Mechanisms of Action Control” at the RUB.
Passive learning through repeated stimulus presentation
In a previous study, the Bochum psychologists reported that the human sense of vision can be changed in the long term by repeatedly exposing subjects to certain visual stimuli for short periods (we reported in May 2011). The task of the participants was to detect changes in the brightness of stimuli. They performed better if they had viewed the stimuli passively for a while first. In the current study, the researchers presented the same task to 29 subjects with the genetic mutation for Huntington’s disease, who, however, did not yet show any symptoms. They also tested 45 control subjects without such mutations in the genome. In both groups, the learning efficiency was better after passive stimulus presentation than without the passive training. Subjects with the Huntington’s mutation, however, increased their performance twice as fast as those without the mutation.
Glutamate may have paradoxical effect
Degenerative diseases of the nervous system are based on complex changes. A key mechanism is an increased release of the neurotransmitter glutamate. However, since glutamate is also important for learning, in some cases it could lead to the paradoxical effect: better learning efficiency despite degeneration of the nerve cells.
Detecting differences in brightness under aggravated conditions
In each experimental run, the subjects saw two consecutive small bars on a computer screen that either had the same or different brightness. Sometimes, however, not only the brightness changed from bar one to bar two, but also the orientation of the bar (vertical or horizontal). “Normally, the distraction stimulus, i.e. the change in orientation, draws all the attention” Christian Beste explains. “But after the passive training with the visual stimuli, the distraction stimulus has no effect at all.” The shift of attention from the non-relevant to the relevant properties of the stimulus was also visible in the electroencephalogram (EEG) in brain areas for early visual processing.
Better performance with stronger mutation
In Huntington’s disease, a short segment of a gene is repeated. The number of repetitions determines when the disease breaks out. In the present study, a greater number of repetitions was, however, also associated with higher learning efficiency. “This shows that neurodegenerative changes can cause paradoxical effects” says Christian Beste. “The everyday view that neurodegenerative changes fundamentally entail deterioration of various functions can no longer be maintained in this dogmatic form.”
A drug designed for diabetes sufferers could have the potential to treat neurodegenerative diseases like Alzheimer’s, a study by scientists at the University of Ulster has revealed.
Type II diabetes is a known risk factor for Alzheimer’s and it is thought that impaired insulin signalling in the brain could damage nerve cells and contribute to the disease.
Scientists believe that drugs designed to tackle Type II diabetes could also have benefits for keeping our brain cells healthy.
To investigate this, Prof Christian Hölscher and his team at the Biomedical Sciences Research Institute on the Coleraine campus used an experimental drug called (Val8)GLP-1.
This drug simulates the activity of a protein called GLP-1, which can help the body control its response to blood sugar. The scientists treated healthy mice with the drug and studied its effects in the brain.
Although it is often difficult for drugs to cross from the blood into the brain, the team found that (Val8)GLP-1 entered the brain and appeared to have no side-effects at the doses tested.
The drug promoted new brain cells to grow in the hippocampus, an area of the brain known to be involved in memory. This finding suggests that as well as its role in insulin signalling, GLP-1 may also be important for the production of new nerve cells in the mouse brain.
The team found that blocking the effect of GLP-1 in the brain made mice perform more poorly on learning and memory task, while boosting it with the drug seemed to have no effect on behaviour.
The new findings, published this week in the journal Brain Research, are part of ongoing research funded by Alzheimer’s Research UK, the leading dementia research charity.
Prof Hölscher, said: “Here at the Biomedical Sciences Research Institute, we are really interested in the potential of diabetes drugs for protecting brain cells from damage and even promoting new brain cells to grow. This could have huge implications for diseases like Alzheimer’s or Parkinson’s, where brain cells are lost.
“It is very encouraging that the experimental drug we tested, (Val8)GLP-1, entered the brain and our work suggests that GLP-1 could be a really important target for boosting memory. While we didn’t see benefits on learning and memory in these healthy mice, we are keen to test the drugs in mice with signs of Alzheimer’s disease, where we could see real improvements.”
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We are pleased to have supported this early stage research, suggesting that this experimental diabetes drug could also promote the growth of new brain cells. While we know losing brain cells is a key feature of Alzheimer’s, there is a long way to go before we would know whether this drug could benefit people with the disease.
"This research will help us understand the factors that keep nerve cells healthy, knowledge that could hold vital clues to tackling Alzheimer’s. With over half a million people in the UK living with the disease, learning more about how to keep our brain cells healthy is of vital importance. Funding for dementia research lags far behind that of other common diseases, but is essential if we are to realise the true potential of research like this.”