New Study IDs Brain Cells That Help Us Learn by Watching Others

-Janice Wood

From infancy, we learn by watching other people, and new research has pinpointed the individual neurons that support this observational learning.

Published in Nature Communications, the study from researchers at the University of California Los Angeles and California Institute of Technology could provide scientists with a better understanding of how the brain goes awry in conditions like learning disorders and social anxiety disorder.

In a further finding, the research team also discovered that neurons in the same region fire in response to schadenfreude — the pleasure of seeing someone else make a blunder or lose a game.

“Observational learning is the cornerstone for our ability to change behavior,” said senior author Dr. Itzhak Fried, a professor of neurosurgery and psychiatry at UCLA’s David Geffen School of Medicine and Semel Institute for Neuroscience and Human Behavior. “It’s human nature to want to learn from other people’s mistakes rather than commit your own.”

“The ability to quickly learn from others can give humans a critical edge over other species,” added lead author Dr. Michael Hill, a former UCLA and Caltech  scientist now based at the Swiss National Science Foundation. “The skill also contributes to someone feeling he or she is a member of one culture versus another.”

Prior to the study, Fried implanted electrodes inside the brains of people with epilepsy being treated at UCLA, a standard medical procedure used to identify the origins of epileptic seizures prior to surgery.

The researchers then used the electrodes to record the activity of individual neurons in the brains of 10 people playing a card game.

Players were instructed to draw a card from one of two decks. One deck included 70 percent of the winning cards, while the other deck contained only 30 percent of the winning cards. Each person took turns choosing cards on his or her own and then watched two other players draw cards from the same decks.

By learning from the results of their own and the other players’ choices, the participants quickly zeroed in on the deck containing better cards.

The research team was surprised to discover that individual neurons deep in the frontal lobe reacted as the patient considered whether they or their opponents would pick a winning card. Called the anterior cingulate cortex, the region plays an important role in high-level functions like decision making, reward anticipation, social interaction and emotion, the researchers explained.

“The firing rate of individual neurons altered according to what the patient expected to happen,” Hill said. “For example, would their opponents win or lose? The same cells also changed their response after the patient discovered whether their prediction was on target, reflecting their learning process.”

The findings suggest that individual nerve cells in the person’s brain used the details gleaned by observing the other players to calculate which deck to choose a card from next, the researchers said.

“The anterior cingulate cortex acts as the central executive of human decision-making, yet we know little about the neuronal machinery at this level,” said Fried, who is also a professor of neurosurgery at the Sackler Faculty of Medicine at Tel Aviv University.

According to the researchers, the findings will help scientists better understand the organization of neurons in the anterior cingulate cortex and exactly what they do.

Fried and Hill propose that active stimulation of the neurons in the anterior cingulate cortex could influence human behavior and have possible benefits for people struggling with learning disabilities or difficulty reading social cues.

The researchers noted that the cells in the same region fired vigorously each time a person won or the other players lost, and decreased their activity whenever the person lost or the other players won.

“While obviously we don’t know precisely what it is that these neurons encode, it’s fascinating to see something like schadenfreude reflected in the activity of individual neurons in the human brain,” Hill said.

Caffeine May Protect Women from Dementia

-Rick Nauert, PhD

A new study of women aged 65 and older discovered a 36 percent reduction in dementia among women who consumed caffeine. Researchers followed the women for over 10 years.

The women self-reported caffeine consumption of more than 261 mg per day or the equivalent to two to three 8-oz cups of coffee per day, five to six 8-oz cups of black tea, or seven to eight 12-ounce cans of cola.

“The mounting evidence of caffeine consumption as a potentially protective factor against cognitive impairment is exciting given that caffeine is also an easily modifiable dietary factor with very few contraindications,” said Ira Driscoll, Ph.D., the study’s lead author and a professor of psychology at the University of Wisconsin-Milwaukee.

“What is unique about this study is that we had an unprecedented opportunity to examine the relationships between caffeine intake and dementia incidence in a large and well-defined, prospectively-studied cohort of women.”

The findings come from participants in the Women’s Health Initiative Memory Study, which is funded by the National Heart, Lung, and Blood Institute. Driscoll and her research colleagues used data from 6,467 community-dwelling, postmenopausal women aged 65 and older who reported some level of caffeine consumption.

Intake was estimated from questions about coffee, tea, and cola beverage intake, including frequency and serving size.

In 10 years or less of follow-up with annual assessments of cognitive function, 388 of these women received a diagnosis of probable dementia or some form of global cognitive impairment. Those who consumed above the median amount of caffeine for this group (with an average intake of 261 mg per day) were diagnosed at a lower rate than those who fell below the median (with an average intake of 64 mg per day).

The researchers adjusted for risk factors such as hormone therapy, age, race, education, body mass index, sleep quality, depression, hypertension, prior cardiovascular disease, diabetes, smoking, and alcohol consumption.

Moderately Vigorous Exercise in Midlife Tied to Greater Cognition in Old Age

-Traci Pedersen

Moderately vigorous physical activity in midlife is linked to better cognition 25 years later, according to a new study involving 3,050 twins from the Finnish Twin Cohort.

While traditional vascular risk factors (elevated blood pressure, hypercholesterolemia, obesity, diabetes, and lack of exercise) have been associated with dementia risk, until now it has remained unclear whether exercise carries other unique benefits for cognition other than reducing these risks. But the link remained even after factoring these out.

“This suggests that the beneficial influence of physical activity on the brain and cognition is not solely based on decreasing vascular risk factors,” says researcher Paula Iso-Markku from the University of Helsinki.

The study was conducted by scientists at the universities of Helsinki, Jyväskylä, and Turku. The twins reported information on their physical activity through questionnaire surveys between 1975 and 1981 (mean age of participants in 1981 was 49), while cognition was assessed by validated telephone interviews between the years 1999 and 2015.

First, the link between exercise and cognition was examined in all participants, and then by comparing later cognition in pairs where one twin was more physically active than the other.

Iso-Markku says that “few long-term, high-quality, follow-up studies on physical activity and cognition have been published, and it has remained unclear what type and amount of exercise is needed to safeguard cognition.”

Importantly, the researchers discovered that cognitive benefits in old age did not continue to increase the more vigorously one had exercised in midlife. In other words, extremely vigorous exercise in midlife did not result in the most superior cognitive abilities later in life.

Instead, a moderate amount of physical activity was sufficient for memory-protecting benefits, and only the most inactive group of twins stood out with a significantly higher risk for cognitive impairment.

“Overall, the study shows that moderately vigorous physical activity, meaning more strenuous than walking, is associated with better cognition after an average of 25 years,” said Professor Urho Kujala from the University of Jyväskylä.

The new results are in accordance with findings on animals which have shown that physical activity increases the amount of growth factors in the brain and improves synaptic plasticity.

Cases of dementia have been on the increase among aging populations worldwide. Although the incidence of dementia seems to have decreased in younger seniors, the total prevalence of the disease is still expected to rise. While no cure exists for dementia as of yet, researchers have produced an abundance of new evidence regarding dementia prevention in the last decade.

The findings are published in the Journal of Alzheimer’s Disease.

10 Days Without Exercise Can Reduce Blood Flow in Brain

-Traci Pedersen

We know that when highly active people stop exercising for one or two weeks, their cardiovascular endurance begins to diminish. But what effect, if any, does an exercise break have on the brain?

This was the focus of a new study by researchers at the University of Maryland School of Public Health. Using MRI brain imaging, the research team studied cerebral blood flow in very healthy and athletic older adults (ages 50-80 years) before and after a 10-day period during which they stopped all exercise.

They found a significant decrease in blood flow to several brain areas, including the hippocampus, after the participants quit their exercise routines.

“We know that the hippocampus plays an important role in learning and memory and is one of the first brain regions to shrink in people with Alzheimer’s disease,” said Dr. J. Carson Smith, associate professor of kinesiology and lead author of the study.

“In rodents, the hippocampus responds to exercise training by increasing the growth of new blood vessels and new neurons, and in older people, exercise can help protect the hippocampus from shrinking. So, it is significant that people who stopped exercising for only 10 days showed a decrease in brain blood flow in brain regions that are important for maintaining brain health.”

The study participants were all “master athletes,” defined as people between the ages of 50 and 80 who had been participating in endurance exercise for at least 15 years and who had recently competed in an endurance event.

To qualify for the study, the participants’ exercise regimens had to involve at least four hours of high intensity endurance training each week. On average, they were running 36 miles each week or the equivalent of a 10K run a day. Not surprisingly, this group had a V02 max above 90 percent for their age. Vo2 max is a measure of the maximal rate of oxygen consumption of an individual and reflects their aerobic physical fitness.

The researchers measured the velocity of blood flow in the brain with an MRI scan while the participants were still following their regular training routine (at peak fitness) and again after 10 days of no exercise.

They discovered that resting cerebral blood flow significantly dropped in eight brain regions, including the areas of the left and right hippocampus and several regions known to be part of the brain’s “default mode network” — a neural network known to deteriorate quickly with a diagnosis of Alzheimer’s disease.

The findings add to the growing scientific evidence of the impact of physical activity on cognitive health.

“We know that if you are less physically active, you are more likely to have cognitive problems and dementia as you age,” said Smith. “However, we did not find any evidence that cognitive abilities worsened after stopping exercising for just 10 days.

“But the take-home message is simple: If you do stop exercising for 10 days, just as you will quickly lose your cardiovascular fitness, you will also experience a decrease in blood brain flow.”

Smith believes this new information could have important implications for brain health in older adults, and points to the need for more research to find out how fast these changes occur, what the long-term effects could be, and how quickly they could be reversed when exercise is resumed.

The findings are published in the journal Frontiers in Aging Neuroscience.

Dopamine Returns to Normal 3 Months After Quitting Smoking

-Traci Pedersen

Three months after quitting smoking, levels of dopamine in the brain return to normal, according to a new study published in the journal Biological Psychiatry. The findings suggest that dopamine deficits found in smokers are due to the smoking itself and are not necessarily a pre-existing risk factor.

A major challenge in understanding substance-related disorders lies in discovering the reasons why only some individuals become addicted, according to first author Dr. Lena Rademacher, postdoctoral fellow at the University of Lübeck in Germany.

Researchers believe that some individuals possess certain traits making them more vulnerable to addiction. They also suspect that brain circuits involving dopamine may be involved. Drugs of abuse release dopamine, and addiction to nicotine is connected to abnormalities in the dopamine system.

But it is still unknown whether smoking induces those abnormalities or if they already exist and contribute to risk of nicotine addiction.

For the study, senior author Dr. Ingo Vernaleken, Professor at RWTH Aachen University in Germany, led a team of researchers to examine dopamine function in chronic smokers before and after long-term cessation.

Using a brain imaging technique called positron emission tomography, the researchers measured the capacity for dopamine production in 30 men who were nicotine-dependent smokers as well as in 15 nonsmokers. After performing an initial scan on all participants, 15 smokers who successfully quit were scanned again after three months of abstinence from smoking and nicotine replacement.

The first scan showed a 15-20 percent reduction in the capacity for dopamine production in smokers compared with nonsmokers. The researchers expected this deficit to remain even after quitting, which would suggest it could be a marker of vulnerability for nicotine addiction. But they discovered that dopamine functioning returned to normal as time went on.

“Surprisingly, the alterations in dopamine synthesis capacity normalized through abstinence,” said Rademacher.

While the role of dopamine in vulnerability toward nicotine addiction cannot be excluded, the findings suggest that altered dopamine function of smokers is a consequence of nicotine consumption rather than the cause.

The findings raise the possibility that treatments might be developed that could help normalize the dopamine system in smokers.

“This study suggests that the first three months after one stops smoking may be a particularly vulnerable time for relapse, in part, because of persisting dopamine deficits. This observation raises the possibility that one might target these deficits with new treatments,” said Dr. John Krystal, editor of Biological Psychiatry.

Source: Elsevier

Mid-Life Forgetfulness May Not Be Decline

-Rick Nauert, PhD

A new study suggests memory decline in mid-life may be the result of a change in what information the brain focuses on during memory formation and retrieval, rather than a decline in brain function.

Memory issues that often present during a person’s fourth decade include the inability to remember details such as where objects have been placed.

Senior author Natasha Rajah, Ph.D., at McGill University’s Douglas Institute, says this reorientation could impact daily life.

“This change in memory strategy with age may have detrimental effects on day-to-day functions that place emphasis on memory for details such as where you parked your car or when you took your prescriptions.”

Brain changes associated with dementia are now thought to arise decades before the onset of symptoms. So a key question in current memory research concerns which changes to the aging brain are normal and which are not.

But Rajah said most of the work on aging and memory has concentrated on understanding brain changes later in life. “So we know little about what happens at midlife in healthy aging and how this relates to findings in late life. Our research was aimed at addressing this issue.”

In this study, 112 healthy adults ranging in age from 19 to 76 years were shown a series of faces. Participants were then asked to recall where a particular face appeared on the screen (left or right) and when it appeared (least or most recently). The researchers used functional MRI to analyze which parts of brain were activated during recall of these details.

Rajah and colleagues found that young adults activated their visual cortex while successfully performing this task. As she explains, “They are really paying attention to the perceptual details in order to make that decision.”

On the other hand, middle-aged and older adults didn’t show the same level of visual cortex activation when they recalled the information. Instead, their medial prefrontal cortex was activated. That’s a part of the brain known to be involved with information having to do with one’s own life and introspection.

Even though middle-aged and older participants didn’t perform as well as younger ones in this experiment, Rajah said it may be wrong to regard the response of the middle-aged and older brains as impairment. “This may not be a ‘deficit’ in brain function per se, but reflects changes in what adults deem ‘important information’ as they age.”

In other words, the middle-aged and older participants were simply focusing on different aspects of the event compared to those in the younger group.

Rajah says that middle-aged and older adults might improve their recall abilities by learning to focus on external rather than internal information. “That may be why some research has suggested that mindfulness meditation is related to better cognitive aging.”

Rajah is currently analyzing data from a similar study to discern if there are any gender differences in middle-aged brain function as it relates to memory. “At mid-life women are going through a lot of hormonal change. So we’re wondering how much of these results is driven by post-menopausal women,’ she said.

The study appears in the journal NeuroImage.

Source: McGill University

Trauma is an Experience, Not an Event

-Santiago Delboy, MBA, MSW, LSW, S-PSB

It seems like “trauma” has become one of those household terms everyone talks about. I took a look at the number of average monthly Google searches for “trauma” in the U.S., and found that it has grown 22% in only one year. As with other terms that became mainstream (for instance “addiction” or “narcissism”), I suspect the price of increased awareness is a diluted understanding of what they really mean.

After hearing my patients talk about their experiences, reflecting on my own upbringing, and studying some of the literature on trauma, I believe the following can be a useful working definition:

Trauma is an experience that overwhelms our capacity to regulate our emotions and results in fragmentation and dissociation.

While this may not be a comprehensive or final definition, I think it captures a few ideas that are important:

  • Trauma impairs our capacity to regulate our emotions. We feel worried, irritated, anxious or afraid, consciously or not, and we cannot self-soothe or seek support from others.
  • Trauma creates fragmentation and dissociation. Whether we understand this as an unconscious defense mechanism (e.g., splitting, projection or repression), as a neurological issue (e.g., thalamus gone offline, hypersensitive amygdala), or both, dissociation is a key trait of trauma.

However, in this post I want to expand on the idea that trauma is not about a past event, but about a present experience.

I think the idea of trauma as a present experience is captured dramatically and beautifully in a 1930 painting by Belgian artist René Magritte.

The Titanic Days

I have liked Magritte since I was a little boy, but I saw “The Titanic Days” (Les jours gigantesques) for the first time a couple of years ago, at a special exhibition at the Art Institute of Chicago.

I was stunned by the power and the violence of this piece. What I see is not a rape attempt happening now, but how a past experience is stored in the woman’s body and felt in the present moment. I see the terror of her frozen expression, reminiscent of the so-called “thousand-yard stare,” the tension of her entire body and the desperate attempt to push back an attacker from a real or imagined past.

I notice the stark contrast of colors in the woman’s body and I see the traumatic struggle between life and death, and the need to keep part of her in the shadows. No words are required to convey the drama, and no words could probably do justice to the horror; trauma, in fact, impairs our capacity to develop a cohesive narrative.

The experience is overwhelming and occupies most of the space on the canvas, yet the atmosphere feels completely desolate: we know nobody will come to her help. Is the blue background a wall, keeping this woman cornered against the attacker living in her body and in her mind or does it suggest an abyss, making the woman one step away from oblivion?

We can only imagine the details of what actually happened in this woman’s past. Was she sexually abused as an adult by a coworker? Was she touched in uncomfortable ways as a young girl by a family friend? Was she somehow sexualized when she was a toddler by her father? How much of what happened was real and how much a creation of her mind?

These are important questions to consider, but not as important as the terror, the isolation, an the helplessness she is experiencing in the present moment. When I stand in front of this painting, much like when I sit across from my patients in therapy, what I see is this woman’s suffering in the here and now.

I don’t need to know all the actual details of her story, but I am curious about the meaning she assigned to it, about how it feels in her body, her mind and her spirit, and about the ways it might be getting in the way of being her full self.

Trauma is Like a Splinter

I remembered Magritte’s painting some months ago, when I read Bessel van der Kolk, a leading trauma researcher, suggesting the metaphor of trauma as a splinter (Van der Kolk, 2014): it is the body’s response to the foreign object that becomes the problem, more than the object itself.

This idea has been around for some time. Almost twenty years ago Peter Lavine, developer of the somatic experiencing approach for trauma treatment, wrote:

Traumatic symptoms are not caused by the triggering event itself. They stem from the frozen residue of energy that has not been resolved and discharged; this residue remains trapped in the nervous system where it can wreak havoc on our bodies and spirits.” – Peter Levine (1997)

It is worth noting that this notion is even older. Not to make the point that everything goes back to Sigmund Freud, but over a hundred years earlier he and his colleague Josef Breuer advanced a similar idea in “Studies on Hysteria:”

Psychical trauma – or more precisely the memory of the trauma – acts like a foreign body which long after its entry must continue to be regarded as the agent that still is at work.” – Josef Breuer and Sigmund Freud (1895)

I think there is value in talking about “traumatic events,” but I believe that it is critical to shift our focus toward the ways in which trauma stays with us. Trauma is not remembered, but reenacted. It is not about something that happened in the past, but about its consequences in the present, about the conscious or unconscious meaning we give to our experience, and how that experience defines how it feels to be in our body and in our mind.

From Traumatic Experience to Healing Experience

The notion of trauma as an experience is valid for traditional PTSD trauma (e.g., when there is a specific event or situation that triggers the traumatic experience, such as sexual abuse, a war or a natural disaster), and for complex developmental trauma, which is more insidious.

Complex trauma is characterized by an upbringing defined by patterns of inconsistency, neglect or abuse. Emotions are not expressed, not allowed, or even punished. A specific “big” event is not necessary; repeated and chronic interpersonal wounds can overwhelm the child’s capacity to regulate emotions, and create fragmentation and dissociation.

Most people I have seen in therapy have experienced some form of developmental trauma. They felt unseen and unheard by physically or emotionally absent parents. They did not feel taken care of, taken seriously, or taken into account. They believed their needs were not important and would ever be met.

They had to carry within, in silence, destructive family secrets. They had to be parents to their parents from a very early age. They needed to constantly perform or pretend to be someone else, in order to feel accepted or loved. They had to learn to soothe themselves. They lived feeling that nothing they did would ever be enough.

All these experiences from the past are re-enacted and experienced in the present, keeping them from feeling safe, loved, worthy and trusting in others or themselves. They get in the way of becoming self-aware, of letting go of control, of developing vulnerable and intimate relationships. They make them feel either in high alert or depleted. These experiences keep them from being fully alive.

The most important thing therapists can do to work through traumatic experiences of this kind, is to offer the opportunity for a healing experience.

The essence of that healing experience is not a matter of technique, approach or theory and goes beyond the promise of providing a safe, calm and reliable environment. I believe the question is about love, authenticity and curiosity.

For me, the question is about being self-aware and curious about my own reactions, about how I think of, feel with, and relate to the person in front of me. It is about being a human being first and a psychotherapist second, which is a difficult task.

Often times I get caught up in the need to make sure that I am saying the right words, giving the best feedback, offering the most insightful interpretation, or providing a useful perspective. Instead, I can trust that my presence, my curiosity, my compassion and my humanity, with its flaws and imperfections, is the first thing that matters.

Do my patients feel heard and seen by me? Would they tell me if they didn’t? Do they feel there is room for their feelings toward me, whether they come from a place of anger, hurt, sadness, joy, love or desire? Can they express them trusting that our relationship will survive? Can they count on me, and trust that I will provide safe boundaries? Can they feel that every part of themselves is acknowledged, accepted and valued?

I believe these are the types of questions that define a healing therapeutic experience. They matter not only because they allow patients to recognize current dysfunctional relationship patterns in their lives, but mainly because they have the potential to provide an experience that was not available to our patients when they were growing up.

We cannot change the past, but we can offer them the opportunity to experience and develop self-awareness, acceptance and unconditional love.

Where did the Joy of Learning Go?

Rekindling Your Child’s Enthusiasm for School

Connect your children to what they learn at school through their interests and past positive experiences so they will WANT to learn what they HAVE to learn.

Where did the joy of learning go?

When school stops being fun, all too frequently, learning stops. Help your child retain that kindergarten enthusiasm of embracing each day with the joy of learning.

Children who appear lazy, oppositional, inattentive, scattered, unmotivated, or inseparable from their social media may not be making voluntary choices. Their brains may be responding to the stress of sustained or frequent boredom.

We know that for most children, kindergarten is anticipated with awe and enthusiasm – especially when one or older siblings are already in school. There certainly can be anxieties, but they revolve around fear of leaving a parent or the security of the home environment. The idea of being a student is exciting. Most kindergarten or first grade students speak passionately about what they learn and do in school. Then, as years progress, burdensome memorization and test preparation are emphasized at the cost of diminished discovery, inquiry, and project-based learning. As school stops engaging children’s imaginations, boredom and frustration replace joy, and learning stops.

Students currently in public high schools in the U.S. are more likely to drop out than ever before. When the reasons for dropping out are examined, almost 80 percent of the students report that the main reason is boredom. When asked what bores them, the most frequent responses are that the material they are taught is either uninteresting or has no relevance to their lives.

The Stress of Boredom Blocks Brain Traffic Flow

Neuroimaging and other research tools continue to yield more data about the brain’s response to stress including sustained or frequent boredom. This comes at a time when boredom is increasingly problematic; as school funding and teacher performance ratings are increasingly tied to test performance. Consequently, there is more time dedicated to repetition, drill, and testing of facts that have no clear personal relevance or value to children.

Cutting edge neuroimaging research reveals significant disturbances in the brain’s information processing circuits in stressful learning environments. Information communication is blocked in these stress states and new learning cannot pass into memory storage. The “thinking, reflective” upper brain cannot downward regulate to direct behaviors, which then become involuntary.

Here’s what happens. The amygdalae are switching stations deep in the brain’s emotional limbic system that are stress-reactive. In the stress state, such as with prolonged or frequent boredom, metabolic activity of these emotional filters increases. When this happens, the ability of the amygdalae to direct input to or from the thinking and reflecting brain, the prefrontal cortex (PFC) is limited.

In the normal state, without high stress, the amygdalae allow input from the senses (what we hear, see, feel, experience) to reach the PFC where it can become long-term memory. The PFC is also the control center that, in the nonstress state, sends communications down to the rest of the brain to consciously and thoughtfully direct our responses, choices, and behaviors.

During high stress, the amygdalae block communication with the PFC and sends input to the lower, reactive brain, where memory is not constructed and behavioral responses are no longer in voluntary control. This is the involuntary fight-flight-freeze response to stress or fear in all mammals – in humans: the act out, zone out, drop out behavior reactions.

Brains Keep Track of Effort That Doesn’t Pay Off

For many children, the stress response to boredom and low personal relevance builds year after year when they do not find learning interesting or relevant. When children’s brains develop negativity to school, the stress state limits their voluntary control to sustain attention in class, do homework carefully, and persevere at challenging classwork.

Their brains learn to automatically resist putting mental effort into activities they have experienced as boring or irrelevant.

This is often the situation when children who are quite intelligent have difficulty with rote memorization. Since memorization is often what is tested it is inaccurately perceived by children as a measure of their intelligence. They develop the belief that their failure to get high grades on rote memory tests means they don’t have the ability to succeed. That mindset is not only inaccurate, but when taken on by your child, means their brains go into the fixed mindset of avoiding challenges and loss of motivation to persevere through setbacks.

Make Learning Personally Relevant

You can help your children keep their brains out of the involuntary, inefficient stress state. Keep them engaged and motivated to put effort into learning at school by connecting their classroom studies to their interests. Connecting them through personal relevance to the topics they study results in less boredom, and the opening of the neural pathways through their amygdalae to their upper, intelligent brains where true learning and creative thinking take place.

You can use strategies so they will WANT to learn what they HAVE to learn. Connect their brains to the topics they will be studying at school by looking with them at photos or videos of family trips, connecting objects they own to the countries they study, reading stories that relate to topics in science, history, and math.

The curiosity prompted by your reminders of their past experiences and current interests becomes a brain bridge ready to link with the information the must learn for school. The Velcro to stick new information is waiting in their brains for their neural circuits to engage learning through positive connections.

Questions as Curiosity Boosters

You’ll further preheat their interest in schoolwork when you ask your children questions that help them personally connect to the current or upcoming school topics. Their brains remain attentive because they are personally interested, and therefore curious, about the answer to the question.

Discussions you promote to bridge your children to their schoolwork will also serve as stronger memory cement if you are an active, attentive listener when they express their opinions about your questions as they learn more about the topic in school. This is not the time to split your focus. To keep them motivated, your children need to know you are truly interested in their ideas and opinions.

The results will more than offset your planning and preparations. Smiles will replace groans and eye-rolls as you use neuroscience to return to your child the joys of learning.

Negativity Turns to Motivation!

Your interventions will help your children avoid the learning turn off to the challenges of today’s fact heavy curriculum and limited opportunities for curiosity and discovery. You will help them construct the brain circuits to become lifelong learners who can transfer and apply what they learn to real-world situations.

They’ll respond to learning more efficiently and store what they learn in their long-term and memory. They will secure learning available not only to retrieve for the test, but also to face the unique challenges and opportunities awaiting them in the 21st century.

-Judy Willis, M.D., M.Ed.

Small Study Shows Memory Loss from Alzheimer’s Can Be Reversed

A small trial of 10 patients has found that broad-based treatment with personalized therapy can reverse memory loss from Alzheimer’s disease.

Results from quantitative MRI and neuropsychological testing show “unprecedented” improvements in the patients with early Alzheimer’s disease (AD) or its precursors following the treatment, according to researchers from the Buck Institute for Research on Aging and the University of California, Los Angeles (UCLA) Easton Laboratories for Neurodegenerative Disease Research.

The study, published in the journal Aging, shows that memory loss can be reversed, and improvement sustained, using a 36-point therapeutic personalized program that involves changes in diet, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry, researchers said.

“All of these patients had either well-defined mild cognitive impairment (MCI), subjective cognitive impairment (SCI), or had been diagnosed with AD before beginning the program,” said Dale Bredesen, M.D., a professor at the Buck Institute and professor at the Easton Laboratories for Neurodegenerative Disease Research at UCLA. “Follow-up testing showed some of the patients going from abnormal to normal.”

Bredesen noted that some patients who had to discontinue work were able to return to work and those struggling at their jobs were able to improve their performance.

According to the researchers, one of the more striking cases was a 66-year-old man whose neuropsychological testing was compatible with a diagnoses of MCI and whose PET scan showed reduced glucose utilization indicative of AD. An MRI showed hippocampal volume at only the 17th percentile for his age.

After 10 months on the protocol, a follow-up MRI showed a dramatic increase of his hippocampal volume to the 75th percentile, with an associated absolute increase in volume of nearly 12 percent, the researchers reported.

In another instance, a 69-year-old entrepreneur who was shutting down his business went on the protocol after 11 years of progressive memory loss. After six months, his wife, co-workers, and he noted an improvement in his memory. A lifelong ability to add columns of numbers rapidly in his head returned and he reported an ability to remember his schedule and recognize faces at work.

After 22 months on the protocol he returned for follow-up quantitative neuropsychological testing. The results showed marked improvements in all categories with his long-term recall increasing from the third to 84th percentile, according to the researchers, who add he is now expanding his business.

Another patient, a 49-year-old woman who noted progressive difficulty with word finding and facial recognition went on the protocol after undergoing quantitative neuropsychological testing at a major university. She had been told she was in the early stages of cognitive decline and was therefore ineligible for an Alzheimer’s prevention program.

After several months on the protocol she noted a clear improvement in recall, reading, navigating, vocabulary, mental clarity, and facial recognition. Her foreign language ability had returned.

Nine months after beginning the program she did a repeat of the neuropsychological testing at the same university site. She no longer showed evidence of cognitive decline, according to the researchers.

All but one of the 10 patients included in the study are at genetic risk for AD, carrying at least one copy of the APOE4 allele, the researchers said. Five of the patients carry two copies of APOE4, which gives them a 10-12 fold increased risk of developing AD.

“We’re entering a new era,” said Bredesen. “The old advice was to avoid testing for APOE because there was nothing that could be done about it. Now we’re recommending that people find out their genetic status as early as possible so they can go on prevention.”

He added that 65 percent of the Alzheimer’s cases in the U.S. involve APOE4, with seven million people carrying two copies of the ApoE4 allele.

According to Bredesen, decades of biomedical research has revealed that an extensive network of molecular interactions is involved in Alzheimer’s disease, suggesting that a broader-based therapeutic approach may be more effective.

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well — the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much,” he said.

“We think addressing multiple targets within the molecular network may be additive, or even synergistic, and that such a combinatorial approach may enhance drug candidate performance, as well.”

While encouraged by the results of the study, Bredesen admits more needs to be done.

“The magnitude of improvement in these 10 patients is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective,” he said. “Even though we see the far-reaching implications of this success, we also realize that this is a very small study that needs to be replicated in larger numbers at various sites.”

Plans for larger studies are underway, he added.

“The Bredesen Protocol,” Bredesen’s book describing the interventions described in the study, will be released by Penguin Random House in May 2017.

Janice Wood

Molecule May Improve Dopamine Function in Parkinson’s

Patients with Parkinson’s disease who supplement with n-acetylcysteine (NAC), a natural molecule with strong antioxidant effects, experience notable improvements in dopamine function, according to a new study published in the journal PLOS ONE.

NAC is an oral supplement that can be found at most nutrition and health food stores. In a medical setting, NAC has been used intravenously to protect the livers of patients who have overdosed on acetaminophen.

Doctors from the Departments of Integrative Medicine, Neurology and Radiology at Thomas Jefferson University show that patients receiving NAC experience improvements in two measures: the observable physical symptoms of the disease as well as in levels of dopamine (the lack of which is thought to contribute to Parkinson’s disease) as shown by brain imaging tests.

Currently, treatments for Parkinson’s disease are limited to those that temporarily replace dopamine in the brain or try to slow the progression of the disease process. Recently, however, researchers have discovered that oxidative stress in the brain may play a vital role in the disease process, and that this stress also lowers levels of glutathione, a chemical produced by the brain to counteract oxidative stress.

Research has shown that NAC helps reduce oxidative damage to brain cells by helping restore the levels of the antioxidant glutathione.

“This study reveals a potentially new avenue for managing Parkinson’s patients and shows that n-acetylcysteine may have a unique physiological effect that alters the disease process and enables dopamine neurons to recover some function,” said senior author Daniel Monti, M.D., M.B.A. Monti is director of the Myrna Brind Center of Integrative Medicine at Thomas Jefferson University.

For the study, Parkinson’s patients who continued their current standard of care treatment, were placed into two groups: The first group received a combination of oral and intravenous (IV) NAC for three months. These patients received 50mg/kg NAC intravenously once per week and 600mg NAC orally twice per day on the non IV days. The second group of patients acted as a control group and received only their standard Parkinson’s treatment.

Patients were evaluated before starting NAC and then after three months of receiving NAC. Control patients were evaluated before the study and then three months later.

The evaluation involved standard clinical measures, including the Unified Parkinson’s Disease Rating Scale (UPDRS), a survey administered by doctors to help determine the stage of disease. The patients also underwent a brain scan via DaTscan SPECT imaging, which measures the amount of dopamine transporter in the basal ganglia, the area most affected by the Parkinson’s disease process.

The findings show that the patients receiving NAC had improvements of four to nine percent in dopamine transporter binding and also had improvements in their UPDRS score of about 13 percent, compared to controls.

“We have not previously seen an intervention for Parkinson’s disease have this kind of effect on the brain,” said first author and neuroimaging expert Andrew Newberg, M.D., professor at the Sidney Kimmel Medical College at Jefferson and Director of Research at the Myrna Brind Center of Integrative Medicine.

The researchers hope the new findings will open up new avenues of treatment for Parkinson’s disease patients.

Source: Thomas Jefferson University