Brain Anatomy May Play Role in Post-Traumatic Stress Disorder

MRI scans found veterans with the disorder had a smaller amygdala, the brain area that controls fear, anxiety

TUESDAY, Nov. 6 (HealthDay News) -- In combat veterans with post-traumatic stress disorder, the area of the brain that controls fear and anxiety responses is much smaller than normal, according to a new study.
The finding is the first to provide evidence that a smaller amygdala is associated with post-traumatic stress disorder (PTSD), but it's not clear whether this smaller size is caused by PTSD or whether people with a smaller amygdala are more likely to develop PTSD, the researchers said.

For the study, MRI brain scans were conducted on 200 combat veterans, half with PTSD and half without, who served in Iraq and Afghanistan since 2001. MRI brains scans of the participants showed that both the right and left amygdala were smaller in those with PTSD.

The researchers also confirmed previous study findings that linked PTSD with a smaller left hippocampus, a region of the brain that plays an important role in memory.

Amygdala size does not appear to be affected by the severity, frequency or duration of the mental trauma that can lead to PTSD, which indicates that such exposures do not cause the amygdala to shrink, said study lead author Dr. Rajendra Morey, assistant professor of psychiatry at Duke University.

This suggests that people with a smaller amygdala to begin with are susceptible to PTSD. Morey and colleagues are conducting further research to determine if that's the case.

"This is one piece in a bigger puzzle to understanding why some people develop PTSD and others do not," Morey said in a university news release. "We are getting closer to that answer."

Prenatal testosterone levels can affect brain function and behaviour later in life

Washington, November 6 (ANI): Testosterone levels early in fetal development influence later sensitivity of brain regions related to reward processing and affect an individual's susceptibility to engage in behaviour, that in extremes, are related to several neuropsychiatric conditions that asymmetrically affect one sex more than the other, a new study has found.

Dr. Michael Lombardo, Prof. Simon Baron-Cohen and colleagues at the University of Cambridge led the study.

Although present at low levels in females, testosterone is one of the primary sex hormones that exerts substantial influence over the emergence of differences between males and females.
In adults and adolescents, heightened testosterone has been shown to reduce fear, lower sensitivity to punishment, increase risk-tasking, and enhance attention to threat. These effects interact substantially with context to affect social behaviour.
This knowledge about the effects of testosterone in adolescence and adulthood suggests that it is related to influencing the balance between approach and avoidance behaviour. These same behaviours are heightened in the teenage years and also emerge in extremes in many neuropsychiatric conditions, including conduct disorder, depression, substance abuse, autism, and psychopathy.

Scientists have long known that sex differences influence many aspects of psychiatric disorders, including age of disease onset, prevalence, and susceptibility. For example, according to the World Health Organization, depression is twice as common in women than men, whereas alcohol dependence shows the reverse pattern.
In addition to many other factors, sex hormone levels are likely to be important factors contributing to sex differences in psychopathology.

However, research to date has mainly focused on sex hormone levels during adolescence and adulthood, when hormone levels are heightened and built upon substantial prior developmental experience. Sex hormone levels are also heightened during critical periods of fetal brain development, but the impact of such prenatal surges in sex hormone levels on subsequent adult brain and behavioural development has received relatively little attention.

"This study is the first to directly examine whether testosterone in fetal development predicts tendencies later in life to engage in approach-related behaviour (e.g., fun-seeking, impulsivity, reward responsivity) and also how it may influence later brain development that is relevant to such behaviours," said first author Lombardo.
In this study, they tested a unique cohort of boys, 8 years of age, whose fetal testosterone had been previously measured from amniotic fluid at 13 weeks gestation. The boys were scanned with functional magnetic resonance imaging technology to assess changes in brain activity while viewing pictures of negative (fear), positive (happy), neutral, or scrambled faces.

They found that increased fetal testosterone predicted more sensitivity in the brain's reward system to positively, compared to negatively, valenced facial cues. This means that reward-related brain regions of boys with higher fetal testosterone levels respond more to positive facial emotion compared to negative facial emotion than boys who with smaller levels of fetal testosterone.

In addition, increased fetal testosterone levels predicted increased behavioural approach tendencies later in life via its influence on the brain's reward system.

Lombardo explained, "This work highlights how testosterone in fetal development acts as a programming mechanism for shaping sensitivity of the brain's reward system later in life and for predicting later tendency to engage in approach-related behaviours. These insights may be especially relevant to a number of neuropsychiatric conditions with skewed sex ratios and which affect approach-related behaviour and the brain's reward system."

Alzheimer's detected decades before symptoms

The shrunken brain of an Alzheimer's patient compared with a healthy one

Researchers have found some of the earliest signs of Alzheimer's disease, more than two decades before the first symptoms usually appear.

Treating the disease early is thought to be vital to prevent damage to memory and thinking.

A study, published in the Lancet Neurology, found differences in the brains of an extended Colombian family predisposed to develop an early form of Alzheimer's.

Experts said the US study may give doctors more time to treat people.

Alzheimer's disease starts long before anyone would notice; previous studies have shown an effect on the brain 10-15 years before symptoms.

It is only after enough brain cells have died that the signs of dementia begin to appear - some regions of the brain will have lost up to 20% of their brain cells before the disease becomes noticeable.

However, doctors fear so much of the brain will have degenerated by this time that it will be too late to treat patients. The failure of recent trials to prevent further cognitive decline in patients with mild to moderate Alzheimer's disease has been partly put down to timing.

Early start 
A team at the Banner Alzheimer's Institute in Arizona looked at a group of patients in Colombia who have familial Alzheimer's. A genetic mutation means they nearly always get the disease in their 40s. Alzheimer's normally becomes apparent after the age of 75.

Brain scans of 20 people with the mutation, aged between 18 and 26, already showed differences compared with those from 24 people who were not destined to develop early Alzheimer's.

The fluid which bathes the brain and spinal cord also had higher levels of a protein called beta-amyloid.
The researchers said differences could be detected "more than two decades before" symptoms would appear in these high-risk patients.

Dr Eric Reiman, one of the scientists involved, said: "These findings suggest that brain changes begin many years before the clinical onset of Alzheimer's disease. 

"They raise new questions about the earliest brain changes involved in the predisposition to Alzheimer's and the extent to which they could be targeted by future prevention therapies."

Prof Nick Fox, from the Institute of Neurology at University College London, said some of his patients had lost a fifth of some parts of their brain by the time they arrived at the clinic.

He told the BBC: "I don't think this pushes us forwards in terms of early diagnosis, we already have markers of the disease.

"The key thing this does is open up the window of early intervention before people take a clinical and cognitive hit."

However, he said this raised the question of how early people would need to be treated - if drugs could be found.

Dr Simon Ridley, the head of research at Alzheimer's Research UK, said: "Although early-onset inherited Alzheimer's is rare and may not entirely represent the more common late-onset form, the findings highlight changes can take place in the brain decades before symptoms show.

"Mapping what changes happen early in the brain will help scientists to improve detection of the disease and allow potential new treatments to be tested at the right time.

"New drugs are being developed and tested to stop amyloid from taking hold, but studies like these show that timing could be crucial for whether these drugs are successful.

Alzheimer's symptoms may be detectable earlier than thought

PARIS: Researchers said on Tuesday they had seen the earliest-ever warning signs of Alzheimer's Disease -- among a high-risk group of 20-somethings -- in the ongoing quest for early detection and prevention.

A major problem in the search for a cure for this debilitating form of dementia is that symptoms appear years after irreversible brain decay has already set in.

For the study, a team of scientists from the United States and Colombia tested 18- to 26-year-old members of an extended Colombian family that share a common ancestor and a genetic predisposition to develop an inherited form of Alzheimer's.

One in three members of the clan carry a gene mutation that will lead to a rare form of the disease which hits people in their 40s, unlike the common variant which presents much later.

A brain scan comparison found that individuals who carry the errant gene have less grey matter in certain areas of the brain than those who don't, scientists wrote in The Lancet medical journal.

They also found that those with the mutation had higher levels in their cerebrospinal fluid of a protein called amyloid beta, implicated in the plaque build-ups found on the brains of Alzheimer's sufferers.

The findings "suggest that neurodegenerative changes occur more than 20 years before symptom onset and somewhat earlier than was suggested by findings from previous MRI studies," Nick Fox of the University College London's Dementia Research Centre said in a comment on the study.

Alzheimer's disease causes two-thirds of dementia cases -- attacking one in 200 people -- the rate is increasing as the world's population ages.

Trial participants, 20 with the fateful gene mutation and 24 without, were not told whether they had it or not. All had normal cognitive abilities at the time of the study.

"The findings... could ultimately lead to improved early detection and better clinical trials of preventative treatments," The Lancet said in a statement.

But the outcome also raises questions about scientists' understanding of how Alzheimer's progresses.
"These findings... raise new questions about the earliest brain changes involved in the predisposition to Alzheimer's and the extent to which they could be targeted by future prevention therapies," research leader Eric Reiman from the Banner Alzheimer's Institute in Arizona said.

Scientists still do not know quite what to make of the plaques and tangles that German doctor Alois Alzheimer first spotted in the brain of a dementia patient who died in 1906.

They disagree on the respective roles of beta amyloid plaque build-ups and of a protein called tau which forms tangles inside the brain cells.

Most test therapies have targeted beta amyloids, but some now suggest it is actually tau killing the brain cells.
According to Fox, the new study questioned existing models of Alzheimer's Disease "on several fronts".
Among other things, "neurodegeneration would seem to be occurring in advance of evidence of plaque deposition", widely thought to cause the brain damage.

Fox said the results should be treated with caution as the trial sample was small and the outcome may not apply to the much more common sporadic, late-onset form of Alzheimer's.

Alzheimer's Disease International (ADI) projects the number of people with dementia will rise from 35.6 million in 2010 to 65.7 million by 2030 and 115.4 million by 2050.

How your brain likes to be treated at revision time

A neuroscience student harnesses his knowledge to advise fellow students about memorising information

Interconnected neurons transfer information using electrical pulses

If you're a student, you rely on one brain function above all others: memory.

These days, we understand more about the structure of memory than we ever have before, so we can find the best techniques for training your brain to hang on to as much information as possible. The process depends on the brain's neuroplasticity, its ability to reorganise itself throughout your life by breaking and forming new connections between its billions of cells.

How does it work? Information is transmitted by brain cells called neurons. When you learn something new, a group of neurons activate in a part of the brain called the hippocampus. It's like a pattern of light bulbs turning on.

Your hippocampus is forced to store many new patterns every day. This increases hugely when you are revising. Provided with the right trigger, the hippocampus should be able to retrieve any pattern. But if it keeps getting new information, the overworked brain might go wrong. That's what happens when you think you've committed a new fact to memory, only to find 15 minutes later that it's disappeared again.

So what's the best way to revise? Here are seven top tips to get information into your brain and keep it there.

Forget about initial letters

Teachers often urge students to make up mnemonics – sentences based on the initial letters of items you're trying to remember. Trouble is, they help you remember the order, but not the names. The mnemonic Kings Prefer Cheese Over Fried Green Spinach can help you recall the order of taxonomy in biology (kingdom, phylum, class, order, family, genus, species) but that's only helpful if you're given the names of the ranks.

The mnemonic is providing you with a cue but, if you haven't memorised the names, the information you want to recall is not there. You're just giving your overflowing hippocampus yet another pattern of activity to store and retrieve.

Repeat yourself

Pathways between neurons can be strengthened over time. Simple repetition – practising retrieving a memory over and over again – is the best form of consolidating the pattern.

Use science to help you retrieve info

Science tells us the ideal time to revise what you've learned is just before you're about to forget it. And because memories get stronger the more you retrieve them, you should wait exponentially longer each time – after a few minutes, then a few hours, then a day, then a few days. This technique is known as spaced repetition.

This also explains why you forget things so quickly after a week of cramming for an exam. Because the exponential curve of memory retrieval does not continue, the process reverses and within a few weeks, you have forgotten everything.

Take regular breaks

Breaks are important to minimise interference. When your hippocampus is forced to store many new (and often similar) patterns in a short space of time, it can get them jumbled up.

The best example of this is when you get a new telephone number. Your old number is still so well-entrenched in your memory that remembering the new one is a nightmare. It's even worse if the new one has a few similarities to the old.

Plan your revision so you can take breaks and revise what you've just learned before moving on to anything new.

Avoid distractions

Attention is the key to memorising. By choosing to focus on something, you give it a personal meaning that makes it easier to remember. In fact, most of our problems when it comes to revision have very little to do with the brain's capacity for remembering things; we just struggle to devote our full attention to the task in hand.

Playing music while revising will make your task harder, because any speech-like sounds, even at low volume, will automatically use up part of the brain's attention capacity.

Sleep is vital

We spend approximately a third of our lives sleeping and it's never as important as during revision time. Sleep plays a critical role in memory consolidation – this is when the brain backs up short-term patterns and creates long-term memories. The process is believed to occur during deep sleep, when the hippocampal neurons pass the patterns of activity to another part of the brain called the neocortex, which is responsible for language and the generation of motor commands.

Recent research in Nature Neuroscience has shed new light on how memories are decluttered and irrelevant information is deleted during this process. This results in the important memories (the pathways that have been strengthened through repetition) becoming easier to access.

Control your emotions

We remember emotionally charged events far better than others, and this is especially the case if the emotion was a positive one. It is not always possible to have warm feelings about your revision, but if you can associate a particular fact with a visual, auditory or emotional experience from the past, then you have a better chance of remembering it, as you have created multiple pathways for retrieval.

Try to reduce anxiety, because it uses up working memory, leaving a much smaller capacity available for processing and encoding new information.

Can FDA help Caitlin Downing battle brain tumor?

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Exercise may protect brain from shrinking

Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Exercise not only protected against such age-related brain changes, but also had a greater effect than mentally and socially stimulating activities.

In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities.

Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the white matter, the “wiring” of the brain's communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and IQ.

As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.”

Because the findings showed only an association, not a causal relationship, the authors could not rule out the possibility that people with less deterioration in their brains were simply more likely to be physically active. But they said that based on their findings, they would advise people to take up physical exercise “whatever their age.”

Possible Cause of Brain Freeze

Damon Winter/The New York Times President Obama and Mitt Romney shaking hands with audience members after their final debate last month.

 

TUESDAY’S PUZZLE — Today’s puzzle is a New York Times debut by a very nice young man named Erik Agard. I’ve had the pleasure of corresponding with Mr. Agard on all things puzzle and humor, so it was a lovely surprise when I saw his name in this week’s queue. We’ll learn more about him after the discussion.
If you haven’t voted early, Mr. Agard has kindly reminded us via circled letters in the long Across entries of the two main political running teams, OBAMA/BIDEN and ROMNEY/RYAN. The fun thing here, though, is not sussing out the running mates. The fun thing here is trying to figure out where Mr. Agard stands in his political leanings.

We’ve got DEM right below President OBAMA, but that’s obvious and doesn’t tell us anything. TEA Party is stuck mysteriously between the Democratic candidates, but I recognized that as the red herring it was so obviously meant to be. What finally gave away Mr. Agard’s clear contempt for both sides? He’s accusing them of a cross-party sex scandal.
That’s correct. Oh, this one is so going to get me that Pulitzer, when they finally add that Best Crossword Blogging category. Only another few hundred phone calls to the Pulitzer Committee and I just know they’ll cave, if they don’t disconnect their phones first.

Anyway, the SEX scandal is uncovered at 51 Across, under RIGHT ON THE MONEY, and continues with a reveal of the turn ONS between BIDEN and ROMNEY. ROMNEY throws OXO hugs and kisses down toward RYAN and ERICA Jong, writer of sensual fiction and poetry, even joins in.
That is journalism, my friends. Reading between the lines. You can thank me later.

On another subject, here is why you should never try to do the crossword puzzle before you’ve had coffee: I filled in the entry at 54 Across, which should have been TAJ as TAL, because my caffeine-deprived brain conflated TAJ and Mahal. That led me to having LAR as 55 Down’s “Pickle holder.” Personally, I’ve always held pickles in my fingers, but for all I know there are fancy people out there with utensils made specifically to avoid having pickle juice run down their wrists. So I looked up LAR, and I will tell you that if there is one thing you do not want, it’s the shock of Google imaging what is supposed to be some kind of fork and seeing pictures of monkeys, automatic weapons, and for some reason, a priest. As always, I’m not quite sure what it is, but let that be a lesson to you all.

Let’s meet Mr. Agard:

Before I regale you with details from my boring life, a public service announcement: if you can vote in today’s election, and you haven’t yet, please do. In case you couldn’t tell from the puzzle, I think the whole democracy thing is pretty neat. Seriously. Please vote.

O.K., we’re on to me now. I’m a sophomore African-American studies major at the University of Maryland (Terp Nation!) I haven’t quite figured out what I’m doing with my life yet, but it will, without a doubt, involve puzzles. I also have a crossword blog! I’m not sure if I’m allowed to plug it here, but if you’re reading this sentence, it means I am most definitely plugging it, and that you should click on the link.

I stumbled upon the punchline for this puzzle in August, and thought to myself, “Self, this would make a great theme for a crossword puzzle! If only there were an election coming up sometime soon.” And the rest, as they say, is… i can’t remember how the expression goes, but this is a thing that happened.

I’m already out of stuff to say – I really do hate talking about myself – but before I go, I’m going to Oscar acceptance speech this thing {Cue “walking off” music — D.A.}
This is a dream come true. I want to thank my family, Will and Paula, the lovely Deb Amlen (whose life I have hopefully not made harder in the process of writing these notes), Mr. stein and all the Blair people, Matt Gaffney, Brendan Emmett Quigley, and most importantly, you. You’re awesome. You made this possible. Thank you for solving, and I hope to see you back here sometime soon.

We hope to see you here again soon too, Mr. Agard.
Let’s move on to the Wednesday puzzle with the most awesome scene in “MR. SMITH Goes to Washington”:
 

Memory Alert: High Blood Pressure May Age Your Brain - Even If You're Under 40

The white and gray matter of the brain are important in memory and thought

Researchers at the University of California at Davis released a study today that should give anyone with even mildly elevated blood pressure pause. It seems that having blood pressure higher than the optimal 120/80 may be aging your brain, putting you at risk for memory problems and eventually for dementia and Alzheimer’s. And this appears to be true even for people in their thirties and even for people with pre-hypertension.

Using data from the highly regarded Framingham Heart Study, the UC Davis team led by professor of neurology Charles DeCarli compared detailed brain scans of 575 people who joined the study in 2009, most in their thirties. DeCarli and his team divided the participants into three groups: hypertensive, pre-hypertensive, and normal blood pressure. They then analyzed the gray and white matter of their brains using high-tech MRIs.

Previous studies have linked high blood pressure with memory loss, Alzheimer’s, and dementia but this study, published online today in the November online version of The Lancet Neurology, appears to be the first one showing that the decline may begin as early as the 30s and 40s. Experts believe that stiffening or hardening of the arteries caused by high blood pressure gradually limits blood flow to the brain, depriving the brain of oxygen over time.

The scans used were both MRIs and diffusion tensor imaging, which obtains a micro view of the brain’s white matter and the axons within it that carry electrical signals between different parts of the brain. According to the researchers, the brains of 30-year-olds with high blood pressure looked similar to the brains of people in their 40s who had normal blood pressure.

DeCarli wants the public to get the message that high blood pressure should be controlled to prevent brain aging, and this is true no matter what age you are. What this would mean is that people in their thirties should regularly get their blood pressure tested, something that most people don’t do until they’re older.

If your blood pressure is elevated, make lifestyle changes (lose weight, exercise, lower your salt intake) or take medication or both to lower it to below 120/80.

General anesthesia may disrupt communication between brain areas

A new study suggests that anesthesia drugs such as propofol work by disrupting communication between brain areas.

Researchers have moved one step closer to understanding how anesthesia drugs work by identifying a component of brain activity that could explain why we lose consciousness under the influence of the drugs, according to a study published Monday in the Proceedings of the National Academy of Sciences.

Though "going under" is an extremely common part of many medical procedures, the mechanism by which it works remains a mystery. This fact has practical ramifications: Some studies have shown that anesthesia can lead to loss of memory and other side effects, something researchers might be able to alleviate if they understand exactly what the drugs do in the body.

One hypothesis for why the drugs cause us to zonk out is that they cause different parts of the brain to lose their "functional integration" -- their ability to work together as a coherent whole. The brain is often thought of as a series of relatively independent areas -- parts of the organ are often referred to as the "face area" or the "vision region." But in order for the whole thing to work correctly, many different areas must work together. If something about anesthesia made this impossible, that could explain why we lose consciousness.

To test whether this was the case, a group of scientists from Harvard University and Massachusetts General Hospital studied the electrical activity of three patients while they were under anesthesia. The three patients were all epileptics, and had been in the hospital to have their epilepsy monitored. As part of the monitoring, doctors implanted an array of electrodes on a part of each patient’s cerebral cortex, the outer shell of the brain. When it came time for doctors to perform the surgery to remove the electrodes, the patients were put under anesthesia.

But before the electrodes were removed, the research team was allowed to use the electrodes to record their brain activity as the patient lost consciousness from the anesthetic propofol. The electrodes allowed the team to record brain activity on multiple spatial scales at once, from recordings of the activity of individual brain cells to the collected electrical activity of thousands of neurons. To keep track of when they lost consciousness, the researchers asked the subjects to push a button in response to a spoken command every so often.
Strikingly, when the subjects lost consciousness, a new element of brain activity, called a “slow oscillation,” immediately arose. A brain oscillation, when visualized, is like a landscape made up of a series of rolling hills. At the peak of the hill, large groups of neurons are firing simultaneously; at the trough, very few are firing. These oscillations are a major feature of normal human brain activity, and they usually occur multiple times per second.

But as soon as the patients lost consciousness, they began to have slow oscillations that occurred less than once per second, something that is not seen during waking brain activity. What’s more, when the researchers looked at a particular type of brain activity called “spiking,” which is generally related to information processing, they found that it only occurred during particular parts of the slow oscillation. In short, spiking had become “locked” to the slow oscillation.

More important, when the researchers compared different parts of the brain, they found that the oscillations were occurring at slightly different times. This likely makes it impossible for the areas to work together even though each individual area appeared to function quite normally.

The results provide a potential explanation for why we lose consciousness when we receive an anesthetic: Propofol prevented different parts of the brain from working together as a unit. If this turns out to be the case and researchers can zone in on the exact mechanisms by which the drugs work, it may be possible to develop more targeted anesthetics with fewer side effects.

When Thinking about Math, The Brains Of Some People Look Like They Are In Pain

Anxiety about math can prompt a response in the brain that’s similar to the one we have when we experience physical pain, according to new research at the University of Chicago. MedicalExpress reports:

“Using brain scans, scholars determined that the brain areas active when highly math-anxious people prepare to do math overlap with the same brain areas that register the threat of bodily harm—and in some cases, physical pain.

‘For someone who has math anxiety, the anticipation of doing math prompts a similar brain reaction as when they experience pain — say, burning one’s hand on a hot stove,’ said Sian Beilock, professor of psychology at the University of Chicago and a leading expert on math anxiety.

Surprisingly, the researchers found it was the anticipation of having to do math, and not actually doing math itself, that looked like pain in the brain. ‘The brain activation does not happen during math performance, suggesting that it is not the math itself that hurts; rather the anticipation of math is painful,” added Ian Lyons, the paper’s coauthor.

Brain scans of the study’s participants showed that the anticipation of math caused a response in the brain similar to physical pain.

The higher a person’s anxiety about math, the more anticipating math activated the posterior insula — a fold of tissue located deep inside the brain just above the ear that is associated with registering direct threats to the body as well as the experience of pain.

The work by Lyons and Beilock suggests that, for those with math anxiety, a painful sense of dread may begin long before a person sits down to take a math test. Previous research has shown that highly math anxious individuals tend to avoid math-related situations and even math-related career paths. The current work suggests that such avoidance stems in part from painful anxiety.

This study points to the value of seeing math anxiety not just as a proxy for poor math ability, but as an indication there can be a real, negative psychological reaction to the prospect of doing math. This reaction needs to be addressed like any other phobia, the researchers said.

Rather than simply piling on math homework for students who are anxious about math, students need active help to become more comfortable with the subject, Beilock said. Beilock’s work has shown, for instance, that writing about math anxieties before a test can reduce one’s worries and lead to better performance.”

That’s a really important take-away at the end: that math anxiety is not something students will just “get over.” This anxiety is real, and it requires interventions that will help them approach the subject with more confidence and equanimity. The alternative, as we know, is a huge population of post-school adults who fear math and avoid it whenever possible — and, most likely, communicate this attitude to their children.