Category: Brain Science

Abnormalities in brain tissue begin several decades before the onset of cognitive decline, but little is known about the lifestyle factors that might slow the onset of decline in middle age.

However, a new longitudinal study from the University of Melbourne has found that regular exercise in middle age is the best lifestyle change a person can make to prevent cognitive decline in their later years, according to this 20-year study.

“The message from our study is very simple. Do more physical activity, it doesn’t matter what.”

As the incidence of Alzheimer’s disease diagnosis doubles every five years after 65, most longitudinal studies examining risk factors and cognitive disease are with adults who are over the age of 60 or 70.

The new study, published in the American Journal of Geriatric Psychiatry, tracked 387 Australian women from the Women’s Healthy Aging Project for two decades. The women were aged 45-55 when the study began in 1992.

Researchers were interested to find out how lifestyle and biomedical factors—such as weight, BMI, and blood pressure—affected memory 20 years down the track, says Cassandra Szoeke, associate professor at the University of Melbourne and director of the Women’s Healthy Aging Project.

“There are few research studies which have data on participants from midlife and have assessed cognition in all their participants in later life. This research is really important because we suspect half the cases of dementia worldwide are most likely due to some type of modifiable risk factor.

“Unlike muscle and vessels, which have the capacity to remodel and reverse atrophy and damage, neuronal cells are not nearly so versatile with damage and cell loss is irreversible.”

Over two decades, Szoeke and colleagues took a wide range of measurements from study participants, taking note of lifestyle factors—including exercise and diet, education, marital and employment status, number of children, physical activity, and smoking.

A slow moving freight train

They also measured hormone levels, cholesterol, height, weight, body mass index, and blood pressure at 11 points throughout the study. Hormone replacement therapy was factored in.

The women were given a Verbal Episodic Memory test in which they were asked to learn a list of 10 unrelated words and attempt to recall them 30 minutes later.

When measuring the amount of memory loss over 20 years, frequent physical activity, normal blood pressure, and high good cholesterol were all strongly associated with better recall.

Once dementia occurs, it is a slow moving freight train to permanent memory loss, Szoeke says. “In our study more weekly exercise was associated with better memory. We now know that brain changes associated with dementia take 20 to 30 years to develop.

“The evolution of cognitive decline is slow and steady, so we needed to study people over a long time period. We used a verbal memory test because that’s one of the first things to decline when you develop Alzheimer’s disease.”

Regular exercise of any type, from walking the dog to mountain climbing, emerged as the number one protective factor against memory loss.

In fact, the beneficial influence of physical activity and blood pressure together compensates the negative influence of age on a person’s mental faculties.

The best effects come from cumulative exercise, that is, how much you do and how often over the course of your life, Szoeke says.

“The message from our study is very simple. Do more physical activity, it doesn’t matter what, just move more and more often. It helps your heart, your body, and prevents obesity and diabetes and now we know it can help your brain. It could even be something as simple as going for a walk, we weren’t restrictive in our study about what type.”

But the key is to start as soon as possible.

“We expected it was the healthy habits later in life that would make a difference but we were surprised to find that the effect of exercise was cumulative. So every one of those 20 years mattered.

“If you don’t start at 40, you could miss one or two decades of improvement to your cognition because every bit helps. That said, even once you’re 50 you can make up for lost time. There is no doubt that intervention is better late than never, but the results of our work indicate that an intervention after 65 will have missed at least 20 years of risk.”

The National Health and Medical Research Council and the Alzheimer’s Association funded the work, which was published in the American Journal of Geriatric Psychiatry.

Source: Republished from Futurity.org as a derivative work under the Attribution 4.0 International license. Original article posted to Futurity by Jane Gardner-Melbourne.

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Members of Alcoholics Anonymous who recited AA prayers after viewing drinking-related images reported less craving for alcohol after praying than after just reading a newspaper.

The reduced cravings in those that prayed corresponded to increased activity in brain regions responsible for attention and emotion as measured by MRI.

Results from the study, which may be the first to explore brain physiology in AA members, appear in the American Journal of Drug and Alcohol Abuse.

“Our findings suggest that the experience of AA over the years had left these members with an innate ability to use the AA experience—prayer in this case―to minimize the effect of alcohol triggers in producing craving,” says senior author Marc Galanter, professor of psychiatry and director of the Division of Alcoholism and Drug Abuse at NYU Langone.

“Craving is diminished in long-term AA members compared to patients who have stopped drinking for some period of time but are more vulnerable to relapse.”

The study results revolve around craving, one of the criteria physicians use to diagnose addiction. Such strong desires can persist even in addicted people who no longer use alcohol or drugs, and AA members recite abstinence-promoting prayers to reduce cravings.

“We wanted to determine what is going on in the brain in response to alcohol-craving triggers, such as passing by a bar or experiencing something upsetting, when long-term AA members are exposed to them,” Galanter says.

CREATING CRAVINGS IN THE LAB

To investigate, Galanter and his colleagues recruited 20 long-term AA members who reported no cravings for alcohol during the week preceding testing. The participants were placed in an MRI scanner and then shown either pictures of alcoholic drinks or people drinking to simulate drinking behavior in a laboratory setting. The pictures were presented twice: first after asking the participant to read neutral material from a newspaper, and again after the participant recited an AA prayer promoting abstinence from alcohol to represent the impact of AA.

According to the study authors, all research subjects reported some degree of craving for alcohol after viewing the images, and less craving after reciting an AA prayer. MRI data revealed that there were changes in parts of the prefrontal cortex, the region of the brain that controls attention, and in brain sites responsible for control of emotion and the semantic reappraisal of emotion, which represents the different ways a people understand situations based on their perspectives.

“This finding suggests that there appears to be an emotional response to alcohol triggers, but that it’s experienced and understood differently when someone has the protection of the AA experience,” Galanter says.

‘SPIRITUAL AWAKENING’

In Galanter’s decade-long research into the role of spirituality in long-term AA members, he and his colleagues have found that members undergo a transition from initially craving alcohol to a new status where they reported little or no craving. This reduction in craving, according to Galanter, is associated with the amount of time that passed following a “spiritual awakening” in AA, which marks a transition to a different attitude toward drinking.

Previous investigations by other researchers of the role of prayer on drinking behavior found that alcohol abusers who reported a spiritual awakening drank less after treatment for alcoholism. Research participants assigned to engage in prayer—unrelated to drinking—every day for four weeks drank about half as much as those who were not.

“Our current findings open up a new field of inquiry into physiologic changes that may accompany spiritual awakening and perspective changes in AA members and others,” says Galanter. He says the study results also support the validity of a long-term AA experience in terms of physiologic changes in the brain.

Earlier this year, Oxford University Press published Galanter’s book, What Is Alcoholics Anonymous?, which provides context for his group’s studies of the psychological effects of AA.

Coauthors are from NYU Langone and Columbia University. The John H. Templeton Foundation supported the work, which is published in the American Journal of Drug and Alcohol Abuse.

Source: Republished from Futurity.org as a derivative work under the Attribution 4.0 International license. Original article posted to Futurity by Greg Williams-NYU.

Featured Photo Credit: frankieleon/Flickr

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By Naja Ferjan Ramirez, University of Washington.

Any adult who has attempted to learn a foreign language can attest to how difficult and confusing it can be. So when a three-year-old growing up in a bilingual household inserts Spanish words into his English sentences, conventional wisdom assumes that he is confusing the two languages.

Research shows that this is not the case.

In fact, early childhood is the best possible time to learn a second language. Children who experience two languages from birth typically become native speakers of both, while adults often struggle with second language learning and rarely attain native-like fluency.

But the question remains: is it confusing for babies to learn two languages simultaneously?

When do babies learn language?

Research shows babies begin to learn language sounds before they’re even born. In the womb, a mother’s voice is one of the most prominent sounds an unborn baby hears. By the time they’re born, newborns can not only tell the difference between their mother’s language and another language, but also show a capability of distinguishing between languages.

Language learning depends on the processing of sounds. All the world’s languages put together comprise about 800 or so sounds. Each language uses only about 40 language sounds, or “phonemes,” which distinguish one language from another.

At birth, the baby brain has an unusual gift: it can tell the difference between all 800 sounds. This means that at this stage infants can learn any language that they’re exposed to. Gradually babies figure out which sounds they are hearing the most.

Between six and 12 months, infants who grow up in monolingual households become more specialized in the subset of sounds in their native language. In other words, they become “native language specialists.” And, by their first birthdays, monolingual infants begin to lose their ability to hear the differences between foreign language sounds.

Studying baby brains

What about those babies who hear two languages from birth? Can a baby brain specialize in two languages? If so, how is this process different then specializing in a single language?

Knowing how the baby brain learns one versus two languages is important for understanding the developmental milestones in learning to speak. For example, parents of bilingual children often wonder what is and isn’t typical or expected, or how their child will differ from those children who are learning a single language.

My collaborators and I recently studied the brain processing of language sounds in 11-month-old babies from monolingual (English only) and bilingual (Spanish-English) homes. We used a completely noninvasive technology called magnetoencephalography (MEG), which precisely pinpointed the timing and the location of activity in the brain as the babies listened to Spanish and English syllables.

We found some key differences between infants raised in monolingual versus bilingual homes.

At 11 months of age, just before most babies begin to say their first words, the brain recordings revealed that:

• Babies from monolingual English households are specialized to process the sounds of English, and not the sounds of Spanish, an unfamiliar language
• Babies from bilingual Spanish-English households are specialized to process the sounds of both languages, Spanish and English.

Here’s a video summarizing our study.

Our findings show that babies’ brains become tuned to whatever language or languages they hear from their caregivers. A monolingual brain becomes tuned to the sounds of one language, and a bilingual brain becomes tuned to the sounds of two languages. By 11 months of age, the activity in the baby brain reflects the language or languages that they have been exposed to.

Is it OK to learn two languages?

This has important implications. Parents of monolingual and bilingual children alike are eager for their little ones to utter the first words. It’s an exciting time to learn more about what the baby is thinking. However, a common concern, especially for bilingual parents, is that their child is not learning fast enough.

We found that the bilingual babies showed an equally strong brain response to English sounds as the monolingual babies. This suggests that bilingual babies were learning English at the same rate as the monolingual babies.

Parents of bilingual children also worry that their children will not know as many words as children who are raised with one language.

To some extent, this concern is valid. Bilingual infants split their time between two languages, and thus, on average, hear fewer words in each. However, studies consistently show that bilingual children do not lag behind when both languages are considered.

Vocabulary sizes of bilingual children, when combined across both languages, have been found to be equal to or greater than those of monolingual children.

Another common concern is that bilingualism causes confusion. Part of this concern arises due to “code switching,” a speaking behavior in which bilinguals combine both languages.

For example, my four-year-old son, who speaks English, Spanish, and Slovene, goes as far as using the Slovene endings on Spanish and English words. Research shows bilingual children code-switch because bilingual adults around them do too. Code-switching in bilingual adults and children is rule-governed, not haphazard.

Unlike monolingual children, bilingual children have another language from which they can easily borrow if they can’t quickly retrieve the appropriate word in one language. Even two-year-olds modulate their language to match the language used by their interlocutor.

Researchers have shown code switching to be part of a bilingual child’s normal language development. And it could even be the beginning of what gives them the extra cognitive prowess known as the “bilingual advantage.”

Bilingual kids are at an advantage

The good news is young children all around the world can and do acquire two languages simultaneously. In fact, in many parts of the world, being bilingual is the norm rather than an exception.

It is now understood that the constant need to shift attention between languages leads to several cognitive advantages. Research has found that bilingual adults and children show an
improved executive functioning of the brain – that is, they are able to shift attention, switch between tasks and solve problems more easily. Bilinguals have also been found to have increased metalinguistic skills (the ability to think about language per se, and understand how it works). There is evidence that being bilingual makes the learning of a third language easier. Further, the accumulating effect of dual language experience is thought to translate into protective effects against cognitive decline with aging and the onset of Alzheimer’s disease.

So, if you want your child to know more than one language, it’s best to start at an early age, before she even starts speaking her first language. It won’t confuse your child, and it could even give her a boost in other forms of cognition.

Naja Ferjan Ramirez, Research Scientist, University of Washington

This article was originally published on The Conversation. Read the original article.

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By Vytas A. Bankaitis, Texas A&M University and Zhigang Xie, Texas A&M University.

Autism spectrum disorders (ASDs) affect about one percent of the world’s population. In the United States alone, about 1 in 68 children are on the spectrum, and between 40 and 60 percent of them are also diagnosed with some degree of intellectual disability.

The annual cost associated with ASD in the United States is high – presently estimated to be US$236-$262 billion. If diagnoses continue to grow at the current pace, it will exceed $460 billion by 2025, more than the total cost of diabetes.

Scientists still aren’t sure what causes ASD, but evidence suggests it’s probably the result of complex interactions between genetic and environmental factors that affect brain development. So far hundreds of genes whose mutations are associated with ASD have been identified. Many of them are known or predicted to play critical roles in the cells that make up the building blocks of the brain.

Learning more about these genes – and their mutations – might help us understand some of the root causes of ASD, and perhaps find ways to lower the risk that a child will have it.

We decided to take a closer look at mutations in one of these genes, called TMLHE, which is required for a critical chemical reaction that lets cells burn fat molecules to produce energy. We wanted to understand how a TMLHE mutation could increase autism risk and whether we could counteract the effect of the mutation.

Neural stem cells and the developing brain

When we examined the effect of TMLHE mutations in mice, we found these mutations specifically affect neural stem cells during early stages of brain development.

Neural stem cells create all of the specialized cells that make up the brain. When they divide to create two “daughter” cells, one typically becomes a specialized brain cell, such as a neuron, and the other remains a neural stem cell.

This means that the population of neural stem cells is maintained, and the brain building work can continue. Although this process occurs throughout one’s lifetime, it is the most active during embryonic brain development.

If the neural stem cell population is not maintained at the proper level when the brain is developing, there won’t be enough stem cells left to produce the right number and right kind of specialized brain cells. The result is an abnormally wired brain.

We find this to be precisely the problem that TMLHE mutations created in mice. Too often, neural stem cell division created two specialized cells, instead of one specialized cell and one neural stem cell.

What does a TMLHE mutation do to neural stem cells?

TMLHE mutations make it difficult for neural stem cells to produce energy, or to maintain a correctly oxidized environment, which is why they often don’t divide properly.

Cells produce energy by processing fat molecules. For this to happen, fat molecules need to get to the mitochondria, the powerhouses of the cell, to be broken down. A nutrient called carnitine helps transport fat to these parts of the cell.

This is where TMLHE comes in. While we can get carnitine from food – milk and meat, for instance – our bodies can also produce it. But the TMLHE gene is required for carnitine synthesis, so a mutation in this gene can lead to carnitine deficiency. This affects energy production in cells and can also result in a cellular environment that is too oxidized for the cell to function properly, which makes problems for the neural stem cell when it divides.

But we also found that this neural stem cell defect is corrected when carnitine is added to TMLHE-deficient cells. This restores their ability to burn fat into energy and to maintain a proper environment within mitochondria, and restores proper cell division behavior to TMLHE-deficient neural stem cells.

TMLHE mutations are surprisingly common

Two recent studies have found that the prevalence of TMLHE mutations in human populations may range from about 1 in 350 to about 1 in 900. In most cases, these people would be unaware that they carry a copy of the defective gene.

Our research raises the possibility that the increased autism risk associated with TMLHE mutations might be effectively managed by making sure the embryo has enough carnitine during critical stages for brain development. It also seems that sufficient carnitine is required at very early stages of pregnancy – far earlier than previously suspected.

Either parent can pass on a defective TMLHE gene. Girls have two copies of the gene, inheriting one from each parent. Boys, however, have only one copy of the gene, which they inherit from the mother. If a male fetus inherits the mutant TMLHE gene, it will be unable to produce its own carnitine and will rely on the mother for its carnitine supply.

Hypothetically, a woman who carries a TMLHE mutation could take supplemental dietary carnitine during pregnancy to try to minimize the associated ASD risk – particularly for male babies.

Carnitine deficiency may be an underestimated ASD risk

While hundreds of genes are associated with ASD risk, the surprisingly high incidence of TMLHE mutations in human beings suggests the impact of carnitine deficiency on ASD risk may be badly underestimated. This is a particularly interesting possibility given that diet might be a significant contributing factor to ASD risk associated with TMLHE mutations.

Results from our mouse study, and a recent study in which an autistic child with a TMLHE mutation was treated with carnitine supplementation, suggest that prenatal carnitine supplementation might well be worth considering. However, more research, particularly clinical trials on human populations, will be needed to further establish the role of carnitine in autism prevention.

Vytas A. Bankaitis, Professor of Chemistry, Texas A&M Health Science Center, Texas A&M University and Zhigang Xie, Assistant Research Scientist, Texas A&M Health Science Center, Texas A&M University

This article was originally published on The Conversation. Read the original article.

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By Joanne Ruthsatz, The Ohio State University.

As a toddler growing up in the 1950s, Richard Wawro threw violent tantrums. Often, he would tap the same piano key for long stretches of time.

When he was three, his parents took him for testing at a nearby hospital. They were told that he was moderately to severely retarded. His family, however, never believed that his IQ was as low as the experts claimed.

A special education teacher began working with Richard when he was six. She introduced him to drawing with crayons, which he took to quickly.

He began filling sketchbooks (and the wallpaper of his Scotland home) with startlingly accurate depictions of cartoon characters like Yogi Bear. When Richard was 12, his artwork astounded a visiting artist who said that his drawings were created “with the precision of a mechanic and the vision of a poet.”

Richard could never read or write well. His speech remained limited. But his involvement with the art world spurred his social development. He participated in dozens of exhibitions and became a well-known artist. His artwork was celebrated by the media and in a documentary, “With Eyes Wide Open.” Both Margaret Thatcher and Pope John Paul II owned Wawro’s originals.

Richard was a savant, an individual with a spike in a particular ability combined with an impairment or disability. In Richard’s case, that underlying condition was autism. Autism is a condition characterized by social and communication challenges, like difficulty making eye contact or making conversation, along with repetitive behaviors or intense interests.

It turns out that many savants have autism. In a 2015 paper, the savant expert Darold Treffert reported that among the congenital savants in his registry, 75 percent had an autism spectrum disorder, a term used to describe a group of disorders with variable symptoms and severity.

Exceptional memory and autism

Not every autistic individual has extraordinary talents.

In fact, autism can be accompanied by serious challenges that last a lifetime (as was also the case for Wawro, whose family handled his daily living needs until he died at age 53).

But when the astounding abilities are there, they are often rooted in extreme memory, excellent attention to detail and passionate interests – traits also linked to autism.

Many autistic kids show exceptional abilities.
Valary, CC BY-NC-ND

My work has been with child prodigies, those astounding individuals who perform at an adult-professional level in a demanding field before adolescence.

In many ways, prodigies look a lot like savants. They have the same preternatural abilities. They have the same prolific output.

But there’s a key difference between the two. While in savants, these extreme abilities are paired with an underlying impairment or disability, prodigies don’t typically have any such disability.

Still, as I recount in my new book, The Prodigy’s Cousin, I have found the overlap between prodigy and autism to be striking. Even though prodigies are not typically autistic, they have the same excellent memories, extreme attention to detail, and passionate interests linked to autism and autistic savants.

The prodigies’ excellent memories were almost immediately apparent. When I investigated nine prodigies across two studies, each one scored in the 99th percentile for this ability. When this group was expanded to 18 prodigies in a 2014 study, the prodigies’ average working memory score was 140 – north of the 95th percentile.

Early work on autism

Reports linking extreme memory and autism date back to the first published reports of Leo Kanner and Hans Asperger, the two scientists credited with identifying autism as an independent condition in the 1940s.

In his landmark 1943 study, Kanner remarked upon his subjects’ “excellent memory for events of several years before, the phenomenal rote memory for poems and names, and the precise recollection of complex patterns and sequences.”

He included a report of a boy, Donald T., with “an unusual memory for faces and names,” who had memorized “an inordinate number of pictures in a set of Compton’s Encyclopedia.” Another, Charles N., could distinguish between 18 symphonies at age one-and-a-half.

Since Kanner’s time, scientists have found that memory in autism is complex. But in a 2015 study, a team of researchers found that more than half of their 200 autistic subjects had notable memories. Treffert has described excellent memory as “integral” for savants in particular.

Prodigies and autism

As part of my 2012 study, the child prodigies I worked with were given the Autism-Spectrum Quotient, a self-administered test designed to measure autistic traits. On attention to detail, they outscored not only the controls, but also those with an autism spectrum disorder.

Attention to detail is another strength associated with autism. Some have described excellent attention to detail as “a universal feature of the autistic brain.” In 2006, the prominent autism researchers Francesca Happé and Uta Frith concluded that there was strong evidence that autism was associated with superiority on “tasks requiring detail-focused processing.”

Child prodigies are also exceptionally passionate about their area of expertise.

Such passionate interests are closely associated with autism. They are even part of autism’s diagnostic criteria.

This trait has been observed since the early days of autism research. Kanner’s 1943 paper includes a description of Alfred L., a child whose mother noted his tendency toward intense interests. As she put it:

He talks of little else while the interest exists, he frets when he is not able to indulge in it (by seeing it, coming in contact with it, drawing pictures of it), and it is difficult to get his attention because of his preoccupation.

This sort of passion can result in prolific output, as it did for Richard Wawro, who created at least 2,453 pictures in his lifetime.

Why do prodigies have autistic relatives?

The link between prodigy and autism could be even deeper than we think.

In addition to drawing from a similar well of cognitive abilities, there appears to be a family link between prodigy and autism. In a study I conducted in 2012, more than half of the prodigies investigated had a close autistic relative. In one instance, a prodigy had five autistic relatives.

Another study I conducted with colleagues at The Ohio State University suggests that prodigies and their autistic relatives may even share a genetic link. We found evidence that the prodigies and their autistic relatives both had a mutation on chromosome one not shared by their non-prodigious, non-autistic relatives.

The same traits that are celebrated in prodigies – like their excellent attention to detail and the passionate interests – are often recognized as strengths in the context of autism, too, though sometimes families report that the extreme nature of autistic interests can take a toll on family life.

This is a real challenge, as are other aspects of autism. Figuring out the best way to support those with autism and their families is essential.

But let’s remember the strengths of autism as well as the challenges.

Kimberly Stephens, coauthor of The Prodigy’s Cousin, contributed to this piece.

Joanne Ruthsatz, Assistant Professor of Psychology, The Ohio State University

This article was originally published on The Conversation. Read the original article.

Featured Image Credit: MIke Wawro, CC BY

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The ominous behaviors that often precede violent acts—stalking, bullying, and possibly sexual aggression—are tied to a distinct part of the hypothalamus, the brain region that also controls body temperature, hunger, and sleep in mammals, new research shows.

The structure is anatomically known as the ventrolateral part of the ventromedial hypothalamus, or VMHvl, because of its central location inside the brain on the underside of the hypothalamus.

“Our study pinpoints the brain circuits essential to the aggressive motivations that build up as animals prepare to attack,” says study senior investigator Dayu Lin, assistant professor at the Neuroscience Institute at New York University Langone Medical Center.

The new findings build on Lin’s ongoing research effort to better understand aggressive motivation, along with related brain biomarkers and biochemical pathways. Its clinical implications are potentially widespread: If the field can learn how to control aggressive motivation, it could lead to better control of these behaviors without the need for sedation. Lin also last month published the results of a mouse study on the origins of rage in the journalCurrent Biology.

Despite these results in mice, which share many brain structures with humans, targeting this part of the human brain with treatments meant to curb aggression remains “only a distant possibility, even if related ethical and legal issues could be resolved,” says Lin. “That said, our results argue that the ventrolateral part of the ventromedial hypothalamus should be studied further as part of future efforts seeking to correct behaviors from bullying to sexual predation.”

MEAN MICE

For the current study, published in the journal Nature Neuroscience, male mice trained to attack weaker male mice were monitored to see how aggressively they tried to gain access to and bully another mouse. One measure was the number of attempts made by aggressive mice to poke their noses through holes that led to another mouse entering their space, and which they could then attack.

While past studies have linked aggressive actions to this part of the brain, the current study specifically tracked the premeditated, motivational aspect of the behavior to the VMHvl.

By using sets of probes that measured nerve activity before, during, and after mice planned to attack, the research team found that nerve cell activity in the VMHvl routinely peaked just before mice began to hole poke, even when the aggressive mice could not yet smell or see their target.

Nerve cell activity in the VMHvl also increased by as much as tenfold during the initial seconds after the weaker target mice appeared. Genetically stopping VMHvl activity ceased nearly all aggressive motivations in mice, but did not inhibit other learned behaviors, such as nose poking for access to a treat.

Lin next plans to investigate which specific nerve cells and circuits in the VMHvl are involved in motivating and carrying out aggression.

Source: Republished from Futurity.org as a derivative work under the Attribution 4.0 International license. Original article posted to Futurity by David March-NYU.

Featured Image Credit:  Emilio Garcia/Flickr

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Neurosurgeons at Washington University in St. Louis unexpectedly found a method to open the brain’s brain-blood barrier in the process of opening the brain’s protective cover and using a laser probe to directly zap brain cancer cells in patients with a deadly form of brain cancer. The unexpected side effect of the laser’s zapping was to open the blood-brain barrier and keep it open for up to six weeks, a new development which would allow for delivery of chemotherapy or other treatments that could help combat their cancer.

In a pilot study, 14 patients with glioblastoma—the most common and aggressive type of brain cancer—underwent minimally invasive laser surgery to treat a recurrence of their tumors. Heat from the laser is known to kill brain tumor cells but, unexpectedly, the technology can also penetrate the blood-brain barrier.

“The laser treatment kept the blood-brain barrier open for four to six weeks, providing us with a therapeutic window of opportunity to deliver chemotherapy drugs to the patients,” says co-corresponding author Eric C. Leuthardt, professor of neurosurgery at Washington University in St. Louis. “This is crucial because most chemotherapy drugs can’t get past the protective barrier, greatly limiting treatment options for patients with brain tumors.

“We are closely following patients in the trial. Our early results indicate that the patients are doing much better on average, in terms of survival and clinical outcomes, than what we would expect. We are encouraged but very cautious because additional patients need to be evaluated before we can draw firm conclusions.”

Glioblastomas are one of the most difficult cancers to treat. Most patients diagnosed with this type of brain tumor survive just 15 months, according to the American Cancer Society.

The new research is part of a larger phase II clinical trial that will involve 40 patients. Twenty patients were enrolled in the pilot study, 14 of whom were found to be suitable candidates for the minimally invasive laser surgery.

The laser technology was approved by the Food and Drug Administration in 2009 as a surgical tool that can be used to treat brain tumors. But the new study marks the first time the laser has been shown to disrupt the blood-brain barrier, which shields the brain from harmful toxins but also inadvertently blocks potentially helpful drugs, such as chemotherapy.

As part of the trial, a widely used chemotherapy—doxorubicin—was given intravenously to 13 patients in the weeks following the laser surgery. Preliminary data indicate that 12 patients showed no evidence of tumor progression during the short, 10-week time frame of the study. One patient experienced tumor growth before chemotherapy was delivered; the tumor in another patient progressed after chemotherapy was administered.

The laser surgery was well-tolerated by the patients in the trial. Most patients went home one to two days afterward and none experienced severe complications. The surgery is performed while a patient lies in an MRI scanner, providing the neurosurgical team with a real-time look at the tumor. Using an incision of only 3 millimeters—about the thickness of two pennies—a neurosurgeon robotically inserts the laser to heat up and kill brain tumor cells at a temperature of about 150 degrees Fahrenheit.

“The laser kills tumor cells, which we anticipated,” Leuthard says, “but, surprisingly, while reviewing MRI scans of our patients, we noticed changes near the former tumor site that looked consistent with the breakdown of the blood-brain barrier.”

He then confirmed and further studied these imaging findings with coauthor Joshua Shimony, associate professor of radiology.

The researchers performed follow-up testing, which showed that the degree of permeability through the blood-brain barrier peaked one to two weeks after surgery but that the barrier remained open for up to six weeks.

Other successful attempts to breach the barrier have left it open for only a short time—about 24 hours—not long enough for chemotherapy to be consistently delivered—or have resulted in only modest benefits. In contrast, the new laser technology leaves the barrier open for weeks—long enough for patients to receive multiple treatments with chemotherapy. And the laser only opens the barrier near the tumor, leaving the protective cover in place in other areas, potentially limiting the harmful effects of chemotherapy drugs in other areas of the brain.

The findings suggest that other exciting approaches such as cancer immunotherapy—which harnesses cells of the immune system to seek out and destroy cancer—also may be useful for patients with glioblastomas. The researchers are planning another clinical trial that combines the laser technology with chemotherapy and immunotherapy as well as trials to test targeted cancer drugs that normally can’t breach the blood-brain barrier.

“We are hopeful this technology opens new avenues to treating these devastating brain tumors that cause great suffering for patients and their families,” Leuthardt says.

The National Cancer Institute of the National Institutes of Health, the Foundation for Barnes-Jewish Hospital,  and Washington University School of Medicine in St. Louis funded the work. The study was published in the journal PLOS ONE

Republished from Futurity.org as a derivative work under the Attribution 4.0 International license. Original article posted to Futurity by Jim Goodwin-WUSTL

Featured Image Credit: NIH Image Gallery/flickr, CC BY

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Jayanthi Maniam, UNSW Australia and Margaret Morris, UNSW Australia

We all know that cola and lemonade aren’t great for our waistline or our dental health, but our new study on rats has shed light on just how much damage sugary drinks can also do to our brain.

The changes we observed to the region of the brain that controls emotional behaviour and cognitive function were more extensive than those caused by extreme early life stress.

It is known that adverse experiences early in life, such as extreme stress or abuse, increase the risk of poor mental health and psychiatric disorders later in life.

The number of traumatic events (accidents; witnessing an injury; bereavement; natural disasters; physical, sexual and emotional abuse; domestic violence and being a victim of crime) a child is exposed to is associated with elevated concentrations of the major stress hormone, cortisol.

There is also evidence that childhood maltreatment is associated with reduced brain volume and that these changes may be linked to anxiety.

What we found

Looking at rats, we examined whether the impact of early life stress on the brain was exacerbated by drinking high volumes of sugary drinks after weaning. As females are more likely to experience adverse life events, we studied female Sprague-Dawley rats.

To model early life trauma or abuse, after rats were born half of the litters were exposed to limited nesting material from days two to nine after birth. They then returned to normal bedding until they were weaned. The limited nesting alters maternal behaviour and increases anxiety in the offspring later in life.

At weaning, half the rats were given unlimited to access to low-fat chow and water to drink, while their sisters were given chow, water and a 25% sugar solution that they could choose to drink. Animals exposed to early life stress were smaller at weaning, but this difference disappeared over time. Rats consuming sugar in both groups (control and stress) ate more calories over the experiment.

The rats were followed until they were 15 weeks old, and then their brains were examined. As we know that early life stress can impact mental health and function, we examined a part of the brain called the hippocampus, which is important for both memory and stress. Four groups of rats were studied – control (no stress), control rats drinking sugar, rats exposed to stress, and rats exposed to stress who drank sugar.

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