Mostrando postagens com marcador neuro. Mostrar todas as postagens
Mostrando postagens com marcador neuro. Mostrar todas as postagens
08 outubro 2016
25 agosto 2016
Sleep ‘resets’ brain connections crucial for memory...
Sleep ‘resets’ brain connections crucial for memory and learning
Discovery that sleeplessness causes neurons to become ‘muddled’ with electrical activity could help develop new treatments for mental health disorders
For Jules Verne it was the friend who keeps us waiting. For Edgar Allan Poe so many little slices of death. But though the reason we spend a third of our lives asleep has so far resisted scientific explanation, research into the impact of sleepless nights on brain function has shed fresh light on the mystery - and also offered intriguing clues to potential treatments for depression.
In a study published, researchers show for the first time that sleep resets the steady build-up of connectivity in the human brain which takes place in our waking hours. The process appears to be crucial for our brains to remember and learn so we can adapt to the world around us.
The loss of a single night’s sleep was enough to block the brain’s natural reset mechanism, the scientists found. Deprived of rest, the brain’s neurons seemingly became over-connected and so muddled with electrical activity that new memories could not be properly laid down.
But Christoph Nissen, a psychiatrist who led the study at the University of Freiburg, is also excited about the potential for helping people with mental health disorders. One radical treatment for major depression is therapeutic sleep deprivation, which Nissen believes works through changing the patient’s brain connectivity. The new research offers a deeper understanding of the phenomenon which could be adapted to produce more practical treatments.
“Why we sleep is a fundamental question. Why do we spend so much of our lives in this brain state? This work shows us that sleep is a highly active brain process and not a waste of time. It’s required for healthy brain function,” said Nissen.
The results are a boost for what is called the synaptic homeostasis hypothesis of sleep, which was developed by scientists at the University of Wisconsin-Madison in 2003. It explains why our brains need to rest after a day spent absorbing all manner of information, from the morning news and the state of the weather, to a chat over lunch and what we must buy for tea.
Known more simply as SHY, the hypothesis states that when we are awake, the synapses that form connections between our brain cells strengthen more and more as we learn and eventually saturate our brains with information. The process requires a lot of energy, but sleep allows the brain to wind down its activity, consolidate our memories, and be ready to start again the next morning.
Writing in the journal Nature Communications, Nissen describes a series of tests that 11 men and nine women aged 19 to 25 took part in, either after a good night’s sleep, or after a night without sleep. On the sleepless night, participants played games, went for walks and cooked food, but were not allowed caffeine. Staff watched them throughout to make sure they stayed awake.
In the first round of experiments, Nissen used magnetic pulses to make neurons fire in the volunteers’ brains and cause a muscle in the left hand to twitch. When sleep deprived, far weaker pulses were sufficient to make the muscles move. This implied that sleepless brains are in a more excitable state, with their neurons more strongly connected than they are after a good night’s sleep.
Nissen next turned to another form of brain stimulation to mimic the way neurons fire when memories are laid down. He found it harder to get the neurons to respond in sleep-deprived people, a sign that the process of writing memories was impaired by sleep loss.
Taken together, the results suggest that sleep allows the brain to calm its activity so memories can be written down. In contrast, the sleep-deprived brain becomes noisy with electrical activity and so feeble at laying down memories that the process is all but blocked. The consequences of sleep loss were clear in a simple memory test, with tired volunteers faring worse than those who were well-rested.
Teasing out how sleep affects brain connections could do more than answer why we snooze so much. Shift workers and military personnel that have to cope with sleep deprivation could benefit from new drugs or countermeasures that restore normal brain connectivity. Blood samples taken from volunteers in the study showed that sleep deprivation lowered levels of a molecule called BDNF, or brain-derived neurotrophic factor, which regulates synaptic connections in the brain.
But Nissen is more excited about the study’s implications for understanding therapeutic sleep deprivation and its impact on depression. “If you deprive people with major depression of sleep for one night, about 60% show a substantial improvement in mood, motivation and cognitive function. We think it works by shifting these patients into a more favourable state,” he said.
Though striking when it works, therapeutic sleep deprivation is not much use because many patients relapse after the subsequent night’s sleep. But that is not the point, Nissen says. “It proves that it’s possible to shift a person’s mood from one state to another within hours. The idea is that we use sleep and sleep deprivation to understand the brain and develop new treatments. If you think about antidepressants or psychotherapy, it can take weeks or months to see any effects.”
Giulio Tononi, a professor of sleep medicine who first proposed SHY at the University of Wisconsin-Madison, said the new study was “truly elegant and powerful” and confirmed experiments that until now had only been performed in animals.
“Sleep is essential, and one main reason is that it allows the brain to learn new things every day while preserving and consolidating the old memories,” Tononi said. “Learning and memory require synaptic activity, which is very energetically expensive and prone to saturation. Sleep allows the brain to renormalize this synaptic activity after it increases in the waking day.”
Lars Westlye, a psychologist at University of Oslo, called the study “wonderful” and said the results could throw light on links between the biology of sleep, more complex brain functions, and severe mental disorders such as schizophrenia and depression. Like Nissen he believes that a clearer understanding of brain connectivity might explain why sleep deprivation can be so effective in people with depression, and plans to study the effect in patients.
“These new results should strongly motivate further studies in patient groups, both to learn more about the roots of the disorders and how to treat them,” Westlye said.
Image Credit: http://ift.tt/1C9uSlB
Source: Guardian Neuroscience (by Ian Sample)
11 setembro 2015
Urging Caution in Wake of “Transmittable" Alzheimer’s...
Urging Caution in Wake of “Transmittable" Alzheimer’s Claim
A provocative new paper published in Nature suggests that neurodegenerative disorders such as Alzheimer’s and Parkinson’s may be transmissible through certain medical procedures. It’s an alarming claim—but one that will require more proof if it’s to be accepted by the scientific community.
Protein Problems
To understand how the researchers came to this conclusion it’s important to consider the way that Creutzfeldt-Jakob disease (CJD) develops in humans. To date, more than 200 individuals have contracted the neurological disease as a result of treatment with human growth hormone (HGH). Prior to 1985, these patients were administered a growth hormone derived from the pituitary glands of human cadavers, some of which were contaminated with prions—abnormal infectious proteins that can fold in structurally variable ways (today, HGH is synthetic so this is no longer a concern). Prions can cause proteins to unfold in unwieldy ways, including some that result in serious health problems, such as CJD.
Similarly, neuroscientists have learned that Alzheimer’s, Parkinson’s, and motor neurone diseases such as prion disease result from the spread of misfolded proteins that kill brain cells, which causes the brain to shrink. These disorders are driven by the spread of two particular misfolded proteins, namely amyloid plaques and tau. And it’s here where the new study, headed by John Collinge and Sebastian Brandner from the University of College London, comes in.
An Unexpected Discovery
While performing an autopsy on eight individuals who died between the ages of 36 and 51, and who caught their CJD from contaminated HGH injections, the researchers unexpectedly discovered severe to moderate grey matter and vascular amyloid beta pathology in four of them. This was a surprise because of the relatively young age of the subjects, and because none of these patients had problematic mutations or predispositions to Alzheimer’s.
The researchers suspect that, when these individuals were administered their HGH treatments, the growth hormone was also contaminated with the amyloid beta protein, which then spread through their brains. This would suggest that the “seeds” responsible for certain neurodegenerative diseases can be transmitted during certain medical procedures or via contaminated surgical instruments.
Caveats Galore
It’s a conclusion that makes sense, and it’s being taken very seriously. The researchers are urging an investigation into other possible routes of prion infection, including blood transfusions and tissue transplantation (this despite the fact that no evidence exists to support such a claim—at least not yet). The concerns of the researchers noted, there are an array of shortcomings to the study.
For one, it’s a purely observational study—one conducted on an excruciatingly small sample of subjects. As The Economist bluntly points out, “this study cannot prove that deposits of amyloid beta were caused by seeds of the protein in contaminated hormone injections.” Moving forward, the researchers will have to determine if old stocks of HGH are indeed contaminated with amyloid proteins (and in fact, that’s exactly what they plan to do).
Again, it’s important to point out that, since 1982, human-derived hormone injections are no longer in use. And just so that we’re exceptionally clear on the matter, people cannot contract Alzheimer’s or Parkinson’s through person-to-person contact.
David Allsop, a professor of Neuroscience at the University of Lancaster,points out some other problems with the study:
I can imagine that this might result in a lot of misleading headlines. What the paper shows is that some people treated with human growth hormone who subsequently went on to develop CJD also show evidence of [amyloid beta] deposits, a key feature of Alzheimer’s disease, in their pituitary glands. What the paper does NOT demonstrate is whether these people would have gone on to develop Alzheimer’s disease had they lived long enough (they died of CJD) or that their pituitary β amyloid deposits were caused by contamination of growth hormone with a ‘rogue’ form of β amyloid. One possible (and indeed likely) explanation is that deposition of the ‘prion protein’ in CJD can result, in some cases, in the co-accumulation of β amyloid.
And indeed, it’s well known from other studies, including animal studies, that certain types of rogue proteins can predispose to accumulation in another.
Allsop concludes thusly:
There is no evidence that Alzheimer’s disease can be transmitted from one person to another, or through use of contaminated surgical instruments, and these results should be interpreted with a great deal of caution.
Read the entire study at Nature: “Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy”.
30 agosto 2015
explore-blog: Oliver Sacks (July 9, 1933 – August 30,...
Oliver Sacks (July 9, 1933 – August 30, 2015).
There is no better way to remember his remarkable mind and spirit than it the incredible story of how he once saved his own life by literature and song.
26 agosto 2015
Brain WavesYour neurons generate electricity to communicate with...
Brain Waves
Your neurons generate electricity to communicate with each other and this electrical activity forms patterns called brain waves.
They can be measured by electroencephalography (EEG), a non-invasive method of recording electrical activity using sensors on the scalp.
Scientists have found five main patterns of brain waves: alpha, beta, delta, gamma and theta. Each brainwave state correlates with a different state of awareness.
Brain waves behind indecisivenessIt’s the same old story:...
Brain waves behind indecisiveness
It’s the same old story: You’re in a restaurant and can’t make up your mind what to order. After studying the menu for some time and many discussions, you eventually choose the steak. But you can’t relax during the meal and keep wondering whether you should have gone for the veal after all. Such difficulties with decisions crop up in all aspects of life, not only food. However, they predominantly affect preference-based decisions, i.e. questions like “what do I prefer – melon or cherries?”. Purely sensory decisions based on sensorial information such as ‘what is bigger – melon or cherry?’ are less prone to indecisiveness.
The more intensive the information flow, the more decisive
How come some people are so uncertain of their preferences and keep making new choices while others know exactly what they like and want? A team headed by Professor Christian Ruff, a neuroeconomist from the University of Zurich, set about investigating this question. The Zurich researchers discovered that the precision and stability of preference decisions do not only depend on the strength of the activation of one or more brain regions. Instead, the key for stable preference choices is the intensity of the communication between two areas of the brain which represent our preferences or are involved in spatial orientation and action planning.
The researchers used transcranial alternating current stimulation, a non-invasive brain stimulation method that enables generation of coordinated oscillations in the activity of particular brain regions. The test subjects did not realize that they were being stimulated. Using this technique, the researchers intensified or reduced the information flow between the prefrontal cortex located directly below the forehead and the parietal cortex just above both ears. The test subjects had to make preference-based or purely sensory decisions about food.
“We discovered that preference-based decisions were less stable if the information flow between the two brain regions was disrupted. Our test subjects were therefore more indecisive. For the purely sensory decisions, however, there was no such effect,” explains Ruff. Consequently, the communication between the two brain regions is only relevant if we have to decide whether we like something and not when we make decisions based on objective facts. There was no evidence of any gender-specific effects in the experiments.
It was not possible to make the decisions more stable by intensifying the information flow. However, the study participants were young, healthy test subjects with highly developed decision-making skills. On the other hand, the results of the study could be used for therapeutic measures in the future – such as in patients who suffer from a high degree of impulsiveness and indecisiveness in the aftermath of brain disorders.
Image: Preference-based decisions were less stable if the information flow between the two brain regions was disrupted. (Credit: UZH)
19 agosto 2015
First almost fully-formed human brain grown in lab An almost...
First almost fully-formed human brain grown in lab
An almost fully-formed human brain has been grown in a lab for the first time, claim scientists from Ohio State University. The team behind the feat hope the brain could transform our understanding of neurological disease.
Though not conscious the miniature brain, which resembles that of a five-week-old foetus, could potentially be useful for scientists who want to study the progression of developmental diseases. It could also be used to test drugs for conditions such as Alzheimer’s and Parkinson’s, since the regions they affect are in place during an early stage of brain development.
The brain, which is about the size of a pencil eraser, is engineered from adult human skin cells and is the most complete human brain model yet developed, claimed Rene Anand of Ohio State University, Columbus, who presented the work today at the Military Health System Research Symposium in Fort Lauderdale, Florida.
Previous attempts at growing whole brains have at best achieved mini-organs that resemble those of nine-week-old foetuses, although these “cerebral organoids” were not complete and only contained certain aspects of the brain. “We have grown the entire brain from the get-go,” said Anand.
Anand and his colleagues claim to have reproduced 99% of the brain’s diverse cell types and genes. They say their brain also contains a spinal cord, signalling circuitry and even a retina.
The ethical concerns were non-existent, said Anand. “We don’t have any sensory stimuli entering the brain. This brain is not thinking in any way.”
Anand claims to have created the brain by converting adult skin cells into pluripotent cells: stem cells that can be programmed to become any tissue in the body. These were then grown in a specialised environment that persuaded the stem cells to grow into all the different components of the brain and central nervous system.
According to Anand, it takes about 12 weeks to create a brain that resembles the maturity of a five-week-old foetus. To go further would require a network of blood vessels that the team cannot yet produce. “We’d need an artificial heart to help the brain grow further in development,” said Anand.
Several researchers said it was hard to judge the quality of the work without access to more data, which Anand is keeping under wraps due to a pending patent on the technique. Many were uncomfortable that the team had released information to the press without the science having gone through peer review.
Zameel Cader, a consultant neurologist at the John Radcliffe Hospital, Oxford, said that while the work sounds very exciting, it’s not yet possible to judge its impact. “When someone makes such an extraordinary claim as this, you have to be cautious until they are willing to reveal their data.”
If the team’s claims prove true, the technique could revolutionise personalised medicine. “If you have an inherited disease, for example, you could give us a sample of skin cells, we could make a brain and then ask what’s going on,” said Anand.
You could also test the effect of different environmental toxins on the growing brain, he added. “We can look at the expression of every gene in the human genome at every step of the development process and see how they change with different toxins. Maybe then we’ll be able to say ‘holy cow, this one isn’t good for you.’”
For now, the team say they are focusing on using the brain for military research, to understand the effect of post traumatic stress disorder and traumatic brain injuries.
Image: The tiny brain, which resembles that of a five-week-old foetus, is not conscious. Ohio State University
11 agosto 2015
Why Can’t We Fall Asleep? BY MARIA KONNIKOVA Did you get...
Why Can’t We Fall Asleep?
Did you get enough sleep last night? Are you feeling fully awake, like your brightest, smartest, and most capable self? This, unfortunately, is a pipe dream for the majority of Americans. “Most of us are operating at suboptimal levels basically always,” the Harvard neurologist and sleep medicine physician Josna Adusumilli told me. Fifty to seventy million Americans, Adusumilli says, have chronic sleep disorders.
In a series of conversations with sleep scientists this May, facilitated by a Harvard Medical School Media Fellowship, I learned that the consequences of lack of sleep are severe. While we all suffer from sleep inertia (a general grogginess and lack of mental clarity), the stickiness of that inertia depends largely on the quantity and quality of the sleep that precedes it. If you’re fully rested, sleep inertia dissipates relatively quickly. But, when you’re not, it can last far into the day, with unpleasant and even risky results.
Many of us have been experiencing the repercussions of inadequate sleep since childhood. Judith Owens, the director of the Center for Pediatric Sleep Disorders at Boston Children’s Hospital, has been studying the effects of school start times on the well-being of school-age kids—and her conclusions are not encouraging. Most adults are fine with about eight hours of sleep, but toddlers need around thirteen hours, including a daytime nap. Teens need around nine and a half hours; what’s more, they tend to be night owls, whose ideal circadian rhythm has them going to bed and waking up late. As schools have pushed their start times earlier and earlier—a trend that first started in the sixties, Owens says—the health effects on students have been severe. “It’s not just sleep loss. It’s circadian disruption,” Owens says. “They have to wake up when their brain tells them to be deeply asleep. Waking a teen at six in the morning is like waking an adult at three at night.”
The result is a kind of constant jet lag—and one that is exacerbated by sleeping in on the weekends. Executive function and emotional responses get worse, hurting everything from judgment to emotional reactivity. The ability to make good decisions can suffer, and kids can become more prone to act out and get depressed. In fact, the rise in A.D.H.D. diagnoses may, in part, be the result of inadequate sleep: in children, symptoms of sleep deprivation include hyperactivity and impaired interpretation of social cues. Owens has seen many such misdiagnoses in her clinical practice. The effects are physical, as well. Children who undersleep are more likely to gain weight and become obese. Even for infants as young as six months, amounts of sleep can predict weight gain three years later.
Schools with healthier start times, on the other hand, see an increase in attendance, test scores, G.P.A.s, and health. In one study in which an intervention pushed start times later, it wasn’t just academic outcomes that improved; car crashes went down by as much as seventy per cent, and self-reported depression rates fell. Even a delay of as little as half an hour, Owens has found, improves outcomes. “It should be about the health and well-being of the students,” she told me, “and not the convenience of adults.”
As we age, unfortunately, our quality of sleep only gets worse. If you sleep six hours a night for twelve days, Adusumilli says—and that’s about how much many Americans sleep all year round—your cognitive and physical performance becomes virtually indistinguishable from that of someone who has been awake for twenty-four hours straight. (The same effect is produced by six days of four-hour nights.) And the performance of someone who has been awake for twenty-four hours straight is similar to that of someone with a blood alcohol level of 0.1 per cent. In other words, “normal” amounts of sleep deprivation have us acting like we’re drunk. (Charles Czeisler recalls presenting these facts to a Times journalist; when the journalist handed in the story, the editor said it couldn’t possibly be true. Most people in the newsroom were sleep-deprived, and they still managed to produce the Timesevery day. Surely an intoxicated newsroom would be incapable of such a feat.)
In the short term, these types of deficits have a significant effect on our performance across the board. Perception deteriorates, along with motor skills: in one study of college basketball players, well-rested players performed better than those who followed their usual schedules. Emotional control suffers—the connection between the prefrontal cortex (where we make executive decisions) and the amygdala (which is associated with fear and other emotions) degrades—and we become more impulsive and prone to depression. And our ability to think and to make sound decisions plummets. We become worse at learning, memory, and simple tasks of arithmetic and analytic reasoning. The rate of accidents and errors rises. In one study, which compared first-year interns at Brigham and Women’s Hospital who worked on a regular schedule to those working on shorter, sixteen-hour shifts that included a nap, the sleep-deprived residents made more than double the number of attentional errors at night—a result that has been replicated multiple times.
Equally troubling are the health impacts in the long term. We become more prone to metabolic and endocrine problems, including weight gain, with a resulting increased risk of diabetes and cardiovascular disease. We decrease our immune function and could increase the risk of multiple types of cancer. We speed up our cognitive decline and increase the risk of dementia.
Even if you start sleeping more today, you may be too late to avoid some of the impacts of sleep deprivation. Because kids’ brains are growing and changing so rapidly, they are more vulnerable to the effects of sleep deprivation than adults; those effects may well follow them throughout life, no matter their habits later on. As for adults, we can recover from relatively short bouts of sleep loss: in one study, the University of Pennsylvania sleep researcher David Dinges found that one night of good sleep was enough to help you rebound from five nights of too little sleep. But recovery from truly chronic sleep deprivation relies on the quality of sleep you are getting. It can take weeks, and sometimes longer, to recover—and we often don’t have the luxury of sleeping ten hours a night for even as much as a week.
Ironically, many of us don’t want to “catch up” on sleep even when we can. We honestly don’t realize that we’re sleep deprived; many of us think we’re just fine with five or six hours a night. We earnestly believe that we’re fully awake and at our best. The fact is, however, that we are very bad at knowing how much sleep is enough.
In one of her studies, Elizabeth Klerman, a sleep scientist at Brigham and Women’s Hospital, allowed people to follow their own sleep schedules for two weeks; they chose how many hours they wanted to be awake, and how many hours they wanted to be asleep. Then, they went into the sleep lab. Klerman was interested in two things: sleep latency, or how long it took them to fall asleep, and sleep duration, or how long they slept. On the second night and during the second day, she told me, they slept an average of twelve and a half hours out of a possible sixteen hours of sleep opportunity, demonstrating a severe sleep deficit. On the first day in the lab, during testing of sleep latency, some fell asleep before the technician had even left the room. Many of the subjects, in other words, were pathologically sleepy. Yet they’d thought they were fully awake and at their best. We all have our “chosen level of uncomfortableness,” Klerman says, but that doesn’t mean we’re actually doing well.
Charles Czeisler has found that we are only aware of the impact of sleep loss on our performance for the first one to two days. After that, we no longer realize that we’re not functioning at our best. “Then, it’s just the new you,” he says. Klerman recalls one participant in another study, which restricted the amount of sleep that subjects were allowed. The subject came back once he was able to sleep normally because he wanted a second chance to fill out the forms that asked him to rate his mental acuity and how well he was functioning. He’d filled them out wrong the first time, he said: after catching up on sleep, he’d realized how impaired he’d been, and wanted a chance to downgrade his ratings. “He’d forgotten what alert felt like,” Klerman says. At the time, he thought he was fully awake and capable. “Why would you expect the brain to be able to police itself?” she asks.
Taken together, the current research on sleep offers us a valuable lesson. We all want to be productive and effective at what we do. But when we try to boost productivity by expanding our waking hours, we aren’t doing anyone any favors. We lose more by skimping on rest than we can ever gain back by adding a few hours to our days. We are less productive, less insightful, less happy, more likely to get sick. And we have no idea just how much we’ve compromised our abilities and health in the process: ask most anyone and they will tell you they do just fine with five, six hours. We systematically undervalue sleep, and yet it is fundamental to our present and future performance. And unlike most anything else, sleep is one of the few things we have to do ourselves. No one can do it for you.
ILLUSTRATION BY MIN HEO
How the Brain Purges Bad MemoriesThe brain is extraordinarily...
How the Brain Purges Bad Memories
The brain is extraordinarily good at alerting us to threats. Loud noises, noxious smells, approaching predators: they all send electrical impulses buzzing down our sensory neurons, pinging our brain’s fear circuitry and, in some cases, causing us to fight or flee. The brain is also adept at knowing when an initially threatening or startling stimulus turns out to be harmless or resolved. But sometimes this system fails and unpleasant associations stick around, a malfunction thought to be at the root of post-traumatic stress disorder (PTSD). New research has identified a neuronal circuit responsible for the brain’s ability to purge bad memories, findings that could have implications for treating PTSD and other anxiety disorders.
Like most emotions, fear is neurologically complicated. But previous work has consistently implicated two specific areas of the brain as contributing to and regulating fear responses. The amygdala, two small arcs of brain tissue deep beneath our temples, is involved in emotional reactions, and it flares with activity when we are scared. If a particular threat turns out to be harmless, a brain region behind the forehead called the prefrontal cortex steps in and the fright subsides. Our ability to extinguish painful memories is known to involve some sort of coordinated effort between the amygdala and the prefrontal cortex. The new study, led by Andrew Holmes at the National Institutes of Health, however, confirms that a working connection between the two brain regions is necessary to do away with fear.
Normally mice that repeatedly listen to a sound previously associated with a mild foot shock will learn that on its own the tone is harmless, and they will stop being afraid. Using optogenetic stimulation technology, or controlling specific neurons and animal behavior using light, the authors found that disrupting the amygdala–prefrontal cortex connection prevents mice from overcoming the negative association with the benign tone. In neurobiology speak, memory “extinction” fails to occur. They also found that the opposite is true—that stimulating the circuit results in increased extinction of fearful memories.
Until now investigators were unsure whether the amygdala–prefrontal cortex communication pathway could on its own control fear extinction; both structures interact with many other brain regions, and so isolating their effects of on behavior was a challenge. Optogenetics made the discovery possible, allowing the NIH group to precisely assess only the connection between the two brain regions in real time, providing a more accurate correlation between neuronal activity and behavior.
Holmes sees the amygdala and prefrontal cortex as two major hubs in a complex communications network. In the case of impaired fear extinction such as PTSD, however, it is just the one connection between the two regions that is faulty, not the hubs themselves. “To regulate fear extinction,” he explains, “I think it will be better to isolate and fix that one line of communication as opposed to trying to reengineer the hubs themselves—it’s their job to carry many lines of communication for all manner of brain functions, most of which are probably working just fine.“
Given the similarities in fear circuitry between rodents and humans, the new findings could inform research into new therapeutic approaches to anxiety disorders, including into medications that act on the fear circuit. Holmes believes that healthy fear extinction relies on “neural plasticity,” the brain’s ability to make new neuronal connections, which is in part influenced by the brain’s own cannabinoids, compounds that regulate neurotransmitters. Drugs that alter the cannabinoid system could provide a way to modify the fear circuit, thereby—possibly—alleviating anxiety.
Neurostimulation technologies, including transcranial magnetic stimulation and even optogenetics, could also potentially be used therapeutically to augment standard anxiety treatments. One such treatment is exposure therapy, in which patients are repeatedly exposed to a stimulus they find abnormally stressful until it no longer causes anxiety. Perhaps externally stimulating the fear circuit in combination with repeated recollections of a painful memory—or repeated exposures to a fear-inducing stimulus—might work together to ease the symptoms of PTSD and other anxiety disorders.
As Holmes points out, it is not unlike when your home Internet connection goes sluggish: "Rather than trying to fix the faulty wire on the telephone pole to help boost your signal—and disrupting many lines of communication—it’s better to just fix the faulty line of communication.”
Image Credit: Thinkstock
30 julho 2015
Here’s What Breaking Up Does to Your Brain When the love...
Here’s What Breaking Up Does to Your Brain
When the love of your life dumps you, you’re going to go a little nuts. But it’s a very specific form of crazy: There are actually conflicting neural systems active inside your brain. It’s like you’re falling in love all over again, only in reverse. Here’s how neuroscience explains it.
Addicted to Love
It doesn’t matter whether you were with your ex-lover for six months, four years, or more – a breakup throws your brain back into the obsession of early love. Everything that reminds you of that person – a photograph, places you used to go together, random thoughts – triggers activity in “reward” neurons inside the caudate nucleus and the ventral tegmental area of the brain. These are the same parts of the brain that light up when scientists put people in the throes of that grossly cute can’t-think-about-anything-else stage of new love into an fMRI machine and ask them to look at photos of their beloved. As it happens, they’re also parts of the brain that respond to cocaine and nicotine.
Turning on the reward neurons releases repeated floods of the neurotransmitter dopamine. And the dopamine activates circuits inside the brain that create a craving for more. That craving gives you motivation, and encourages you to try out other behaviors that will help you get more of whatever it is you need. In the case of romance, the thing you need more of is your beloved.
As a romantic relationship develops into a long term partnership, that obsession fades away, even though thoughts of your partner still tickle the brain’s reward systems. But after a breakup, all those old can’t-get-enough feelings come flooding back. The brain’s reward systems are still expecting their romantic ‘fix’, but they’re not getting the responses they expect. And like someone in the depths of a drug addiction, they turn up the volume in an effort to get you to respond.
In this new context, the reward system is now the part of your brain that’s going to motivate you do something really dumb. Like drunk calling your ex, or initiating breakup sex.
Lucy Brown, a neuroscientist at Einstein College of Medicine who has studied romantic responses in the brain, explains that the motivation is more extreme than for other forms of social rejection because romance ties into more primal parts of the brain. “Other kinds of social rejection are much more cognitive,” she says. “[Romantic rejection] is a life changing thing, and involves systems that are at the same level as feeling hungry or thirsty.”
No wonder it hurts.
The Pain is Real
When your lover leaves you, chances are you’re going to feel it. Your chest gets tight, you feel sick to your stomach, or maybe there’s that sinking sensation that accompanies terrible news. Two studies that looked at brain activity inside people who were deep in the throes of a breakup found that the reward regions weren’t the only systems lit up inside their brains. They also saw activity in brain regions that control distress and the response to physical pain. Specifically, the parts of the brain that collect pain sensations from the outside world were quiet, but the systems they tie to–the systems that control how the body reacts to pain–were busy telling the body that something awful was happening.
And since the brain controls the body, turning on those systems can trigger a cascade of effects: for example, releasing stress hormones which in turn affect the heart, the digestive system, even the immune system. In some extreme cases, the stress can make the heart weaken and bulge, creating a condition called takotsubo cardiomyopathy or “broken heart syndrome,” which can sometimes lead to death.
Fortunately, those sorts of extreme stress responses are rare. But the pain of a romantic rejection can still last a long time. There’s a lot of variation from one person to the next, but Brown says the painful feelings usually fade away over the course of about six months to two years. But the pain is a natural part of the process. Breakups hurt because they turn on a basic system that gets us to make and maintain meaningful connections with other people. “It’s a system to try to keep us together”, Brown explains. “When we have little separations, these feelings get us to work hard to get close to the person again. If two people are cooperating, it works.” When they’re not, it’s as much of a hurt as a cut or a broken bone.
What Were They Thinking? And What Can You Do?
So far, all the “breakup fMRI” experiments have looked at brain activity in dump-ees. Like you, science still has no idea what’s going on in the brain of a dump-er. Logic suggests there must be some mechanism that can slowly erode and weaken connections in the brain’s attachment pathways. We do know that neural connections that aren’t used in sensory pathways can get pruned away, so perhaps this type of neural rewriting can also slowly change the way your lover feels about you until one day, those warm feelings of romantic attachment are gone.
And then comes that “We have to talk” visit.
But when you’re heartbroken, there’s no reason that you can’t try things that encourage your brain to rewire itself. In fact, there’s evidence that immediately after a breakup your brain is working hard to get you to move on. Those same brain scans of the heartbroken that showed their brains were awash in pain and desire also had activity in regions of the frontal cortex that inhibit impulses and redirect behavior.
In short, explains Brown, your brain is trying to regulate your mixed-up emotions, prevent you from doing at least some of the crazy things you feel compelled to try, and help you start putting your life back together. It will take time to get over it. But over time, the brain activity of romantic obsession will go away. Until then, Brown suggests trying a little memory rewriting of your own. “When the thought of that person comes up, instead of thinking how great [the relationship] was, think about how bad that person was for you instead.”
[Mearns 1991 | Aron et al. 2005 | Wittstein et al. 2005 | Smith and Vale 2006 | Acevedo et al. 2010 | Fisher et al. 2010 | Kross et al. 2011 | Cooper et al. 2014 | Eisenberger 2015]
Illustration by Jim Cooke
26 julho 2015
22 julho 2015
we-are-star-stuff: How to Deal with a Seizure This short guide...
How to Deal with a Seizure
This short guide is going to be by no means complete, and won’t be able to help every single case, but having some information is better than none, and taking a few moments to read may just save you, your friend, your family, or some random stranger from pain or even death. (This guide is written for Grand Mal Seizures - the “stereotypical” seizure that involves fainting and convulsion of the entire body).
DO:
- DO put the person having the seizure on the floor, laying them on their side. If they were standing, unfortunately, they probably ended up there on their own. Try to cushion the fall if possible, taking special precautions to the head. If they are sitting on a chair, then carefully bring them to the floor and lay them on their side in an open space.
- DO turn their head to the side on the floor. Many people having seizures vomit during the seizure, so do not put them on their back, or they may choke.
- DO loosen any collar or tie or anything constricting the body/neck/throat if possible.
- DO put something soft under the person’s head (a jacket or pillow if you have one).
- DO keep track of how long the seizure was, where it started (left leg? right arm?), the colour of their skin (was their face turning green? purple?), and anything else that stuck out to you (what were they doing right before they got the seizure? was there blood in the corner of the mouth (indication that they bit their tongue)? etc) so that you can convey it to the medical specialists who come.
- DO call the ambulance if the person is not known to have epilepsy or seizure disorder. If they do have seizure disorder/epilepsy, but the seizure continues for more than a few minutes, call the ambulance anyways. Especially if the color of the skin changes (could mean oxygen is not getting to the brain and rest of body).
DON’T:
- DON’T try to “stop” the seizure by hugging them or holding them down. It’s not going to happen. Let the seizure run its course. You can hurt either or both of you by clutching the person, whether it be the other person pulling muscles or you getting punched in the face.
- DON’T put anything in the person’s mouth. They can choke on it and die, or bite pieces of whatever it is and die. Some people vomit during seizures, and that and whatever is stuffed in the mouth will not go well together either - the fluid needs to come out, not get stuck in the mouth.
- DON’T stick your finger or spoon or anything into the other person’s mouth, even if they have something in there. At best, your finger is going to get bitten very badly, and at worst, the person is going to chip their tooth on the spoon or slice up their mouth.
This is very important: when they regain consciousness, please try to be as calm as possible, especially if the person has never had a grand mal seizure before. It is very disorienting to wake up from a seizure. Usually, the world is very dizzy and foggy. It takes at least a few minutes to land back to earth, even after the initial “waking up”. So speak calmly, explain the situation slowly, and don’t get irritated when they don’t seem to understand what you are saying, or stare at you blankly.
Remember: seizures can happen to anybody given the “correct” circumstances.
20 julho 2015
Device delivers drugs to brain via remote control A team of...
Device delivers drugs to brain via remote control
A team of researchers has developed a wireless device the width of a human hair that can be implanted in the brain and activated by remote control to deliver drugs.
The technology, demonstrated for the first time in mice, one day may be used to treat pain, depression, epilepsy and other neurological disorders in people by targeting therapies to specific brain circuits, according to the researchers at Washington University School of Medicine in St. Louis and the University of Illinois at Urbana-Champaign.
The research is a major step forward in pharmacology and builds on earlier work in optogenetics, a technology that makes individual brain cells sensitive to light and then activates those targeted populations of cells with flashes of light. Because it’s not yet practical to re-engineer human neurons, the researchers made the tiny wireless devices capable of delivering drugs directly into the brain, with the remote push of a button.
“In the future, it should be possible to manufacture therapeutic drugs that could be activated with light,” said co-principal investigator Michael R. Bruchas, PhD, associate professor of anesthesiology and neurobiology at Washington University. “With one of these tiny devices implanted, we could theoretically deliver a drug to a specific brain region and activate that drug with light as needed. This approach potentially could deliver therapies that are much more targeted but have fewer side effects.”
Previous attempts to deliver drugs or other agents, such as enzymes or other compounds, to experimental animals have required the animals to be tethered to pumps and tubes that restricted their movement. But the new devices were built with four chambers to carry drugs directly into the brain. By activating brain cells with drugs and with light, the scientists are getting an unprecedented look at the inner workings of the brain.
“This is the kind of revolutionary tool development that neuroscientists need to map out brain circuit activity,” said James Gnadt, PhD, program director at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NIH). “It’s very much in line with the goals of the NIH’s BRAIN Initiative.”
The NIH BRAIN (Brain Research through Advancing Innovative Technologies) Initiative is a program designed to accelerate the development and application of new technologies to shed light on the complex links between brain function and behavior.
The new devices ultimately may help people with neurological disorders and other problems, according to co-first authors Jae-Woong Jeong, PhD, a former postdoctoral researcher at the University of Illinois and now assistant professor of electrical, computer and energy engineering at the University of Colorado, Boulder, and Jordan G. McCall, PhD, a graduate student in the Bruchas lab.
“Now, we literally can deliver drug therapy with the press of a button,”McCall said. “We’ve designed it to exploit infrared technology, similar to that used in a TV remote. If we want to influence an animal’s behavior with light or with a particular drug, we can simply point the remote at the animal and press a button.”
Jeong added: “The device embeds microfluid channels and microscale pumps, but it is soft like brain tissue and can remain in the brain and function for a long time without causing inflammation or neural damage.”
As part of the study, the researchers showed that by delivering a drug to one side of an animal’s brain, they could stimulate neurons involved in movement, which caused the mouse to move in a circle.
In other mice, shining a light directly onto brain cells expressing a light-sensitive protein prompted the release of dopamine, a neurotransmitter that rewarded the mice by making them feel good. The mice then returned to the same location in a maze to seek another reward. But the researchers were able to interfere with that light-activated pursuit by remotely controlling the release of a drug that blocks the action of dopamine on its receptors.
The researchers also believe that similar, more flexible devices could have applications in areas of the body other than the brain, including peripheral organs.
“We’ve successfully produced and demonstrated an implantable, cellular-scale microfluidic and micro-optical interface to biology, with application opportunities not only in the brain but in other parts of the nervous system and other organs as well,” said the study’s other co-principal investigator, John A. Rogers, PhD, professor of materials science and engineering at the University of Illinois.
For now, the devices contain only four chambers for drugs, but in the future, the researchers hope to incorporate a design much like a printer’s ink cartridge so that drugs can continue to be delivered to specific cells in the brain, or elsewhere in the body, for as long as required without the need to replace the entire device.
Images: Tiny, implantable devices are capable of delivering light or drugs to specific areas of the brain, potentially improving drug delivery to targeted regions of the brain and reducing side effects. Eventually, the devices may be used to treat pain, depression, epilepsy and other neurological disorders in people. Credit: ALEX DAVID JEREZ ROMAN
Unleashing the Potential of Stem Cells The hippocampus, a...
Unleashing the Potential of Stem Cells
The hippocampus, a region of the brain important for learning, memory, and mood, contains a large number of stem cells. These cells are undifferentiated, meaning they have the potential to become different types of specialized cells. This image shows stems cells (cells with black dots) in the hippocampus of an adult mouse. While most of the stem cells are dormant, they can be activated to generate new neurons in a process called neurogenesis. Researchers have identified two distinct types of hippocampal stem cells, which they speculate may generate neurons that regulate learning and mood differently. In the future, scientists hope to learn more about these cells and the roles they may play in learning and mood disorders
Image credit: Jhaveri, et al. The Journal of Neuroscience, 2015.
18 julho 2015
A colorized scanning electron microscope picture of a nerve...
A colorized scanning electron microscope picture of a nerve ending that has been broken open to reveal the synaptic vesicles (orange and blue) beneath the cell membrane.
Attribution: Tina Carvalh
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