Posts tagged brain
Articles and news from the latest research reports.
Neuroscience offers a glimpse into the mind - and our future
Hassan Rasouli recently accomplished a remarkable feat: He lifted his thumb in a way that suggests he was making a thumbs-up gesture.
The feat was a remarkable one since doctors at Sunnybrook Health Sciences Centre in Toronto had diagnosed him as being in a persistent vegetative state (PVS), a mysterious condition in which patients appear to be awake but show no clinical signs of conscious awareness.
The condition first came to prominence in 1998 when family members, and then courts and politicians, engaged in a protracted battle over the care of Floridian Terri Schiavo. The matter was finally settled in 2005 when Schiavo, who was in a persistent vegetative state, was removed from life support and died.
Doctors at Sunnybrook similarly wanted to transfer Rasouli to palliative care, but Rasouli’s family refused. The doctors therefore sought a court order, and the Supreme Court of Canada heard arguments in the case on Monday.
The court’s decision might not affect Rasouli since, given his ability to give a thumbs-up gesture, he is no longer considered to be in a persistent vegetative state (PVS). But the case could have a profound impact on the many other patients who have been diagnosed as being in a PVS, as it could answer pressing legal questions about when someone can be removed from life support, and who has the authority to order that such support be discontinued.
The Rasouli case also raises further troubling questions of fact: Was Rasouli’s ability to give a thumbs-up gesture an indication that his condition had improved, or was he never in a persistent vegetative state? Was he, and other people similarly diagnosed, always consciously aware, but, thanks to being trapped in a paralyzed body, unable to express his thoughts?
(Illustration by Bert Dodson)
Controversial Surgery for Addiction Burns Away Brain’s Pleasure Center
How far should doctors go in attempting to cure addiction? In China, some physicians are taking the most extreme measures. By destroying parts of the brain’s “pleasure centers” in heroin addicts and alcoholics, these neurosurgeons hope to stop drug cravings. But damaging the brain region involved in addictive desires risks permanently ending the entire spectrum of natural longings and emotions, including the ability to feel joy.
In 2004, the Ministry of Health in China banned this procedure due to lack of data on long term outcomes and growing outrage in Western media over ethical issues about whether the patients were fully aware of the risks.
However, some doctors were allowed to continue to perform it for research purposes—and recently, a Western medical journal even published a new study of the results. In 2007, The Wall Street Journal detailed the practice of a physician who claimed he performed 1000 such procedures to treat mental illnesses such as depression, schizophrenia and epilepsy, after the ban in 2004; the surgery for addiction has also since been done on at least that many people.
The ethical minefield of using neuroscience to prevent crime
On the evening of March 10, 2007, Abdelmalek Bayout, an Algerian citizen living in Italy, brutally stabbed to death Walter Perez, a fellow immigrant from Colombia. Bayout admitted to the crime, saying he was provoked by Perez, who ridiculed him for wearing eye makeup.
According to Nature magazine, Bayout’s defence argued that he was mentally ill at the time of the offence. The court accepted that argument and, although it found Bayout guilty of the crime, imposed on him a reduced prison sentence of nine years and two months.
Bayout nevertheless appealed the judgment, and the Court of Appeal ordered a new psychiatric report. That report showed, among other things, that Bayout had low levels of the neurotransmitter monoamine oxidase A (MAO-A) — an important development given that previous research discovered that men who had low MAO-A levels and who had been abused as children were more likely to be convicted of violent crimes as adults.
Ultimately, the Court of Appeal further reduced Bayout’s sentence by a year, with Judge Pier Valerio Reinotti describing the MAO-A evidence as “particularly compelling.”
Upon a brief review of the scientific evidence, certain glaring problems with the court’s judgment quickly become apparent. Most obviously, the research showing an association between low MAO-A levels and violence tells us nothing about Bayout’s — or any specific individual’s — propensity for violence. Indeed, while a significant percentage of men with low MAO-A levels commit violent offences, the majority do not.
Yet the fact that the court allowed such evidence to influence its verdict suggests that neuroscience, while not eliminating criminal responsibility, might lead courts to conclude that defendants with certain neurological deficits are less responsible than those with “normal” brains.
There is, in fact, a precedent for this, and it’s one that few people question. Adolescents in virtually every country are subject to differential sentencing, and in many cases to an entirely separate system of justice, because their neurobiology renders them less blameworthy, less responsible than adults.
Indeed, while the limbic system, or emotional centre of the brain, is typically mature by the age of 16, the prefrontal cortex, which is associated with one’s capacity to control emotions, is not fully developed, in most people, until the early 20s. Hence according to what’s sometimes called the “two systems” theory, the imbalance in development of the limbic system and the PFC explains the risk taking and emotional behaviour that is characteristic of adolescence. And it justifies our treating adolescents as less responsible than adults.
There are, of course, substantial differences between adolescents and adults with neurological deficits, the most obvious being that most adolescents will outgrow the developmental imbalance. But the basic principle — that people who suffer from neurological aberrations that render them less capable of controlling their behaviour should be held less blameworthy — seems to have swayed the Italian Court of Appeal.
But not just the Italian Court of Appeal. While the “MAO-A defence” has been tried and failed in many courts around the world, recent research led by University of Utah psychologist Lisa Aspinwall suggests that many judges, when presented with neurobiological evidence, are inclined to reduce defendants’ sentences.
Hacking the Human Brain: The Next Domain of Warfare
It’s been fashionable in military circles to talk about cyberspace as a “fifth domain” for warfare, along with land, space, air and sea. But there’s a sixth and arguably more important warfighting domain emerging: the human brain.
This new battlespace is not just about influencing hearts and minds with people seeking information. It’s about involuntarily penetrating, shaping, and coercing the mind in the ultimate realization of Clausewitz’s definition of war: compelling an adversary to submit to one’s will. And the most powerful tool in this war is brain-computer interface (BCI) technologies, which connect the human brain to devices.
Current BCI work ranges from researchers compiling and interfacing neural data such as in the Human Conectome Project to work by scientists hardening the human brain against rubber hose cryptanalysis to technologists connecting the brain to robotic systems. While these groups are streamlining the BCI for either security or humanitarian purposes, the reality is that misapplication of such research and technology has significant implications for the future of warfare.
Where BCIs can provide opportunities for injured or disabled soldiers to remain on active duty post-injury, enable paralyzed individuals to use their brain to type, or allow amputees to feel using bionic limbs, they can also be exploited if hacked. BCIs can be used to manipulate … or kill.
Recently, security expert Barnaby Jack demonstrated the vulnerability of biotechnological systems by highlighting how easily pacemakers and implantable cardioverter-defibrillators (ICDs) could be hacked, raising fears about the susceptibility of even life-saving biotechnological implants. This vulnerability could easily be extended to biotechnologies that connect directly to the brain, such as vagus nerve stimulation or deep-brain stimulation.
Outside the body, recent experiments have proven that the brain can control and maneuver quadcopter drones and metal exoskeletons. How long before we harness the power of mind-controlled weaponized drones – or use BCIs to enhance the power, efficiency, and sheer lethality of our soldiers?
Given that military research arms such as the United States’ DARPA are investing in understanding complex neural processes and enhanced threat detection through BCI scan for P300 responses, it seems the marriage between neuroscience and military systems will fundamentally alter the future of conflict.
And it is here that military researchers need to harden the systems that enable military application of BCIs. We need to prevent BCIs from being disrupted or manipulated, and safeguard against the ability of the enemy to hack an individual’s brain.
The possibilities for damage, destruction, and chaos are very real. This could include manipulating a soldier’s BCI during conflict so that s/he were forced to pull the gun trigger on friendlies, install malicious code in his own secure computer system, call in inaccurate coordinates for an air strike, or divulge state secrets to the enemy seemingly voluntarily. Whether an insider has fallen victim to BCI hacking and exploits a system from within, or an external threat is compelled to initiate a physical attack on hard and soft targets, the results would present major complications: in attribution, effectiveness of kinetic operations, and stability of geopolitical relations.
Like every other domain of warfare, the mind as the sixth domain is neither isolated nor removed from other domains; coordinated attacks across all domains will continue to be the norm. It’s just that military and defense thinkers now need to account for the subtleties of the human mind … and our increasing reliance upon the brain-computer interface.
Regardless of how it will look, though, the threat is real and not as far away as we would like – especially now that researchers just discovered a zero-day vulnerability in the brain.
Placebo and the Brain: How Does it Work?
Placebo, the positive effect of a drug that lacks any beneficial ingredients, has been researched for centuries but remain a mystery for psychologists and neuroscientists alike. Although there is now a considerable amount of amassed knowledge of how placebo can be induced, through which mechanisms it works, and which individuals are susceptible to the effect, the explicit answer to why and how our brains have the ability to ‘cure’ themselves under certain circumstances is yet to be found. Having dived into the literature on the phenomenon, a picture has emerged in which one of the brain’s greatest tricks can be better understood and the fascinating implications it has for how we look at the body-mind distinction.
What is termed a placebo is usually defined in research trying to pin down its nature as the treatment that results in a change in symptom or condition that differs from the natural course of the specific disease. Placebo effects have been shown for mainly relief of pain, but also in studies of depression, parkinson’s, and anxiety. While the sugar pill is still in use, we now know that there are a two factors that are crucial for a placebo effect to occur. These are the level of expectancy and desire to get better/not get worse that the patient feels and both are in turn sensitive to a host of psychosocial variables such as their faith in medical staff, the emotional tone of the physician-patient interaction (whether it is optimistic or pessimistic for example), memories of past experiences with the effects of medicine, and so on.
While some individuals show reliable placebo effects, others do not and the underlying causes have recently been suggested to be tied to our individual genetic makeup. Researchers from the Harvard Program for Placebo Studies found that the magnitude of the placebo effect was tied to genes coding for an anzyme that regulates the levels of dopamine in various regions of the brain. Dopamine plays a key role in processing of reward, pain, memory, and learning, all areas in which the placebo effect has been demonstrated. The study, led by Kathryn Hall, concluded that persons whose genes promote an upregulation of the levels of dopamine in the brain also exhibit the greatest placebo effects. In other studies examining release of another group of transmitters called opioids, which regulate the activity in areas that code for pain, higher amounts of opioids were matched to the size of the placebo effect found.
As for where the effect originates, research using brain imaging have found that when a real drug is compared to the effects of a placebo very similar areas show activation but some areas, such as the lateral and central prefrontal cortex, show a greater response in the placebo condition. This part of the brain is often described as overseeing and exerting control over other processing in the brain and act as a connecting point for different streams of information that build up our expectations and desires.
So, how can this knowledge about the placebo effect influence the way doctors discuss, promote, and administer their own treatments? Surely, if we know that an encouraging prognosis given together with a sugar pill can be as effective in some cases as a pharmacological product but without the side- effects, we should be using that. However, having doctors treat their patients through deception leads to obvious problems such as public mistrust in the profession. A finding from the scientists at the very same Harvard program for placebo studies might have the answer. They namely demonstrated that the placebo effect remained when participants were told explicitly that the treatment they were given was in effect useless.
Better understanding of the cause of Alzheimer’s disease
Alzheimer’s disease is the most common form of dementia, affecting over 35 million people worldwide. It is generally assumed that the clumping of beta-amyloid (Aß) protein causes neuronal loss in patients. Medication focuses on reducing Aß42, one of the most common proteins and the most harmful. University of Twente PhD student Annelies Vandersteen is refining the current approach. She explains: “The results of my research provide a broader understanding of the processes that lead to Alzheimer’s disease and in this way may help to bring about new medication”.
The Aß protein occurs in the body in various lengths, ranging from 33 to 49 amino acids. The shorter varieties are regarded as ‘safe’, unlike the longer ones – Aß42 and longer – which are highly aggregating. Current therapeutic strategy tries to reduce the clumping of Aß42, and its harmful effects, by limiting the release of Aß42. Reducing Aß42 production at the same time results in a rise in Aß38 levels. Vandersteen comments: “One of the findings of my research is that small amounts of Aß38 can in fact increase or temper the clumping and toxic effects of longer Aß proteins. The processes that result in Alzheimer’s disease are determined by the whole spectrum of Aß proteins. So the picture is far less black and white than has been assumed so far, and less common forms of Aß are far less harmless than we thought.”
The study
Vandersteen examined the protein mixtures in a laboratory situation. She devised a series of experiments based on a computer-calculated hypothesis. The behaviour of the various Aß proteins and mixtures was studied in detail and described using various biophysical techniques. The influence of the various Aß proteins and mixtures on neurons was then studied in a cell culture.
(Source: alphagalileo.org)
Countering brain chemical could prevent suicides
Researchers have found the first proof that a chemical in the brain called glutamate is linked to suicidal behavior, offering new hope for efforts to prevent people from taking their own lives.
Writing in the journal Neuropsychopharmacology, Michigan State University’s Lena Brundin and an international team of co-investigators present the first evidence that glutamate is more active in the brains of people who attempt suicide. Glutamate is an amino acid that sends signals between nerve cells and has long been a suspect in the search for chemical causes of depression.
“The findings are important because they show a mechanism of disease in patients,” said Brundin, associate professor of translational science and molecular medicine in MSU’s College of Human Medicine. “There’s been a lot of focus on another neurotransmitter called serotonin for about 40 years now. The conclusion from our paper is that we need to turn some of that focus to glutamate.”
Brundin and colleagues examined glutamate activity by measuring quinolinic acid – which flips a chemical switch that makes glutamate send more signals to nearby cells – in the spinal fluid of 100 patients in Sweden. About two-thirds of the participants were admitted to a hospital after attempting suicide and the rest were healthy.
They found that suicide attempters had more than twice as much quinolinic acid in their spinal fluid as the healthy people, which indicated increased glutamate signaling between nerve cells. Those who reported the strongest desire to kill themselves also had the highest levels of the acid.
The results also showed decreased quinolinic acid levels among a subset of patients who came back six months later, when their suicidal behavior had ended.
The findings explain why earlier research has pointed to inflammation in the brain as a risk factor for suicide. The body produces quinolinic acid as part of the immune response that creates inflammation.
Brundin said anti-glutamate drugs are still in development, but could soon offer a promising tool for preventing suicide. In fact, recent clinical studies have shown the anesthetic ketamine – which inhibits glutamate signaling – to be extremely effective in fighting depression, though its side effects prevent it from being used widely today.
In the meantime, Brundin said physicians should be aware of inflammation as a likely trigger for suicidal behavior. She is partnering with doctors in Grand Rapids, Mich., to design clinical trials using anti-inflammatory drugs.
“In the future, it’s likely that blood samples from suicidal and depressive patients will be screened for inflammation,” Brundin said. “It is important that primary health care physicians and psychiatrists work closely together on this.”
A Key Gene for Brain Development
About one in ten thousand babies is born with an abnormally small head. The cause for this disorder – which is known as microcephaly – is a defect in the develoment of the embryonic brain. Children with microcephaly are severely retarded and their life expectancy is low. Certain cases of autism and schizophrenia are also associated with the dysregulation of brain size.
The causes underlying impaired brain development can be environmental stress (such as alcohol abuse or radiation) or viral infections (such as rubella) during pregnancy. In many cases, however, a mutant gene causes the problem.
David Keays, a group leader at the IMP, has now found a new gene which is responsible for Microcephaly. Together with his PhD-student Martin Breuss, he was able to identify TUBB5 as the culprit. The gene is responsible for making tubulins, the building blocks of the cell’s internal skeleton. Whenever a cell moves or divides, it relies on guidance from this internal structure, acting like a scaffold.
The IMP-researchers, together with collaborators at Monash University (Victoria, Australia), were able to interfere with the function of the TUBB5 in the brains of unborn mice. This led to massive disturbances in the stem cell population and impaired the migration of nerve cells. Both, the generation of large numbers of neurons from the stem cell reservoir and their correct positioning in the cortex, are essential for the development of the mammalian brain.
To determine whether the findings are also relevant in humans, David Keays collaborates with clinicians from the Paris-Sorbonne University. The French team led by Jamel Chelly, examined 120 patients with pathological brain structures and severe disabilities. Three of the children were found to have a mutated TUBB5-gene.
This information will prove vital to doctors treating children with brain disease. It will allow the development of new genetic tests which will form the basis of genetic counseling, helping parents plan for the future. By understanding how different genes cause brain disorders, it is hoped that one day scientists will be able to create new drugs and therapies to treat them.
The new findings by the IMP-researchers are published in the current issue of the journal “Cell Reports”. For David Keays, understanding the function of TUBB5 is the key to understanding brain development. “Our project shows how research in the lab can help improve lives in the clinic”, he adds.
The paper “Mutations in the β-tubulin Gene TUBB5 Cause Microcephaly with Structural Brain Abnormalities” is published on December 13, 2012, in the online Journal Cell Reports.
Pursuing literary immortality illuminates how the mind works
The initial excitement of hearing a new song fades as it’s replayed to death. That’s because the brain naturally functions as a kind of ticking time bomb, obliterating the thrill of artistic sounds, images and words by making them familiar over time.
So the artist, musician or author’s challenge is to create a work that retains its freshness, according to Case Western Reserve University’s Michael Clune in his new book Writing Against Time (Stanford University Press). And, for the artist, musician or writer, creating this newness with each work is a race against “brain time.”
In his book, Clune explained how neurobiological forces designed for our survival naturally make interest in art fade. But the forces don’t stop artists from trying for timelessness.
While the phenomenon is true for all art, the assistant professor of English focused on the intersection of literature and science, describing what writers can do to block or slow that natural erosion over time. Clune builds on his interest in how the brain destroys a lasting enjoyment of art. He has written about and reported on the topic in the neuroscience journal Behavioral and Brain Sciences.
The brain gradually defeats that initial excitement with boredom, which Clune described as “this dull feeling that your senses have died.”
As writers fight to ward off the reader’s boredom with striking new forms, metaphors and images, the brain works just as fast to extinguish it.
“We are evolutionarily designed so that we focus on new objects and ignore familiar ones,” Clune said. “When the mind confronts a new object, our perception is intense and vivid, but it soon dies with familiarity. Every minute, this feeling fades as the mind grasps the object.”
Brain cells activated, reactivated in learning and memory
Memories are made of this, the song says. Now neuroscientists have for the first time shown individual mouse brain cells being switched on during learning and later reactivated during memory recall. The results are published Dec. 13 in the journal Current Biology.
We store episodic memories about events in our lives in a part of a brain called the hippocampus, said Brian Wiltgen, now an assistant professor at the Center for Neuroscience and Department of Psychology at the University of California, Davis. (Most of the work was conducted while Wiltgen was working at the University of Virginia.) In animals, the hippocampus is important for navigation and storing memories about places.
"The exciting part is that we are now in a position to answer a fundamental question about memory," Wiltgen said. "It’s been assumed for a long time that the hippocampus is essential for memory because it drives reactivation of neurons (nerve cells) in the cortex. The reason you can remember an event from your life is because the hippocampus is able to recreate the pattern of cortical activity that was there at the time."
According to this model, patients with damage to the hippocampus lose their memories because they can’t recreate the activity in the cortex from when the memory was made. Wiltgen’s mouse experiment makes it possible to test this model for the first time.