1. Exercising can protect the brain from Alzheimer’s disease

    May 26, 2017 by Ashley

    From the University of British Columbia Okanagan campus press release:

    The evidence is clear. Physical activity is associated with a reduced risk of Alzheimer’s disease, says a panel of researchers and not-for-profit leaders, led by UBC’s Okanagan campus.

    The researchers also confirmed that regular physical activity may improve the performance of daily activities for people afflicted with Alzheimer’s. Their conclusions may have significant implications for the 1.1 million Canadians affected directly or indirectly by dementia.

    “As there is no current cure for Alzheimer’s, there is an urgent need for interventions to reduce the risk of developing it and to help manage the symptoms,” says study first author Kathleen Martin Ginis, professor in UBC Okanagan’s School of Health and Exercise Sciences. “After evaluating all the research available, our panel agrees that physical activity is a practical, economical and accessible intervention for both the prevention and management of Alzheimer’s disease and other dementias.”

    Martin Ginis and her cohort reviewed data from more than 150 research articles about the impact of physical activity on people with Alzheimer’s. Some of the work explored how physical activity improves the patient’s quality of life and the others examined the risk of developing Alzheimer’s based on the amount of activity in which an individual participated.

    The panel concluded that regular physical activity improves activities of daily living and mobility in in older adults with Alzheimer’s and may improve general cognition and balance. They also established that older adults not diagnosed with Alzheimer’s who are physically active, were significantly less likely to develop the disease compared to people who were inactive.

    “This is exciting work,” says Martin Ginis. “From here we were able to prepare a consensus statement and messaging which not only has community backing, but is also evidence-based. Now we have the tool to promote the protective benefit of physical activity to older adults. I’m hopeful this will move the needle on this major health concern.”

    Alzheimer’s disease is the most common form of dementia, characterized by progressive neurodegeneration that results in severe cognitive impairment, compromised physical ability and loss of independence. The number of worldwide cases is expected to increase from 30.8 million in 2010 to more than 106 million in 2050.


  2. Spread of tau protein measured in brains of Alzheimer’s patients

    May 25, 2017 by Ashley

    From the Karolinska Institutet press release:

    In a new study presented in Molecular Psychiatry, researchers at Karolinska Institutet have measured how deposits of the pathological protein tau spread through the brain over the course of Alzheimer’s disease. Their results show that the size of the deposit and the speed of its spread differ from one individual to the next, and that large amounts of tau in the brain can be linked to episodic memory impairment.

    Already in a very early phase of Alzheimer’s disease there is an accumulation of tau in the brain cells, where its adverse effect on cell function causes memory impairment. It is therefore an attractive target for vaccine researchers. For the present study, Professor Agneta Nordberg at Karolinska Institutet’s Department of Neurobiology, Care Sciences and Society and her doctoral student Konstantinos Chiotis along with the rest of her team used PET brain imaging to measure the spread of tau deposits as well as the amyloid plaque associated with Alzheimer’s disease, and charted the energy metabolism of the brain cells. They then examined how these three parameters changed over the course of the disease.

    “There’s been an international race to measure tau spread, and we probably got there first,” says Professor Nordberg. “There are no previous reports on how tau deposits spread after 17 months into the disease. Our results can improve understanding of tau accumulation in Alzheimer’s disease, help ongoing research to quantify the effect of tau vaccines, and enable early diagnosis.”

    The study included 16 patients at different stages of Alzheimer’s disease from the memory unit at Karolinska Hospital in Huddinge. The patients were given a series of neurological memory tests and underwent PET scans at 17-month intervals. While all 16 participants had abundant amyloid plaque deposition in the brain, the size and speed of spread of their tau deposits differed significantly between individuals.

    “We also saw a strong direct correlation between size of deposit and episodic memory impairment,” continues Professor Nordberg. “This could explain why the disease progresses at such a varying rate from one patient to the other. That said, tau doesn’t seem to have much of an effect on the global general memory, which is more reasonably related to brain metabolism.”

    The study was conducted in collaboration with Uppsala University, where the PET scans were performed.


  3. Study expands understanding of how the brain encodes fear memory

    May 19, 2017 by Ashley

    From the UC Riverside press release:

    Research published by scientists at the University of California, Riverside on “fear memory” could lead to the development of therapies that reduce the effects of post-traumatic stress disorder (PTSD).

    To survive in a dynamic environment, animals develop adaptive fear responses to dangerous situations, requiring coordinated neural activity in the hippocampus, medial prefrontal cortex (mPFC), and amygdala – three brain areas connected to one another. A disruption of this process leads to maladaptive generalized fear in PTSD, which affects 7 percent of the U.S. population.

    Jun-Hyeong Cho, an assistant professor of cell biology and neuroscience and Woong Bin Kim, a postdoctoral researcher in Cho’s lab, have now found that a population of hippocampal neurons project to both the amygdala and the mPFC, and that it is these neurons that efficiently convey information to these two brain areas to encode and retrieve fear memory for a context associated with an aversive event.

    The study, which appeared in the May 10 print issue of the Journal of Neuroscience, is the first to quantify these “double-projecting” hippocampal neurons and explain how they convey contextual information more efficiently for fear responses, compared to hippocampal neurons that project only to either the mPFC or the amygdala.

    “This study, done using a mouse model, expands our understanding of how associative fear memory for a relevant context is encoded in the brain,” said Cho, the lead author of the study and a member of the UCR School of Medicine’s Center for Glial-Neuronal Interactions, “and could inform the development of novel therapeutics to reduce pathological fear in PTSD.”

    To visualize the double-projecting hippocampal neurons, Cho and Kim used a tracing method in which hippocampal neurons that project to different brain areas were labeled with fluorescence proteins with different colors. The pair also developed a novel approach of electrophysiological recordings and optogenetics to examine how exactly the double-projecting neurons connected to the mPFC and amygdala. (These experimental approaches can be used to examine other brain areas that project to multiple targets.)

    “We were surprised to find that as much as 17 percent of hippocampal neurons that projected to the amygdala or the mPFC were, in fact, double-projecting neurons,” Cho said. “Although previous studies demonstrated the existence of double-projecting hippocampal neurons, neuroscientists largely ignored them when studying the role of neural pathways between the hippocampus, amygdala and mPFC in contextual fear learning.”

    Cho explained that the acquisition (encoding) and retrieval of contextual fear memory requires coordinated neural activity in the hippocampus, amygdala and mPFC. The hippocampus encodes context cues, the amygdala stores associations between a context and an aversive event, and the mPFC signals whether a defensive response is appropriate in the present context.

    Context is broadly defined as the set of circumstances around an event. In contextual fear conditioning, experimental subjects are placed in an emotionally neutral context (such as a room) and presented an aversive stimulus (such as an electrical shock). Then, they learn to associate the context with the aversive event, and show fear responses (such as freezing behavior) when placed subsequently in that context.

    “Our study suggests that double-projecting hippocampal neurons can facilitate synchronized neural activity in the mPFC and amygdala that is implicated in learned fear,” he said. “It is by modulating the activity of the mPFC and basal amygdala that these double-projecting hippocampal neurons contribute to the acquisition and retrieval of fear memory for a context associated with an aversive event.”

    Cho also explained that multiple projections from single neurons appear to be a general feature of the neural circuits in the brain and could promote synchronized neural activity and long-term changes in the efficiency of neural communication.

    The study came about when, a few years ago, Cho and Kim were selectively labeling and stimulating hippocampal neurons that project to the mPFC, and examining how this manipulation affects fear memory formation in mice. When they carefully examined the brain tissue, they found that labeled hippocampal neurons also projected to the amygdala.

    “We initially thought there was something wrong with our experiments,” Kim, the postdoctoral researcher, said. “But, when we repeated the experiments, the same pattern was observed consistently. We realized that this could be an exciting finding that may account for how contextual information is processed and conveyed between brain areas for the formation of fear memory for the context associated with an aversive event.”

    Next, to better understand the role of double-projecting hippocampal neurons in fear learning and memory, Cho and Kim plan to selectively silence these neurons and examine how this manipulation impacts the formation of fear memory for a context associated with an aversive event.


  4. New hope for patients with primary progressive aphasia

    May 18, 2017 by Ashley

    From the Baycrest Centre for Geriatric Care press release:

    A Baycrest Health Sciences researcher and clinician has developed the first group language intervention that helps individuals losing the ability to speak due to a rare form of dementia, and could help patients maintain their communication abilities for longer.

    Primary Progressive Aphasia (PPA) is a unique language disorder that involves struggles with incorrect word substitutions, mispronounced words and/or difficulty understanding simple words and forgetting names of familiar objects and people. With PPA, language function declines before the memory systems, which is the opposite of Alzheimer’s disease.

    Dr. Regina Jokel, a speech-language pathologist at Baycrest’s Sam and Ida Ross Memory Clinic and a clinician-scientist with the Rotman Research Institute (RRI), has developed the first structured group intervention for PPA patients and their caregivers. This intervention could also help treat patients with other communication problems, such as mild cognitive impairment (a condition that is likely to develop into Alzheimer’s). The results of her pilot program were published in the Journal of Communication Disorders on April 14, 2017.

    “This research aims to address the needs of one of the most underserviced populations in language disorders,” says Dr. Jokel. “Individuals with PPA are often referred to either Alzheimer’s programs or aphasia centres. Neither option is appropriate in this case, which often leaves individuals with PPA adrift in our health care system. Our group intervention has the potential to fill the existing void and reduce demands on numerous other health services.”

    Language rehabilitation has made headway in managing the disorder, but there are limited PPA treatment options, adds Dr. Jokel.

    Dr. Jokel is one of the few researchers in the world studying this disease. She was motivated to acquire her PhD. and devise the intervention after encountering her first PPA patient more than 25 years ago.

    “When I realized the patient had PPA, I ran to the rehabilitation literature thinking that he needed to start some sort of therapy. I ran a search and came up with nothing. Absolutely nothing,” says Jokel. “That’s when I thought, ‘It’s time to design something.'”

    The 10-week intervention included working on language activities, learning communication strategies and receiving counselling and education for both patients and their caregivers. During the pilot program, patients either improved or remained unchanged on communication assessments for adults with communication disorders. Their caregivers also reported being better prepared to manage psychosocial issues and communication challenges and had more knowledge of PPA and the disease’s progression.

    “In progressive disorders, any sign of maintaining current level of function should be interpreted as success,” says Dr. Jokel. “Slowing the progression and maintenance of communication abilities should be the most important goal.”

    For the study’s next steps, Dr. Jokel has received support from a Brain Canada-Alzheimer’s Association partnership grant to assess the therapy’s impact on the language skills of PPA patients. With support from the Ontario Brain Institute, she is also collaborating with RRI brain rehabilitation scientist, Dr. Jed Meltzer, to explore the effect of brain stimulation on patients also undergoing language therapy.


  5. Study suggests cannabis reverses aging processes in the brain

    May 13, 2017 by Ashley

    From the University of Bonn press release:

    Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel). Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia. The results are now presented in the journal Nature Medicine.

    Like any other organ, our brain ages. As a result, cognitive ability also decreases with increasing age. This can be noticed, for instance, in that it becomes more difficult to learn new things or devote attention to several things at the same time. This process is normal, but can also promote dementia. Researchers have long been looking for ways to slow down or even reverse this process.

    Scientists at the University of Bonn and The Hebrew University of Jerusalem (Israel) have now achieved this in mice. These animals have a relatively short life expectancy in nature and display pronounced cognitive deficits even at twelve months of age. The researchers administered a small quantity of THC, the active ingredient in the hemp plant (cannabis), to mice aged two, twelve and 18 months over a period of four weeks.

    Afterwards, they tested learning capacity and memory performance in the animals — including, for instance, orientation skills and the recognition of other mice. Mice who were only given a placebo displayed natural age-dependent learning and memory losses. In contrast, the cognitive functions of the animals treated with cannabis were just as good as the two-month-old control animals. “The treatment completely reversed the loss of performance in the old animals,” reported Prof. Andreas Zimmer from the Institute of Molecular Psychiatry at the University of Bonn and member of the Cluster of Excellence ImmunoSensation.

    Years of meticulous research

    This treatment success is the result of years of meticulous research. First of all, the scientists discovered that the brain ages much faster when mice do not possess any functional receptors for THC. These cannabinoid 1 (CB1) receptors are proteins to which the substances dock and thus trigger a signal chain. CB1 is also the reason for the intoxicating effect of THC in cannabis products, such as hashish or marihuana, which accumulate at the receptor. THC imitates the effect of cannabinoids produced naturally in the body, which fulfil important functions in the brain. “With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces,” says Prof. Zimmer. “When the activity of the cannabinoid system declines, we find rapid ageing in the brain.”

    To discover precisely what effect the THC treatment has in old mice, the researchers examined the brain tissue and gene activity of the treated mice. The findings were surprising: the molecular signature no longer corresponded to that of old animals, but was instead very similar to that of young animals. The number of links between the nerve cells in the brain also increased again, which is an important prerequisite for learning ability. “It looked as though the THC treatment turned back the molecular clock,” says Zimmer.

    Next step: clinical trial on humans

    A low dose of the administered THC was chosen so that there was no intoxicating effect in the mice. Cannabis products are already permitted as medications, for instance as pain relief. As a next step, the researchers want to conduct a clinical trial to investigate whether THC also reverses ageing processes in the brain in humans and can increase cognitive ability.

    The North Rhine-Westphalia science minister Svenja Schulze appeared thrilled by the study: “The promotion of knowledge-led research is indispensable, as it is the breeding ground for all matters relating to application. Although there is a long path from mice to humans, I feel extremely positive about the prospect that THC could be used to treat dementia, for instance.”


  6. Exercise study offers hope in fight against Alzheimer’s

    May 10, 2017 by Ashley

    From the University of Maryland press release:

    Could the initiation of a simple walking exercise program help older adults to reverse declines in key brain regions? A new study led by University of Maryland School of Public Health researchers adds more information about how physical activity impacts brain physiology and offers hope that it may be possible to reestablish some protective neuronal connections. Dr. J. Carson Smith, associate professor of kinesiology, and colleagues explored how a 12-week walking intervention with older adults, ages 60-88, affected functionality of a brain region known to show declines in people suffering from mild cognitive impairment (MCI) or Alzheimer’s disease.

    “The brain’s posterior cingulate cortex (PCC)/precuneus region is a hub of neuronal networks which integrates and disperses signals,” explains Dr. J. Carson Smith, senior author of the paper published in the Journal of Alzheimer’s Disease and director of the Exercise for Brain Health Laboratory. “We know that a loss of connectivity to this hub is associated with memory loss and amyloid accumulation, both signs of MCI and Alzheimer’s.”

    For this reason, reduced connectivity to the PCC/precuneus region is seen as a potential biomarker to detect cognitive impairment even before symptoms of MCI or AD may appear. It is also a potential target to test the effectiveness of interventions such as exercise to improve brain function in those exhibiting symptoms of MCI.

    Dr. Smith’s research team recruited two groups — one with 16 healthy elders and another with 16 elders diagnosed with mild cognitive impairment to participate in an exercise intervention that included walking for 30 minutes, four times a week (at 50-60 % of heart rate reserve) for three months.

    Before and after the exercise intervention, participants in both groups underwent fMRI brain scans to assess functional connectivity between multiple brain regions and the PCC/precuneus. After completing the intervention, both groups showed improved ability to remember a list of words; however only the MCI group showed increased connectivity to the PCC/precuneus hub, which was evident in 10 regions spanning the frontal, parietal, temporal and insular lobes, and the cerebellum.

    “These findings suggest that the protective effects of exercise training on cognition may be realized by the brain re-establishing communication and connections among the brain’s so-called default mode network, which may possibly increase the capacity to compensate for the neural pathology associated with Alzheimer’s disease,” said Dr. Smith.

    While it is unclear yet whether the effects of exercise training can delay further cognitive decline in patients diagnosed with MCI, the neural network connectivity changes documented in this study provide hope that exercise training may stimulate brain plasticity and restore communication between brain regions that may have been lost through Alzheimer’s disease. The specificity of these effects in the MCI group further suggest that exercise may be particularly useful in those who have already experienced mild memory loss. Future studies planned by Dr. Smith’s team aim to include exercise control conditions, and to incorporate exercise combined with cognitive engagement, among healthy older adults who are at increased risk for Alzheimer’s disease.


  7. Brain tissue structure could explain link between fitness and memory

    May 7, 2017 by Ashley

    From the University of Illinois at Urbana-Champaign press release:

    Studies have suggested a link between fitness and memory, but researchers have struggled to find the mechanism that links them. A new study by University of Illinois researchers found that the key may lie in the microstructure of the hippocampus, a region in the middle of the brain involved in memory processes.

    Aron Barbey, a professor of psychology, led a group of researchers at the Beckman Institute for Advanced Science and Technology at Illinois that used a specialized MRI technique to measure the structural integrity of the hippocampus in healthy young adults and correlated it with their performances on fitness and memory tests. They found that viscoelasticity, a measure of structural integrity in brain tissue, was correlated with fitness and memory performance — much more so than simply looking at the size of the hippocampus.

    “Using a new tool to examine the integrity of the hippocampus in healthy young adults could tell us more about how this region functions and how to predict decline for early intervention,” Barbey said. “By the time we look at diseased states, it’s often too late.”

    Prior research led by Illinois psychology professor Neal Cohen, who is also a co-author on the new paper, demonstrated that the hippocampus is critical for relational memory and that the integrity of this region predicts a host of neurodegenerative diseases. To date, much research on the hippocampus’ structure has focused on its size.

    Studies in developing children and declining older adults have found strong correlations between hippocampal size and memory. However, size does not seem to matter as much in healthy young adults, said postdoctoral researcher Hillary Schwarb. The Illinois group looked instead at the microstructure of the tissue, using an emerging neuroimaging tool called magnetic resonance elastography. The method involves an MRI scan, but with a pillow under the subject’s head vibrating at a very low amplitude — as gentle as driving on the interstate, Schwarb said. The vibration is the key to measuring the structural integrity of the hippocampus.

    “It’s a lot like sending ripples through a still pond — if there’s some large thing like a boulder under the surface, the ripples are going to displace around it,” Schwarb said. “We are sending waves through the brain and reconstructing the displacements into a map we can look at and measure.”

    The study, published in the journal NeuroImage, found that those who performed better on the fitness test tended to also perform better on the memory task, confirming a correlation the group had noticed before. But by adding the information on the structure of the hippocampus, the researchers were able to find a possible pathway for the link. They found that the subjects with higher fitness levels also had more elastic tissue in the hippocampus. The tissue structure, in turn, was associated with memory.

    “We found that when the hippocampus is more elastic, memory is better. An elastic hippocampus is like a firm foam mattress pad that pops right back up after you get up,” said study co-author Curtis Johnson, a former graduate researcher at the Beckman Institute who is now a professor at the University of Delaware. “When the hippocampus is more viscous, memory is worse. A viscous hippocampus is like a memory-foam mattress that holds its shape even after you get up.”

    The results suggest that the viscoelasticity of the hippocampus may be the mediating factor in the relationship between fitness and memory in healthy young adults.

    “It also shows us that magnetic resonance elastography is a useful tool for understanding tissue microstructure, and that microstructure is important to cognition,” Schwarb said. “This provides us a new level of analysis for studying the human brain.”


  8. Low levels of ‘memory protein’ linked to cognitive decline in Alzheimer’s disease

    by Ashley

    From the Johns Hopkins Medicine press release:

    Working with human brain tissue samples and genetically engineered mice, Johns Hopkins Medicine researchers together with colleagues at the National Institutes of Health, the University of California San Diego Shiley-Marcos Alzheimer’s Disease Research Center, Columbia University, and the Institute for Basic Research in Staten Island say that consequences of low levels of the protein NPTX2 in the brains of people with Alzheimer’s disease (AD) may change the pattern of neural activity in ways that lead to the learning and memory loss that are hallmarks of the disease.

    This discovery, described online in the April 25 edition of eLife, will lead to important research and may one day help experts develop new and better therapies for Alzheimer’s and other forms of cognitive decline.

    AD currently affects more than five million Americans.

    Clumps of proteins called amyloid plaques, long seen in the brains of people with AD, are often blamed for the mental decline associated with the disease. But autopsies and brain imaging studies reveal that people can have high levels of amyloid without displaying symptoms of AD, calling into question a direct link between amyloid and dementia.

    This new study shows that when the protein NPTX2 is “turned down” at the same time that amyloid is accumulating in the brain, circuit adaptations that are essential for neurons to “speak in unison” are disrupted, resulting in a failure of memory.

    “These findings represent something extraordinarily interesting about how cognition fails in human Alzheimer’s disease,” says Paul Worley, M.D., a neuroscientist at the Johns Hopkins University School of Medicine and the paper’s senior author. “The key point here is that it’s the combination of amyloid and low NPTX2 that leads to cognitive failure.”

    Since the 1990s, Worley’s group has been studying a set of genes known as “immediate early genes,” so called because they’re activated almost instantly in brain cells when people and other animals have an experience that results in a new memory.

    The gene NPTX2 is one of these immediate early genes that gets activated and makes a protein that neurons use to strengthen “circuits” in the brain.

    “Those connections are essential for the brain to establish synchronized groups of ‘circuits’ in response to experiences,” says Worley. “Without them, neuronal activation cannot be effectively synchronized and the brain cannot process information.”

    Worley says he was intrigued by previous studies indicating altered patterns of activity in brains of individuals with Alzheimer’s. Worley’s group wondered whether altered activity was linked to changes in immediate early gene function.

    To get answers, the researchers first turned to a library of 144 archived human brain tissue samples to measure levels of the protein encoded by the NPTX2 gene. NPTX2 protein levels, they discovered, were reduced by as much as 90 percent in brain samples from people with AD compared with age-matched brain samples without AD. By contrast, people with amyloid plaques who had never shown signs of AD had normal levels of NPTX2. This was an initial suggestion of a link between NPTX2 and cognition.

    Prior studies had shown NPTX2 to play an essential role for developmental brain wiring and for resistance to experimental epilepsy. To study how lower-than-normal levels of NPTX2 might be related to the cognitive dysfunction of AD, Worley and his collaborators examined mice bred without the rodent equivalent of the NPTX2 gene.

    Tests showed that a lack of NPTX2 alone wasn’t enough to affect cell function as tested in brain slices. But then the researchers added to mice a gene that increases amyloid generation in their brain. In brain slices from mice with both amyloid and no NPTX2, fast-spiking interneurons could not control brain “rhythms” important for making new memories. Moreover, a glutamate receptor that is normally expressed in interneurons and essential for interneuron function was down-regulated as a consequence of amyloid and NPTX2 deletion in mouse and similarly reduced in human AD brain.

    Worley says that results suggest that the increased activity seen in the brains of AD patients is due to low NPTX2, combined with amyloid plaques, with consequent disruption of interneuron function. And if the effect of NPTX2 and amyloid is synergistic — one depending on the other for the effect — it would explain why not all people with high levels of brain amyloid show signs of AD.

    The team then examined NPTX2 protein in the cerebrospinal fluid (CSF) of 60 living AD patients and 72 people without AD. Lower scores of memory and cognition on standard AD tests, they found, were associated with lower levels of NPTX2 in the CSF. Moreover, NPTX2 correlated with measures of the size of the hippocampus, a brain region essential for memory that shrinks in AD. In this patient population, NPTX2 levels were more closely correlated with cognitive performance than current best biomarkers — including tau, a biomarker of neurodegenerative diseases, and a biomarker known as A-beta-42, which has long been associated with AD. Overall, NPTX2 levels in the CSF of AD patients were 36 to 70 percent lower than in people without AD.

    “Perhaps the most important aspect of the discovery is that NPTX2 reduction appears to be independent of the mechanism that generates amyloid plaques. This means that NPTX2 represents a new mechanism, which is strongly founded in basic science research, and that has not previously been studied in animal models or in the context of human disease. This creates many new opportunities,” says Worley.

    “One immediate application may be to determine whether measures of NPTX2 can be helpful as a way of sorting patients and identifying a subset that are most responsive to emerging therapies.” Worley says. For instance, drugs that disrupt amyloid may be more effective in patients with relatively high NPTX2. His group is now providing reagents to companies to assess development of a commercial test that measures NPTX2 levels.

    More work is needed, Worley adds, to understand why NPTX2 levels become low in AD and how that process could be prevented or slowed.


  9. Study suggests rosemary aroma can aid children’s working memory

    May 4, 2017 by Ashley

    From the British Psychological Society press release:

    Exposure to the aroma of rosemary essential oil can significantly enhance working memory in children.

    This is one the findings of a study presented today, Thursday 4 May 2017, by Dr Mark Moss and Victoria Earle of Northumbria University at the British Psychological Society Annual Conference in Brighton.

    Dr Mark Moss said: “Our previous study demonstrated the aroma of rosemary essential oil could enhance cognition in healthy adults. Knowing how important working memory is in academic achievement we wanted to see if similar effects could be found in school age children in classroom settings.”

    A total of 40 children aged 10 to 11 took part in a class based test on different mental tasks. Children were randomly assigned to a room that had either rosemary oil diffused in it for ten minutes or a room with no scent.

    The children were tested individually, seated at the table opposite the researcher. After introducing herself to the child the researcher said: “You are here to play some memory games. Please don’t be nervous but try the best you can to remember what I ask you to.”

    Analysis revealed that the children in the aroma room received significantly higher scores than the non-scented room. The test to recall words demonstrated the greatest different in scores.

    Dr Moss said: “Why and how rosemary has this effect is still up for debate. It could be that aromas affect electrical activity in the brain or that pharmacologically active compounds can be absorbed when adults are exposed.

    “We do know that poor working memory is related to poor academic performance and these findings offers a possible cost effective and simple intervention to improve academic performance in children. The time is ripe for large-scale trials of aroma application in education settings.”


  10. Caudate stimulation enhances human associative learning

    May 3, 2017 by Ashley

    From the American Association of Neurological Surgeons (AANS) press release:

    Associative learning allows an individual to acquire an association between a sensory cue and an outcome resulting from a specific response. Associative learning plays a vital role in the ability to learn new associations that allow human beings to optimally respond to the world around them. Research in humans and primates supports an important role for the caudate in associative learning. Our objective was to determine whether caudate stimulation could modulate associative learning in humans and to examine the neural circuitry involved in this process.

    Two subjects who underwent depth electrode placement for monitoring of refractory epilepsy were included in the study. During recording from intracranial electrodes, subjects participated in an associative learning task requiring them to learn associates presented image with a button press. For half of the presented images, bilateral caudate stimulation was performed at 2 mA and 200 Hz for one second during the feedback epoch after correct responses. Authors calculated the learning curve for stimulated and non-stimulated images using a state space model and calculated average power at electrode contacts in different spectral bands during the response and feedback epochs of the task and examined for correlation with the learning curve.

    Caudate stimulation during correct feedback significantly improved associative learning. Stimulated image associations were learned more rapidly than non-stimulated image associations. Learning was associated with increased low gamma (30-55 Hz) power in the nucleus accumbens and increased theta (3-8 Hz) power in the dorsolateral prefrontal cortex.

    Caudate stimulation during reinforcement of correct association enhances learning and is associated with power changes in both dopaminergic circuitry involved in reward processing and areas involved in associative processes. This supports a role for the caudate in integrating reward information with associations. Furthermore, this suggests a new potential target for neuromodulation in human memory disorders.