Posts tagged cerebellum
Articles and news from the latest research reports.
Did standing up change our brains?
Although lots of animals are smart, humans are even smarter. How and why do we think and act so differently from other species?
A young boy’s efforts while learning to walk have suggested a new explanation, in a new journal paper jointly authored by his father and grandfather, both academics at the University of Sydney.
In the latest issue of the scientific journal, Frontiers in Neuroscience, the son-and-father team Mac and Rick Shine suggest that the big difference between humans and other species may lie in how we use our brains for routine tasks.
They advance the idea that the key to exploiting the awesome processing power of our brain’s most distinctive feature - the cortex - may have been to liberate it from the drudgery of controlling routine activities.
And that’s where young Tyler Shine, now two years old, comes into the story. When Tyler was first learning to walk, his doting father and grandfather noticed that every step took Tyler’s full attention.
But before too long, walking became routine, and Tyler was able to start noticing other things around him. He was better at maintaining his balance, which freed up his attention to focus on more interesting tasks, like trying to get into mischief.
How did Tyler improve? His father and grandfather suggest that he did so by transferring the control of his balance to ‘lower’ parts of the brain, freeing up the powerful cortex to focus on unpredictable challenges, such as a bumpy floor covered in stray toys.
"Any complicated task - like driving a car or playing a musical instrument - starts out consuming all our attention, but eventually becomes routine," Mac Shine says.
"Studies of brain function suggest that we shift the control of these routine tasks down to ‘lower’ areas of the brain, such as the basal ganglia and the cerebellum.
"So, humans are smart because we have automated the routine tasks; and thus, can devote our most potent mental faculties to deal with new, unpredictable challenges.
"What event in the early history of humans made us change the way we use our brains?
Watching Tyler learn to walk suggested that it was the evolutionary shift from walking on all fours, to walking on two legs.
"Suddenly our brains were overwhelmed with the complicated challenge of keeping our balance - and the best kind of brain to have, was one that didn’t waste its most powerful functions on controlling routine tasks."
So, the Shines believe, those first pre-humans who began to stand upright faced a new evolutionary pressure not just on their bodies, but on their brains as well.
"New technologies are allowing us to look inside the brain while it works, and we are learning an enormous amount," Mac Shine says.
"But in order to interpret those results, we need new ideas as well. I’m delighted that my son has played a role in suggesting one of those ideas."
"Hopefully, by the time he is watching his own son learn to walk, we will be much closer to truly understanding the greatest mystery of human existence: how our brains work."
Genetic legacy from the Ottoman Empire: Single mutation causes rare brain disorder
An international team of researchers have identified a previously unknown neurodegenerative disorder and discovered it is caused by a single mutation in one individual born during the height of the Ottoman Empire in Turkey about 16 generations ago.
(Image caption: An fMRI scan of the brain of a patient with CLP1 mutation reveals severe atrophy of the brainstem (red line) and cerebellum (blue) as well as lack of formation of the corpus callosum (green), which connects both sides of the cerebrum (yellow), which is also atrophied. The lines outline approximately the expected sizes of the brain areas. A study traced the mutation to a single individual born in Turkey during the Ottoman Empire, some 16 generations ago.)
The genetic cause of the rare disorder was discovered during a massive analysis of the individual genomes of thousands of Turkish children suffering from neurological disorders.
“The more we learn about basic mechanisms behind rare forms of neuro-degeneration, the more novel insights we can gain into more common diseases such as Alzheimer’s or Lou Gehrig’s Disease,” said Murat Gunel, the Nixdorff-German Professor of Neurosurgery, and professor of genetics and neurobiology at Yale.
Gunel is a senior co-author of one of two papers published in the April 24 issue of the journal Cell that document the devastating effects of a mutation in the CLP1 gene. Gunel and colleagues at Yale Center for Mendelian Genomics along with Joseph Gleeson’s group at University of California-San Diego compared DNA sequencing results of more than 2,000 children from different families with neurodevelopmental disorders. In four apparently unrelated families, they identified the exact same mutation in the CLP1 gene. Working with the Frank Bass group from the Netherlands, the researchers also studied how CLP1 mutations interfered with the transfer of information encoded within genes to cells’ protein-making machinery.
The discovery of the identical mutation in seemingly unrelated families originally from eastern Turkey suggested an ancestral mutation, dating back several generations, noted the researchers.
Affected children suffer from intellectual disability, seizures, and delayed or absent mental and motor development, and their imaging studies show atrophy affecting the cerebral cortex, cerebellum, and the brain stem.
The second Cell paper by researchers from Baylor School of Medicine and Austria also found the identical founder mutation in CLP1 in another 11 children from an additional five families originally from eastern Turkey.
Gunel said that the high prevalence of consanguineous marriages [between closely related people] in Turkey and the Middle East leads to these rare recessive genetic neurodegenerative disorders. Affected children inherit mutations in the same gene from both of their parents, who are closely related to each other, such as first cousins. Without consanguinity between parents, children are very unlikely to inherit two mutations in the same gene.
“By dissecting the genetic basis of these neurodevelopmental disorders, we are gaining fundamental insight into basic physiological mechanisms important for human brain development and function” Gunel said. “We learn a lot about normal biology by studying what happens when things go wrong.”
(Source: news.yale.edu)
Neuroscientists discover brain circuits involved in emotion
Neuroscientists have discovered a brain pathway that underlies the emotional behaviours critical for survival.
New research by the University of Bristol, published in the Journal of Physiology, has identified a chain of neural connections which links central survival circuits to the spinal cord, causing the body to freeze when experiencing fear.
Understanding how these central neural pathways work is a fundamental step towards developing effective treatments for emotional disorders such as anxiety, panic attacks and phobias.
An important brain region responsible for how humans and animals respond to danger is known as the PAG (periaqueductal grey), and it can trigger responses such as freezing, a high heart rate, increase in blood pressure and the desire for flight or fight.
This latest research has discovered a brain pathway leading from the PAG to a highly localised part of the cerebellum, called the pyramis. The research went on to show that the pyramis is involved in generating freezing behaviour when central survival networks are activated during innate and learnt threatening situations.
The pyramis may therefore serve as an important point of convergence for different survival networks in order to react to an emotionally challenging situation.
Dr Stella Koutsikou, first author of the study and Research Associate in the School of Physiology and Pharmacology at the University of Bristol, said: “There is a growing consensus that understanding the neural circuits underlying fear behaviour is a fundamental step towards developing effective treatments for behavioural changes associated with emotional disorders.”
Professor Bridget Lumb, Professor of Systems Neuroscience, added: “Our work introduces the novel concept that the cerebellum is a promising target for therapeutic strategies to manage dysregulation of emotional states such as panic disorders and phobias.”
The researchers involved in this work are all members of Bristol Neuroscience which fosters interactions across one of the largest communities of neuroscientists in the UK.
Professor Richard Apps said: “This is a great example of how Bristol Neuroscience brings together expertise in different fields of neuroscience leading to exciting new insights into brain function.”
Muscle-controlling Neurons Know When They Mess Up
Whether it is playing a piano sonata or acing a tennis serve, the brain needs to orchestrate precise, coordinated control over the body’s many muscles. Moreover, there needs to be some kind of feedback from the senses should any of those movements go wrong. Neurons that coordinate those movements, known as Purkinje cells, and ones that provide feedback when there is an error or unexpected sensation, known as climbing fibers, work in close concert to fine-tune motor control.
A team of researchers from the University of Pennsylvania and Princeton University has now begun to unravel the decades-spanning paradox concerning how this feedback system works.
At the heart of this puzzle is the fact that while climbing fibers send signals to Purkinje cells when there is an error to report, they also fire spontaneously, about once a second. There did not seem to be any mechanism by which individual Purkinje cells could detect a legitimate error signal from within this deafening noise of random firing.
Using a microscopy technique that allowed the researchers to directly visualize the chemical signaling occurring between the climbing fibers and Purkinje cells of live, active mice, the Penn team has for the first time shown that there is a measurable difference between “true” and “false” signals.
This knowledge will be fundamental to future studies of fine motor control, particularly with regards to how movements can be improved with practice.
The research was conducted by Javier Medina, assistant professor in the Department of Psychology in Penn’s School of Arts and Sciences, and Farzaneh Najafi, a graduate student in the Department of Biology. They collaborated with postdoctoral fellow Andrea Giovannucci and associate professor Samuel S. H. Wang of Princeton University.
It was published in the journal Cell Reports.
The cerebellum is one of the brain’s motor control centers. It contains thousands of Purkinje cells, each of which collects information from elsewhere in the brain and funnels it down to the muscle-triggering motor neurons. Each Purkinje cell receives messages from a climbing fiber, a type of neuron that extends from the brain stem and sends feedback about the associated muscles.
“Climbing fibers are not just sensory neurons, however,” Medina said. “What makes climbing fibers interesting is that they don’t just say, ‘Something touched my face’; They say, ‘Something touched my face when I wasn’t expecting it.’ This is something that our brains do all the time, which explains why you can’t tickle yourself. There’s part of your brain that’s already expecting the sensation that will come from moving your fingers. But if someone else does it, the brain can’t predict it in the same way and it is that unexpectedness that leads to the tickling sensation.”
Not only does the climbing fiber feedback system for unexpected sensations serve as an alert to potential danger — unstable footing, an unseen predator brushing by — it helps the brain improve when an intended action doesn’t go as planned.
“The sensation of muscles that don’t move in the way the Purkinje cells direct them to also counts as unexpected, which is why some people call climbing fibers ‘error cells,’” Medina said. “When you mess up your tennis swing, they’re saying to the Purkinje cells, ‘Stop! Change! What you’re doing is not right!’ That’s where they help you learn how to correct your movements.
“When the Purkinje cells get these signals from climbing fibers, they change by adding or tweaking the strength of the connections coming in from the rest of the brain to their dendrites. And because the Purkinje cells are so closely connected to the motor neurons, the changes to those synapses are going to result in changes to the movements that Purkinje cell controls.”
This is a phenomenon known as neuroplasticity, and it is fundamental for learning new behaviors or improving on them. That new neural pathways form in response to error signals from the climbing fibers allows the cerebellum to send better instructions to motor neurons the next time the same action is attempted.
The paradox that faced neuroscientists was that these climbing fibers, like many other neurons, are spontaneously activated. About once every second, they send a signal to their corresponding Purkinje cell, whether or not there were any unexpected stimuli or errors to report.
“So if you’re the Purkinje cell,” Medina said, “how are you ever going to tell the difference between signals that are spontaneous, meaning you don’t need to change anything, and ones that really need to be paid attention to?”
Medina and his colleagues devised an experiment to test whether there was a measurable difference between legitimate and spontaneous signals from the climbing fibers. In their study, the researchers had mice walk on treadmills while their heads were kept stationary. This allowed the researchers to blow random puffs of air at their faces, causing them to blink, and to use a non-invasive microscopy technique to look at how the relevant Purkinje cells respond.
The technique, two-photon microscopy, uses an infrared laser and a reflective dye to look deep into living tissue, providing information on both structure and chemical composition. Neural signals are transmitted within neurons by changing calcium concentrations, so the researchers used this technique to measure the amount of calcium contained within the Purkinje cells in real time.
Because the random puffs of air were unexpected stimuli for the mice, the researchers could directly compare the differences between legitimate and spontaneous signals in the eyelid-related Purkinje cells that made the mice blink.
“What we have found is that the Purkinje cell fills with more calcium when its corresponding climbing fiber sends a signal associated with that kind of sensory input, rather than a spontaneous one,” Medina said. “This was a bit of a surprise for us because climbing fibers had been thought of as ‘all or nothing’ for more than 50 years now.”
The mechanism that allows individual Purkinje cells to differentiate between the two kinds of climbing fiber signals is an open question. These signals come in bursts, so the number and spacing of the electrical impulses from climbing fiber to Purkinje cell might be significant. Medina and his colleagues also suspect that another mechanism is at play: Purkinje cells might respond differently when a signal from a climbing fiber is synchronized with signals coming elsewhere from the brain.
Whether either or both of these explanations are confirmed, the fact that individual Purkinje cells are able to distinguish when their corresponding muscle neurons encounter an error must be taken into account in future studies of fine motor control. This understanding could lead to new research into the fundamentals of neuroplasticity and learning.
“Something that would be very useful for the brain is to have information not just about whether there was an error but how big the error was — whether the Purkinje cell needs to make a minor or major adjustment,” Medina said. “That sort of information would seem to be necessary for us to get very good at any kind of activity that requires precise control. Perhaps climbing fiber signals are not as ‘all-or-nothing’ as we all thought and can provide that sort of graded information”
Family problems experienced in childhood and adolescence affect brain development
New research has revealed that exposure to common family problems during childhood and early adolescence affects brain development, which could lead to mental health issues in later life.
The study led by Dr Nicholas Walsh, lecturer in developmental psychology at the University of East Anglia, used brain imaging technology to scan teenagers aged 17-19. It found that those who experienced mild to moderate family difficulties between birth and 11 years of age had developed a smaller cerebellum, an area of the brain associated with skill learning, stress regulation and sensory-motor control. The researchers also suggest that a smaller cerebellum may be a risk indicator of psychiatric disease later in life, as it is consistently found to be smaller in virtually all psychiatric illnesses.
Previous studies have focused on the effects of severe neglect, abuse and maltreatment in childhood on brain development. However the aim of this research was to determine the impact, in currently healthy teenagers, of exposure to more common but relatively chronic forms of ‘family-focused’ problems. These could include significant arguments or tension between parents, lack of affection or communication between family members, physical or emotional abuse, and events which had a practical impact on daily family life and might have resulted in health, housing or school problems.
Dr Walsh, from UEA’s School of Psychology, said: “These findings are important because exposure to adversities in childhood and adolescence is the biggest risk factor for later psychiatric disease. Also, psychiatric illnesses are a huge public health problem and the biggest cause of disability in the world.
“We show that exposure in childhood and early adolescence to even mild to moderate family difficulties, not just severe forms of abuse, neglect and maltreatment, may affect the developing adolescent brain. We also argue that a smaller cerebellum may be an indicator of mental health issues later on. Reducing exposure to adverse social environments during early life may enhance typical brain development and reduce subsequent mental health risks in adult life.”
The study, which was conducted with the University of Cambridge and the Medical Research Council Cognition and Brain Sciences Unit, Cambridge, is published in the journal NeuroImage: Clinical.
The 58 teenagers who took part in the brain scanning were drawn from a larger study of 1200 young people, whose parents were asked to recall any negative life events their children had experienced between birth and 11 years of age. The interviews took place when the children were aged 14 and of the 58, 27 were classified as having been exposed to childhood adversities. At ages 14 and 17 the teenagers themselves also reported any negative events and difficulties they, their family or closest friends had experienced during the previous 12 months.
A “significant and unexpected” finding was that the participants who reported stressful experiences when aged 14 were subsequently found to have increased volume in more regions of the brain when they were scanned aged 17-19. Dr Walsh said this could mean that mild stress occurring later in development may ‘inoculate’ teenagers, enabling them to cope better with exposure to difficulties in later life, and that it is the severity and timing of the experiences that may be important.
“This study helps us understand the mechanisms in the brain by which exposure to problems in early-life leads to later psychiatric issues,” said Dr Walsh. “It not only advances our understanding of how the general psychosocial environment affects brain development, but also suggests links between specific regions of the brain and individual psychosocial factors. We know that psychiatric risk factors do not occur in isolation but rather cluster together, and using a new technique we show how the general clustering of adversities affects brain development.”
The researchers also found at that those who had experienced family problems were more likely to have had a diagnosed psychiatric illness, have a parent with a mental health disorder and have negative perceptions of their how their family functioned.
Aging brains need ‘chaperone’ proteins
The word “chaperone” refers to an adult who keeps teenagers from acting up at a dance or overnight trip. It also describes a type of protein that can guard the brain against its own troublemakers: misfolded proteins that are involved in several neurodegenerative diseases.
Researchers at Emory University School of Medicine have demonstrated that as animals age, their brains are more vulnerable to misfolded proteins, partly because of a decline in chaperone activity.
The researchers were studying a model of spinocerebellar ataxia, but the findings have implications for understanding other diseases, such as Alzheimer’s, Parkinson’s and Huntington’s. They also identified targets for potential therapies: bolstering levels of either a particular chaperone or a growth factor in brain cells can protect against the toxic effects of misfolded proteins.
The results were published this week in the journal Neuron.
Scientists led by Shihua Li, MD, and Xiao-Jiang Li, MD, PhD devised a system in which production of a misfolding-prone protein that causes a form of spinocerebellar ataxia can be triggered artificially in mice at various ages. Both Li’s are professors of human genetics at Emory University School of Medicine. The first author of the paper is BCDB graduate student Su Yang.
Spinocerebellar ataxia is an inherited neurodegenerative disease in which patients develop gait problems and a loss of coordination in mid-life, because of atrophy of the cerebellum. There are several types, each caused by a mutation in a different gene.
Most of the mutations that cause spinocerebellar ataxia involve an expansion of a “polyglutamine repeat" in a protein. Having the same protein building block (the amino acid glutamine) repeated dozens of times alters the protein’s function and makes it more likely to misfold and clump together. The misfolded proteins are toxic and interfere with the normal forms of the same protein.
Huntington’s disease is caused by a similar polyglutamine repeat. Misfolded proteins also play roles in Alzheimer’s and Parkinson’s, although their production is not driven by an inherited polyglutamine repeat in those diseases.
Li’s team was trying to distinguish between two possibilities. One was that the duration of mutant protein accumulation is important for disease severity; aging might allow more misfolded proteins to accumulate and become toxic over time.
Instead, the scientists observed that older animals develop disease more quickly after mutant protein production is triggered. The mutant protein accumulates more quickly in 9- and 14-month old mice than in 3-month old mice, suggesting that aged neurons are more vulnerable to the effects of the misfolded protein.
Chaperones are proteins whose job is to “prevent improper liaisons" between other proteins; they prevent the sticky regions of proteins from grabbing something they’re not supposed to. Li’s team identified a particular chaperone called Hsc70 whose activity declines with age in the brain, while others’ activity does not.
To confirm Hsc70’s importance, the researchers showed that boosting cells’ levels of Hsc70 can bolster their ability to cope with misfolded proteins. Injecting mice in the cerebellum with a virus that forces cells to make more Hsc70 can slow degeneration. The researchers found that the mutant protein interferes with production of a growth factor called MANF (mesenchephalic astrocyte-derived neurotrophic factor) in the cerebellum and that Hsc70 can prevent this interference. Injection of a virus that forces cells to make more MANF can also slow degeneration.
Potentially, small molecules that increase Hsc70 or MANF levels could be used for treating spinocerebellar ataxia, says Xiao-Jiang Li.
(Source: news.emory.edu)
How metabolism and brain activity are linked
A new study by scientists at McGill University and the University of Zurich shows a direct link between metabolism in brain cells and their ability to signal information. The research may explain why the seizures of many epilepsy patients can be controlled by a specially formulated diet.
(Image caption: Neurons in the cerebellum. Credit: Bowie Lab/McGill University)
The findings, published Jan. 16 in Nature Communications, reveal that metabolism controls the processes that inhibit brain activity, such as that involved in convulsions. The study uncovers a link between how brain cells make energy and how the same cells signal information – processes that neuroscientists have often assumed to be distinct and separate.
“Inhibition in the brain is commonly targeted in clinical practice,” notes Derek Bowie, Canada Research Chair in Receptor Pharmacology at McGill and corresponding author of the study. “For example, drugs that alleviate anxiety, induce anesthesia, or even control epilepsy work by strengthening brain inhibition. These pharmacological approaches can have their drawbacks, since patients often complain of unpleasant side effects.”
The experiments showed an unexpected link between how the mitochondria of brain cells make energy and how the same cells signal information. Brain cells couple these two independent functions by using small chemical messengers, called reactive oxygen species (or ROS), that are normally associated with signaling cell death. While ROS are known to have roles in diseases of aging, such as Alzheimer’s and Parkinson’s, the new study shows they also play important roles in the healthy brain.
The findings emerged from an ongoing collaboration between Prof. Bowie’s laboratory in McGill’s Department of Pharmacology and Therapeutics and a research team headed by Dr. Jean-Marc Fritschy, Professor of Pharmacology at the University of Zurich and current director of the Neuroscience Center Zurich (ZNZ). The researchers have the longer term aim of trying to understand why the seizures of many epilepsy patients — especially young children – can be treated with a high-fat, low-carbohydrate diet known as the ketogenic diet.
The idea that diet can control seizures was noticed as far back as ancient Greece, during periods of fasting. From the 1920s until the 1950s, the ketogenic diet was widely used to treat epilepsy patients. With the introduction of anticonvulsant drugs in the 1950s, the dietary approach fell out of favour with doctors. But because anticonvulsant drugs don’t work for 20% to 30% of patients, there has been a resurgence in use of the ketogenic diet.
“Since our study shows that brain cells have their own means to strengthen inhibition,” explains Prof Bowie, “our work points to potentially new ways in which to control a number of important neurological conditions including epilepsy.”
(Source: mcgill.ca)
For centuries, the brain was a mystery. Only in the last few decades have scientists begun to unravel its secrets. In recent years, using the latest technology and powerful computers further key discoveries have been made.
However, much remains to be understood about how the brain works. Here are five important areas of study attempting to unlock the last secrets of the brain.
How to fix it
When we think, move, speak, dream and even love - it all happens in the grey matter. But our brains are not simply one colour. White matter matters too.
Much of the research into dementia has focused on the tell-tale plaques of beta amyloid and tau protein tangles which occur in the grey matter.
But one British scientist, Dr Atticus Hainsworth says the white matter - and its blood supply - may be equally important.
The white colour results from fatty sheaths around the axons - which are extensions of the nerve cell bodies and help the cells to communicate.
He is using banks of donated brains, in Oxford and Sheffield, to analyse white matter for potential triggers such as leaking blood vessels.
"Some of the cases had an MRI or CT scan and that information can help give more clues about whether there was disease in the white matter - and what its basis might be," says Dr Hainsworth.
If leaking blood vessels in white matter do play a key role in the development of dementia then it may offer up a another potential route for new drug therapies.
How to make us all geniuses
For years caffeine was used to enhance alertness. But popping a pill to get straight-A’s may soon become the norm.
At Cambridge University neuroscientist Barbara Sahakian is investigating cognitive enhancers - drugs which make us smarter.
She studies how they can improve the performance of surgeons or pilots and asks if they could even be used to make us more entrepreneurial.
But she warns that there is no long-term safety information on these drugs and as a society we need to talk about their use.
She says the scientific and ethical challenges created by drugs which affect the production of brain chemicals like dopamine and noradrenaline - which induce pleasurable or “fight or flight” responses - need to be debated in order to decide whether drug-tests become routine before taking an exam.
Dr Sahakian adds: “I frequently talk to students about cognitive-enhancing drugs and a lot of students take them for studying and exams.
"But other students feel angry about this, they feel those students are cheating."
How can we harness our unconscious?
People need to be on top of their game when mastering skills like playing a musical instrument or detecting a bomb.
But research suggests that our unconscious can be harnessed to help us excel.
Repeatedly playing a tricky piece of music obviously helps develop a familiarity with the bits that are most difficult.
But cellist Tania Lisboa, who’s also a researcher in the Centre for Performance Science at London’s Royal College of Music, says it also helps to send the trickier parts of a piece from her conscious to the unconscious part of her brain.
After hours of practice, a fluent musician’s brain stores how to play the piece in an area at the back of the brain called the cerebellum - literally “the little brain”.
Neuroscientist Prof Anil Seth, of Sussex University, says: “It has more brain cells than the rest of the brain put together.
"It helps to promote fluid movements.. So the conscious effort of learning how to bow a cello is moved from the cortical areas which are involved when it’s new or difficult over to the cerebellum, which is very good at producing unconscious fluent behaviour on demand."
Music and defence may not appear to have much in common, but the unconscious can also help detect potential threats, whether it’s a suspicious person in a crowd or the presence of an improvised explosive device.
The unconscious brain is really good at spotting patterns - a skill which Paul Sajda at Colombia University in New York exploits - right at the boundary of the conscious/sub-conscious.
"I can flash 10 images a second and if one of those images has something out of the ordinary..that will essentially cause me to re-orient my brain to that image - but I’m not exactly aware of what that is."
Brain activity is monitored whilst the analyst looks at images so that researchers can later see which images triggered reactions.
What dreams are for
It’s just 60 years since scientists in Chicago first noted the tell-tale “rapid eye movement” or REM sleep which we now associate with dreaming.
But our fascination with dreams dates back at least 5,000 years to ancient Mesopotamia when people believed that the soul moved out of a sleeping body to visit the places they dreamed of.
REM sleep - which occurs every 90 minutes or so - begins with signals from the base of the brain which eventually reach the cerebral cortex - the outer layer of the brain which is responsible for learning and thought.
These nerve impulses are also directed to the spinal cord, inducing temporary paralysis of the limbs.
Prof Robert Stickgold, from the Beth Israel Deaconess Medical Center for Sleep and Cognition in Boston, believes that dreams are vital for processing memory associations.
He has asked the subjects of some of his sleep studies to play Tetris - and then noted their descriptions of how they floated amongst geometric shapes in their dreams.
He’s an admirer of Japanese scanning research where the scientists could “read” the dreams of subjects as they had MRI scans.
But he says it’s hard to get people to sleep in a noisy, expensive scanner.
And the future? “I would like to see research which reveals the rules for dream construction - and how it relates to the larger concept of memory processing during sleep.”
One even more elusive goal: how to dream just happy dreams and ditch the bad ones, especially nightmares.
Can we cure unreachable pain?
Excruciating chronic pain is one of medicine’s most difficult problems to solve.
Untouched by conventional treatments like painkilling drugs, surgeons are now testing their theory that deep brain stimulation could provide relief.
It is a brain surgery technique which involves electrodes being inserted to reach targets deep inside the brain.
The target areas are stimulated via the electrodes which are connected to a battery-powered pacemaker surgically placed under the patient’s collar bone.
One of the pioneers of this technique is Prof Tipu Aziz at the John Radcliffe Hospital in Oxford.
Deep brain stimulation has been used in the past for Parkinson’s disease and depression, and is now being trialled on obsessive compulsive disorder patients as well as those in chronic pain.
One of his patients, Clive, has suffered from terrible pain for nearly a decade after an operation to remove a disc in his neck.
"Sometimes I thought that if I had an axe, I’d chop my own arm off, if I thought it would get rid of the pain."
The doctors explained to him that his brain was getting signals from his arm to his brain confused and that the electrodes could help.
In Clive’s case this was an area of the brain called the anterior cingulate.
A week after his surgery he was one of the fortunate 70% of patients for whom the deep brain stimulation provides relief.
"It’s great to be out of that pain now. Since having the implant I can sit down for longer, I am able to walk further, everything is an improvement."
Prof Aziz is treating medical conditions. But he is aware of ethical dilemmas which could arise if the technique was applied to other areas.
"Putting electrodes in targets to improve memory.
"Or you could put electrodes into people to make them indifferent to danger and create the perfect soldier."
Ballet dancers’ brains adapt to stop them feeling dizzy
Scientists have discovered differences in the brain structure of ballet dancers that may help them avoid feeling dizzy when they perform pirouettes.
The research suggests that years of training can enable dancers to suppress signals from the balance organs in the inner ear.
The findings, published in the journal Cerebral Cortex, could help to improve treatment for patients with chronic dizziness. Around one in four people experience this condition at some time in their lives.
Normally, the feeling of dizziness stems from the vestibular organs in the inner ear. These fluid-filled chambers sense rotation of the head through tiny hairs that sense the fluid moving. After turning around rapidly, the fluid continues to move, which can make you feel like you’re still spinning.
Ballet dancers can perform multiple pirouettes with little or no feeling of dizziness. The findings show that this feat isn’t just down to spotting, a technique dancers use that involves rapidly moving the head to fix their gaze on the same spot as much as possible.
Researchers at Imperial College London recruited 29 female ballet dancers and, as a comparison group, 20 female rowers whose age and fitness levels matched the dancers’.
The volunteers were spun around in a chair in a dark room. They were asked to turn a handle in time with how quickly they felt like they were still spinning after they had stopped. The researchers also measured eye reflexes triggered by input from the vestibular organs. Later, they examined the participants’ brain structure with MRI scans.
In dancers, both the eye reflexes and their perception of spinning lasted a shorter time than in the rowers.
Dr Barry Seemungal, from the Department of Medicine at Imperial, said: “Dizziness, which is the feeling that we are moving when in fact we are still, is a common problem. I see a lot of patients who have suffered from dizziness for a long time. Ballet dancers seem to be able to train themselves not to get dizzy, so we wondered whether we could use the same principles to help our patients.”
The brain scans revealed differences between the groups in two parts of the brain: an area in the cerebellum where sensory input from the vestibular organs is processed and in the cerebral cortex, which is responsible for the perception of dizziness.
The area in the cerebellum was smaller in dancers. Dr Seemungal thinks this is because dancers would be better off not using their vestibular systems, relying instead on highly co-ordinated pre-programmed movements.
“It’s not useful for a ballet dancer to feel dizzy or off balance. Their brains adapt over years of training to suppress that input. Consequently, the signal going to the brain areas responsible for perception of dizziness in the cerebral cortex is reduced, making dancers resistant to feeling dizzy.
“If we can target that same brain area or monitor it in patients with chronic dizziness, we can begin to understand how to treat them better.”
Another finding in the study may be important for how chronic dizzy patients are tested in the clinic. In the control group, the perception of spinning closely matched the eye reflexes triggered by vestibular signals, but in dancers, the two were uncoupled.
“This shows that the sensation of spinning is separate from the reflexes that make your eyes move back and forth,” Dr Seemungal said. “In many clinics, it’s common to only measure the reflexes, meaning that when these tests come back normal the patient is told that there is nothing wrong. But that’s only half the story. You need to look at tests that assess both reflex and sensation.”
Experimental Compound Reverses Down Syndrome-Like Learning Deficits In Mice
Researchers at Johns Hopkins and the National Institutes of Health have identified a compound that dramatically bolsters learning and memory when given to mice with a Down syndrome-like condition on the day of birth. As they report in the Sept. 4 issue of Science Translational Medicine, the single-dose treatment appears to enable the cerebellum of the rodents’ brains to grow to a normal size.
The scientists caution that use of the compound, a small molecule known as a sonic hedgehog pathway agonist, has not been proven safe to try in people with Down syndrome, but say their experiments hold promise for developing drugs like it.
“Most people with Down syndrome have a cerebellum that’s about 60 percent of the normal size,” says Roger Reeves, Ph.D., a professor in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine. “We treated the Down syndrome-like mice with a compound we thought might normalize the cerebellum’s growth, and it worked beautifully. What we didn’t expect were the effects on learning and memory, which are generally controlled by the hippocampus, not the cerebellum.”
Reeves has devoted his career to studying Down syndrome, a condition that occurs when people have three, rather than the usual two, copies of chromosome 21. As a result of this “trisomy,” people with Down syndrome have extra copies of the more than 300 genes housed on that chromosome, which leads to intellectual disabilities, distinctive facial features and sometimes heart problems and other health effects. Since the condition involves so many genes, developing treatments for it is a formidable challenge, Reeves says.
For the current experiments, Reeves and his colleagues used mice that were genetically engineered to have extra copies of about half of the genes found on human chromosome 21.
The mice have many characteristics similar to those of people with Down syndrome, including relatively small cerebellums and difficulty learning and remembering how to navigate through a familiar space. (In the case of the mice, this was tested by tracking how readily the animals located a platform while swimming in a so-called water maze.)
Based on previous experiments on how Down syndrome affects brain development, the researchers tried supercharging a biochemical chain of events known as the sonic hedgehog pathway that triggers growth and development. They used a compound — a sonic hedgehog pathway agonist — that could do just that.
The compound was injected into the Down syndrome-like mice just once, on the day of birth, while their cerebellums were still developing. “We were able to completely normalize growth of the cerebellum through adulthood with that single injection,” Reeves says.
But the research team went beyond measuring the cerebellums, looking for changes in behavior, too. “Making the animals, synthesizing the compound and guessing the right dose were so difficult and time-consuming that we wanted to get as much data out of the experiment as we could,” Reeves says. The team tested the treated mice against untreated Down syndrome-like mice and normal mice in a variety of ways, and found that the treated mice did just as well as the normal ones on the water maze test.
Reeves says further research is needed to learn why exactly the treatment works, because their examination of certain cells in the hippocampus known to be involved in learning and affected by Down syndrome appeared unchanged by the sonic hedgehog agonist treatment. One idea is that the treatment improved learning by strengthening communication between the cerebellum and the hippocampus, he says.
As for the compound’s potential to become a human drug, the problem, Reeves says, is that altering an important biological chain of events like sonic hedgehog would likely have many unintended effects throughout the body, such as raising the risk of cancer by triggering inappropriate growth. But now that the team has seen the potential of this strategy, they will look for more targeted ways to safely harness the power of sonic hedgehog in the cerebellum. Even if his team succeeds in developing a clinically useful drug, however, Reeves cautions that it wouldn’t constitute a “cure” for the learning and memory-related effects of Down syndrome. “Down syndrome is very complex, and nobody thinks there’s going to be a silver bullet that normalizes cognition,” he says. “Multiple approaches will be needed.”
(Source: newswise.com)