Posts tagged brain
Articles and news from the latest research reports.
Equations reveal the rebellious rhythms at the heart of nature
From the beating of our hearts to the proper functioning of our brains, many systems in nature depend on collections of ‘oscillators’; perfectly-coordinated, rhythmic systems working together in flux, like the cardiac muscle cells in the heart.
Unless they act together, not much happens. But when they do, powerful changes occur. Cooperation between neurons results in brain waves and cognition, synchronized contractions of cardiac cells cause the whole heart to contract and pump the blood around the body. Lasers would not function without all the atomic oscillators acting in unison. Soldiers even have to break step when they reach a bridge in case oscillations caused by their marching feet cause the bridge to collapse.
But sometimes those oscillations go wrong.
Writing in the journal Nature Communications, scientists at Lancaster University report the possibility of “glassy states” and a “super-relaxation” phenomenon, which might appear in the networks of tiny oscillators within the brain, heart and other oscillating entities.
To uncover these phenomena, they took a new approach to the solution of a set of equations proposed by the Japanese scientist Yoshiki Kuramoto in the 1970s. His theory showed it was possible in principle to predict the properties of a system as a whole from a knowledge of how oscillators interacted with each other on an individual basis.
Therefore, by looking at how the microscopic cardiac muscle cells interact we should be able to deduce whether the heart as a whole organ will contract properly and pump the blood round. Similarly, by looking at how the microscopic neurons in the brain interact, we might be able to understand the origins of whole-brain phenomena like thoughts, or dreams, or amnesia, or epileptic fits.
Physicists Dmytro Iatsenko, Professor Peter McClintock, and Professor Aneta Stefanovska have reported a far more general solution of the Kuramoto equations than anyone has achieved previously, with some quite unexpected results.
One surprise is that the oscillators can form “glassy” states, where they adjust the tempos of their rhythms but otherwise remain uncoordinated with each other, thus giving birth to some kind of “synchronous disorder” rather like the disordered molecular structure of window glass. Furthermore and even more astonishingly, under certain circumstances the oscillators can behave in a totally independent manner despite being tightly coupled together, the phenomenon the authors call “super-relaxation”.
These results raise intriguing questions. For example, what does it mean if the neurons of your brain get into a glassy state?
Dmytro Iatsenko, the PhD student who solved the equations, admitted the results posed more questions than they answered.
“It is not fully clear yet what it might mean if, for example, this happened in the human body, but if the neurons in the brain could get into a “glassy state” there might be some strong connection with states of the mind, or possibly with disease.”
Lead scientist Professor Aneta Stefanovska said: “With populations of oscillators, the exact moment when something happens is far more important than the strength of the individual event. This new work reveals exotic changes that can happen to large-scale oscillations as a result of alterations in the relationships between the microscopic oscillators. Because oscillations occur in myriads of systems in nature and engineering, these results have broad applicability.”
Professor Peter McClintock said: “The outcome of the work opens doors to many new investigations, and will bring enhanced understanding to several seemingly quite different areas of science.”
Beyond the Damaged Brain
Until the past few decades, neuroscientists really had only one way to study the human brain: Wait for strokes or some other disaster to strike people, and if the victims pulled through, determine how their minds worked differently afterward. Depending on what part of the brain suffered, strange things might happen. Parents couldn’t recognize their children. Normal people became pathological liars. Some people lost the ability to speak — but could sing just fine.
These incidents have become classic case studies, fodder for innumerable textbooks and bull sessions around the lab. The names of these patients — H. M., Tan, Phineas Gage — are deeply woven into the lore of neuroscience.
When recounting these cases today, neuroscientists naturally focus on these patients’ deficits, emphasizing the changes that took place in their thinking and behavior. After all, there’s no better way to learn what some structure in the brain does than to see what happens when it shorts out or otherwise gets destroyed.
A young man lies unconscious on the table, his head clamped firmly in place. His eyes are closed. The hair over his left temple has been shaved.
Continue reading: How a surgeon installs seizure sensors inside a skull
(Image courtesy: University of Utah, Department of Neurosurgery)
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."
Scientists find brain region that helps you make up your mind
One of the smallest parts of the brain is getting a second look after new research suggests it plays a crucial role in decision making.
A University of British Columbia study published today in Nature Neuroscience says the lateral habenula, a region of the brain linked to depression and avoidance behaviours, has been largely misunderstood and may be integral in cost-benefit decisions.
“These findings clarify the brain processes involved in the important decisions that we make on a daily basis, from choosing between job offers to deciding which house or car to buy,” says Prof. Stan Floresco of UBC’s Dept. of Psychology and Brain Research Centre (BRC). “It also suggests that the scientific community has misunderstood the true functioning of this mysterious, but important, region of the brain.”
In the study, scientists trained lab rats to choose between a consistent small reward (one food pellet) or a potentially larger reward (four food pellets) that appeared sporadically. Like humans, the rats tended to choose larger rewards when costs—in this case, the amount of time they had to wait before receiving food–were low and preferred smaller rewards when such risks were higher.
Previous studies suggest that turning off the lateral habenula would cause rats to choose the larger, riskier reward more often, but that was not the case. Instead, the rats selected either option at random, no longer showing the ability to choose the best option for them.
The findings have important implications for depression treatment. “Deep brain stimulation – which is thought to inactivate the lateral habenula — has been reported to improve depressive symptoms in humans,” Floresco says. “But our findings suggest these improvements may not be because patients feel happier. They may simply no longer care as much about what is making them feel depressed.”
Background
Floresco, who conducted the study with PhD candidate Colin Stopper, says more investigation is needed to understand the complete brain functions involved in cost-benefit decision processes and related behaviour. A greater understanding of decision-making processes is also crucial, they say, because many psychiatric disorders, such as schizophrenia, stimulant abuse and depression, are associated with impairments in these processes.
The lateral habenula is considered one of the oldest regions of the brain, evolution-wise, the researchers say.
Hawking: ‘in the future brains could be separated from the body’
Professor Stephen Hawking has predicted that it could be possible to preserve a mind as powerful as his on a computer - but not with technology existing today.
The cosmologist, 71, said the brain operates in a similar way to a computer programme, meaning it could in theory be kept running without a body to power it.
Prof Hawking was speaking after the premiere of a new biopic about his life, which he narrates himself, at the Cambridge Film Festival.
Asked about whether a person’s consciousness can live on after they die, he said: “I think the brain is like a programme in the mind, which is like a computer, so it’s theoretically possible to copy the brain onto a computer and so provide a form of life after death.
"However, this is way beyond our present capabilities. I think the conventional afterlife is a fairy tale for people afraid of the dark."
The film tells the story of Prof Hawking’s life, from his childhood in Oxford to his current home in Cambridge where he lives with the help of a group of carers.
It addresses how he moved from being diagnosed with motor neurone disease at the age of 21, and being told he had three years left to live, to becoming the world’s most famous living scientist.
Addressing his condition, which has afflicted him for half a century, he says in the film: “Keeping an active mind has been vial to my survival,as has been maintaining a sense of humour.”
Speaking before the premiere on Thursday, Kip Thorne, the American physicist and a close friend of Prof Hawking, said: “I think his handicap allowed him to do science he may not otherwise have done.
"He is the most stubborn man I know and that stubbornness and that drive is in part motivated by his disability."
Researchers Identify Conditions Most Likely to Kill Encephalitis Patients
People with severe encephalitis — inflammation of the brain — are much more likely to die if they develop severe swelling in the brain, intractable seizures or low blood platelet counts, regardless of the cause of their illness, according to new Johns Hopkins research.
The Johns Hopkins investigators say the findings suggest that if physicians are on the lookout for these potentially reversible conditions and treat them aggressively at the first sign of trouble, patients are more likely to survive.
“The factors most associated with death in these patients are things that we know how to treat,” says Arun Venkatesan, M.D., Ph.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine and leader of the study published in the Aug. 27 issue of the journal Neurology.
Experts consider encephalitis something of a mystery, and its origins and progress unpredictable. While encephalitis may be caused by a virus, bacteria or autoimmune disease, a precise cause remains unknown in 50 percent of cases. Symptoms range from fever, headache and confusion in some, to seizures, severe weakness or language disability in others. The most complex cases can land patients in intensive care units, on ventilators, for months. Drugs like the antiviral acyclovir are available for herpes encephalitis, which occurs in up to 15 percent of cases, but for most cases, doctors have only steroids and immunosuppressant drugs, which carry serious side effects.
“Encephalitis is really a syndrome with many potential causes, rather than a single disease, making it difficult to study,” says Venkatesan, director of the Johns Hopkins Encephalitis Center.
In an effort to better predict outcomes for his patients, Venkatesan and his colleagues reviewed records of all 487 patients with acute encephalitis admitted to The Johns Hopkins Hospital and Johns Hopkins Bayview Medical Center between January 1997 and July 2011. They focused further attention on patients who spent at least 48 hours in the ICU during their hospital stays and who were over the age of 16. Of those 103 patients, 19 died. Patients who had severe swelling in the brain were 18 times more likely to die, while those with continuous seizures were eight times more likely to die. Those with low counts in blood platelets, the cells responsible for clotting, were more than six times more likely to die than those without this condition.
The findings can help physicians know which conditions should be closely monitored and when the most aggressive treatments — some of which can come with serious side effects — should be tried, the researchers say. For example, it may be wise to more frequently image the brains of these patients to check for increased brain swelling and the pressure buildup that accompanies it.
Venkatesan says patients with cerebral edema may do better if intracranial pressure is monitored continuously and treated aggressively. He cautioned that although his research suggests such a course, further studies are needed to determine if it leads to better outcomes for patients.
Similarly, he says research has yet to determine whether aggressively treating seizures and low platelet counts also decrease mortality.
Venkatesan and his colleagues are also developing better guidelines for diagnosing encephalitis more quickly so as to minimize brain damage. Depending on where in the brain the inflammation is, he says, the illness can mimic other diseases, making diagnosis more difficult.
Another of the study’s co-authors, Romergryko G. Geocadin, M.D., an associate professor of neurology who co-directs the encephalitis center and specializes in neurocritical care, says encephalitis patients in the ICU are “the sickest of the sick,” and he fears that sometimes doctors give up on the possibility of them getting better.
“This research should give families — and physicians — hope that, despite how bad it is, it may be reversible,” he says.
(Source: newswise.com)
Researchers Gain Insight into How Ion Channels Control Heart and Brain Electrical Activity
Virginia Commonwealth University researchers studying a special class of potassium channels known as GIRKs, which serve important functions in heart and brain tissue, have revealed how they become activated to control cellular excitability.
The findings advance the understanding of the interaction between a family of signaling proteins called G proteins, and a special type of cell membrane ion pore called G protein-sensitive, inwardly rectifying potassium (GIRK) channels. The findings may one day help researchers develop targeted drugs to treat conditions of the heart such as atrial fibrillation.
In the study, published this week in the Online First section of Science Signaling, a publication of the American Association for the Advancement of Science (AAAS), researchers used a computational approach to predict the interactions between G proteins and a GIRK channel.
Rahul Mahajan, a M.D./Ph.D. candidate in the VCU School of Medicine’s Department of Physiology and Biophysics, undertook this problem for his dissertation work, under the mentorship of Diomedes E. Logothetis, Ph.D., chair of the Department of Physiology and Biophysics and the John D. Bower Endowed Chair in Physiology in the VCU School of Medicine. They developed a model and tested its predictions in cells, demonstrating how G proteins cause activation of GIRKs.
“Malfunctions of GIRK channels have been implicated in chronic atrial fibrillation, as well as in drug abuse and addiction,” said Logothetis, who is an internationally recognized leader in the study of ion channels and cell signaling mechanisms.
“Understanding the structural mechanism of Gβγ activation of GIRK channels could lead to rational based drug design efforts to combat chronic atrial fibrillation.”
In chronic atrial fibrillation, the GIRK channel is believed to be inappropriately open. According to Logothetis, if researchers are able to target only the specific site that keeps the channel inappropriately open, then any unrelated channels could be left unaltered, thus avoiding unwanted side effects.
Crystal structures of GIRK channels, which preceded the current study, have revealed two constrictions of the ion permeation pathway that researchers call “gates”: one at the inner leaflet of the membrane bilayer and the other close by in the cytosol, which is the liquid found inside cells.
“The structure of the Gβγ -GIRK1 complex reveals that Gβγ inserts a part of it in a cleft formed by two cytosolic loops of two adjacent channel subunits,” Logothetis said. “This is also the place where alcohols bind to activate the channel. One can think of this cleft as a clam that has its shells either open or shut closed. Stabilization of this cleft in the ‘open’ position stabilizes the cytosolic gate in the open state.”
GIRKs are activated when they interact with G proteins coupled to receptors bound to stimulatory hormones or neurotransmitters. In heart tissue, acetylcholine released by the vagus nerve activates these channels, which hyperpolarize the membrane potential and slow heart rate. In brain tissue, GIRKs inhibit excitation by acting at postsynaptic cells.
G proteins are composed of three subunits, a, b, and g. Since 1987, researchers have known that the Gbgsubunits directly activate the atrial GIRK channel, but an atomic resolution picture of how the two proteins interact remained elusive until now.
Moving forward, the team would like to use computational and experimental approaches to build and test the structures of the rest of the components of the G protein complex – for example, the Ga subunits and the G protein-coupled receptor – around the Gβγ-channel complex, which is the structure the team has already achieved.
This Is How Your Brain Becomes Addicted to Caffeine
Within 24 hours of quitting the drug, your withdrawal symptoms begin. Initially, they’re subtle: The first thing you notice is that you feel mentally foggy, and lack alertness. Your muscles are fatigued, even when you haven’t done anything strenuous, and you suspect that you’re more irritable than usual.
Over time, an unmistakable throbbing headache sets in, making it difficult to concentrate on anything. Eventually, as your body protests having the drug taken away, you might even feel dull muscle pains, nausea and other flu-like symptoms.
This isn’t heroin, tobacco or even alcohol withdrawl. We’re talking about quitting caffeine, a substance consumed so widely (the FDA reports thatmore than 80 percent of American adults drink it daily) and in such mundane settings (say, at an office meeting or in your car) that we often forget it’s a drug—and by far the world’s most popular psychoactive one.
Like many drugs, caffeine is chemically addictive, a fact that scientists established back in 1994. This past May, with the publication of the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), caffeine withdrawal was finally included as a mental disorder for the first time—even though its merits for inclusion are symptoms that regular coffee-drinkers have long known well from the times they’ve gone off it for a day or more.
Why, exactly, is caffeine addictive? The reason stems from the way the drug affects the human brain, producing the alert feeling that caffeine drinkers crave.
Soon after you drink (or eat) something containing caffeine, it’s absorbed through the small intestine and dissolved into the bloodstream. Because the chemical is both water- and fat-soluble (meaning that it can dissolve in water-based solutions—think blood—as well as fat-based substances, such as our cell membranes), it’s able to penetrate the blood-brain barrier and enter the brain.
Structurally, caffeine closely resembles a molecule that’s naturally present in our brain, called adenosine (which is a byproduct of many cellular processes, including cellular respiration)—so much so, in fact, that caffeine can fit neatly into our brain cells’ receptors for adenosine, effectively blocking them off. Normally, the adenosine produced over time locks into these receptors and produces a feeling of tiredness.
When caffeine molecules are blocking those receptors, they prevent this from occurring, thereby generating a sense of alertness and energy for a few hours. Additionally, some of the brain’s own natural stimulants (such as dopamine) work more effectively when the adenosine receptors are blocked, and all the surplus adenosine floating around in the brain cues the adrenal glands to secrete adrenaline, another stimulant.
For this reason, caffeine isn’t technically a stimulant on its own, says Stephen R. Braun, the author or Buzzed: the Science and Lore of Caffeine and Alcohol, but a stimulant enabler: a substance that lets our natural stimulants run wild. Ingesting caffeine, he writes, is akin to “putting a block of wood under one of the brain’s primary brake pedals.” This block stays in place for anywhere from four to six hours, depending on the person’s age, size and other factors, until the caffeine is eventually metabolized by the body.
In people who take advantage of this process on a daily basis (i.e. coffee/tea, soda or energy drink addicts), the brain’s chemistry and physical characteristics actually change over time as a result. The most notable change is that brain cells grow more adenosine receptors, which is the brain’s attempt to maintain equilibrium in the face of a constant onslaught of caffeine, with its adenosine receptors so regularly plugged (studies indicate that the brain also responds by decreasing the number of receptors for norepinephrine, a stimulant). This explains why regular coffee drinkers build up a tolerance over time—because you have more adenosine receptors, it takes more caffeine to block a significant proportion of them and achieve the desired effect.
This also explains why suddenly giving up caffeine entirely can trigger a range of withdrawal effects. The underlying chemistry is complex and not fully understood, but the principle is that your brain is used to operating in one set of conditions (with an artificially-inflated number of adenosine receptors, and a decreased number of norepinephrine receptors) that depend upon regular ingestion of caffeine. Suddenly, without the drug, the altered brain chemistry causes all sorts of problems, including the dreaded caffeine withdrawal headache.
The good news is that, compared to many drug addictions, the effects are relatively short-term. To kick the thing, you only need to get through about 7-12 days of symptoms without drinking any caffeine. During that period, your brain will naturally decrease the number of adenosine receptors on each cell, responding to the sudden lack of caffeine ingestion. If you can make it that long without a cup of joe or a spot of tea, the levels of adenosine receptors in your brain reset to their baseline levels, and your addiction will be broken.
Autism affects different parts of the brain in women and men
Autism affects different parts of the brain in females with autism than males with autism, a new study reveals. The research is published today in the journal Brain as an open-access article.
Scientists at the Autism Research Centre at the University of Cambridge used magnetic resonance imaging to examine whether autism affects the brain of males and females in a similar or different way. They found that the anatomy of the brain of someone with autism substantially depends on whether an individual is male or female, with brain areas that were atypical in adult females with autism being similar to areas that differ between typically developing males and females. This was not seen in men with autism.
“One of our new findings is that females with autism show neuroanatomical ‘masculinization’,” said Professor Simon Baron-Cohen, senior author of the paper. “This may implicate physiological mechanisms that drive sexual dimorphism, such as prenatal sex hormones and sex-linked genetic mechanisms.”
Autism affects 1% of the general population and is more prevalent in males. Most studies have therefore focused on male-dominant samples. As a result, our understanding of the neurobiology of autism is male-biased.
“This is one of the largest brain imaging studies of sex/gender differences yet conducted in autism. Females with autism have long been under-recognized and probably misunderstood,” said Dr Meng-Chuan Lai, who led the research project. “The findings suggest that we should not blindly assume that everything found in males with autism applies to females. This is an important example of the diversity within the ‘spectrum’.”
Dr Michael Lombardo, who co-led the study, added that although autism manifests itself in many different ways, grouping by gender may help provide a better understanding of this condition.
He said: “Autism as a whole is complex and vastly diverse, or heterogeneous, and this new study indicates that there are ways to subgroup the autism spectrum, such as whether an individual is male or female. Reducing heterogeneity via subgrouping will allow research to make significant progress towards understanding the mechanisms that cause autism.”