Chapter 7. Life-Span Development of the Brain and Behavior
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By Jane E. Brody Barrett Treadway, now 3½, has never been the best of sleepers, but her sleep grew increasingly worse in the last year and a half. She gets up several times a night, often climbs into her parents’ bed and creates havoc with their nights. “We’ve known for a long time that she snores, but until a mother-daughter trip in May when we shared a bed, I didn’t realize that this was not simply snoring,” her mother, Laura, told me. “She repeatedly stopped breathing, then started again with a loud snort that often woke her up and kept me up all night.” Barrett has sleep apnea, a condition most often diagnosed in adults and usually associated with obesity. But neither of those attributes describes Barrett, who is young and lithe, although the condition is somewhat more common in overweight children. In most cases, the problem results when, during sleep, the child’s airway is temporarily obstructed by enlarged tonsils or adenoids or both — lymphoid tissues in the back of the throat — hence the name obstructive sleep apnea. When breathing stops for 10 or more seconds, the rising blood level of carbon dioxide prompts the brain to take over and restart breathing, typically accompanied by a loud snore or snort. Rarely, a child may have what is called central sleep apnea, in which the brain temporarily fails to signal the muscles that control breathing. Experts say that between 1 percent and 3 percent of children have sleep apnea that, if untreated, can disrupt far more than a family’s restful nights. Affected children simply do not get enough restorative sleep to assure normal development. If not corrected, the condition can result in hyperactivity and attention problems in school that are often mistaken for attention deficit hyperactivity disorder (A.D.H.D.) and sometimes mistreated with a stimulant that only makes matters worse. © 2015 The New York Times Company
Alexandra Sims Intelligent people are not only smarter than the average person - it seems they could also live longer as well. A study by the London School of Economics found that smarter siblings are more likely to outlive their less clever brothers and sisters, with genetics accounting for 95 per cent of the connection between intelligence and life span. The scientists examined the differences in longevity between identical twins, who share all of their genes and non-identical twins, who on average share half of their genes. Writing in the International Journal of Epidemiology, scientists noted the difference in intellect between the twins and the age at which they died. Focusing on three different twin studies from Sweden, Denmark and the United States the researchers examined sets of twins for whom both intelligence and age of death had been recorded in pairs where at least one of the twins had died. In both types of twins it was found that the smarter of the two lived longer, but this effect was far more prominent in non-identical twins. Rosalind Arden, a research associate at the LSE, told The Times that "the association between top jobs and longer lifespans is more a result of genes than having a big desk.” She added though that the research does not mean parents can "deduce your child’s likely lifespan from how he or she does in their exams this summer”.
Qazi Rahman In a recent Guardian article , Simon Copland argued that it is very unlikely people are born gay (or presumably any other sexual orientation). Scientific evidence says otherwise. It points strongly to a biological origin for our sexualities. Finding evidence for a biological basis should not scare us or undermine gay, lesbian and bisexual (LGB) rights (the studies I refer to do not include transgendered individuals, so I’ll confine my comments to lesbian, gay and bisexual people). I would argue that understanding our fundamental biological nature should make us more vigorous in promoting LGB rights. Let’s get some facts and perspective on the issue. Evidence from independent research groups who studied twins shows that genetic factors explain about 25-30% of the differences between people in sexual orientation (heterosexual, gay, lesbian, and bisexual). Twin studies are a first look into the genetics of a trait and tell us that there are such things as “genes for sexual orientation” (I hate the phrase “gay gene”). Three gene finding studies showed that gay brothers share genetic markers on the X chromosome; the most recent study also found shared markers on chromosome 8. This latest research overcomes the problems of three prior studies which did not find the same results. Gene finding efforts have issues, as Copland argues, but these are technical and not catastrophic errors in the science. For example, complex psychological traits have many causal genes (not simply “a gay gene”). But each of these genes has a small effect on the trait so do not reach traditional levels of statistical significance. In other words, lots of genes which do influence sexual orientation may fall under the radar. But scientific techniques will eventually catch up. In fact there are more pressing problems that I would like to see addressed, such as the inadequate research on female sexuality. Perhaps this is due to the stereotype that female sexuality is “too complex” or that lesbians are rarer than gay men. © 2015 Guardian News and Media Limited
Sara Reardon After years of disappointment, clinical-trial results released on 22 July suggest that antibody treatments may produce small improvements in people with Alzheimer’s disease. The drugs — Eli Lilly’s solanezumab and Biogen’s aducanumab — target the amyloid-β protein that accumulates in the brains of people with Alzheimer’s. Many researchers question whether the findings will hold up, given that antibody drugs against amyloid have failed in every previous test against the disease. Details of the results were presented at the Alzheimer's Association International Conference in Washington DC. Lilly, of Indianapolis, Indiana, says that in a trial with 440 participants, solanezumab seemed to slow the cognitive decline of people with mild Alzheimer’s by about 30%. The loss of mental acuity in these patients over 18 months was equivalent to the deterioration that participants with a similar level of Alzheimer's disease in a placebo group experienced in just 12 months. Lilly snatched this small victory from the jaws of defeat. In 2012, the company reported no difference between patients who had taken solanezumab for 18 months and those who had received a placebo. But when the company reanalyzed that trial it found a slight improvement in participants whose symptoms were mild when the trial began. Lilly continued the test for six months and began giving solanezumab to the 440-member control group, whose disease was by then more advanced. © 2015 Nature Publishing Group,
Jon Hamilton The face of Alzheimer's isn't always old. Sometimes it belongs to someone like Giedre Cohen, who is 37, yet struggles to remember her own name. Until about a year ago, Giedre was a "young, healthy, beautiful" woman just starting her life, says her husband, Tal Cohen, a real estate developer in Los Angeles. Now, he says, "her mind is slowly wasting away." People like Giedre have a rare gene mutation that causes symptoms of Alzheimer's to appear before they turn 60. Until recently, people who inherited this gene had no hope of avoiding dementia and an early death. Now there is a glimmer of hope, thanks to a project called DIAN TU that is allowing them to take part in a study of experimental Alzheimer's drugs. The project also could have a huge payoff for society, says Dr. Randall Bateman, a professor of neurology at Washington University in St. Louis. "It's highly likely," he says, that the first drug able to prevent or delay Alzheimer's will emerge from studies of people genetically destined to get the disease. Giedre Cohen enrolled in the DIAN TU study in 2013, when she still had no symptoms of Alzheimer's, her husband says. Their story began more than a decade earlier. In 2002, Tal Cohen was on a trip to Miami to attend a wedding. He met Giedre, who was born in Lithuania, and the two fell in love. © 2015 NPR
Link ID: 21211 - Posted: 07.23.2015
By Warren Cornwall The number of U.S. school children placed in special education programs due to autism more than tripled from 2000 to 2010, to nearly 420,000. But a new study argues much of that increase likely came as educators swapped one diagnosis for another. The overall percentage of kids diagnosed with a collection of brain development problems that includes autism remained unchanged, suggesting that children who used to be labeled with conditions such as “intellectual disability” were in fact autistic. “If you asked me, ‘Is there a real increase in the prevalence of autism?’ maybe there is, but probably much lower than the reported magnitude,” says Santhosh Girirajan, a geneticist at Pennsylvania State University (Penn State), University Park. In the new study, Girirajan and colleagues combed through data collected in each state for approximately 6.2 million U.S. school children with disabilities who are enrolled in special education programs. The information is collected each year under the federal Individuals with Disabilities Education Act. Based on his or her diagnosis, each child was assigned to one of 13 broader categories, ranging from autism to physical challenges such as blindness. Between 2000 and 2010, the number of children in the autism category more than tripled from 93,624 in 2000 to 419,647 a decade later. Yet nearly two-thirds of that increase was matched by a decline in the rate at which children were labeled as having an “intellectual disability.” The number of kids in that category fell from 637,270 to 457,478. © 2015 American Association for the Advancement of Science.
Link ID: 21207 - Posted: 07.23.2015
By Sandhya Somashekhar NEW WESTMINSTER, B.C. — Alanna Whitney was a weird kid. She had a strange knack for pronouncing long words. Anchovies on pizza could send her cowering under a table. Her ability to geek out on subjects such as Greek mythology and world religions could be unsettling. She drank liquids obsessively, and in her teens, her extreme water intake landed her in the hospital. Years later, she found a word that explained it all: Autistic. Instead of grieving, she felt a rush of relief. “It was the answer to every question I’d ever had,” she recalled. “It was kind of like a go-ahead to shed all of those things I could or couldn’t do and embrace myself for who I am.” So it came to be that Whitney, 24, was arranging strawberries and store-bought cookies on platters at the Queensborough Community Center for a celebration of “Autistic Pride Day,” her shoulder-length hair dyed mermaid green to match her purse and sandals. A bowl of orange earplugs sat nearby in case any of the guests found the ambient sounds overwhelming. Whitney is part of a growing movement of autistic adults who are finding a sense of community, identity and purpose in a diagnosis that most people greet with dread. These “neurodiversity” activists contend that autism — and other brain afflictions such as dyslexia and attention deficit hyperactivity disorder — ought to be treated not as a scourge to be eradicated but rather as a difference to be understood and accepted.
Link ID: 21206 - Posted: 07.23.2015
By James Gallagher Health editor, BBC News website The first hints a drug can slow the progression of Alzheimer's disease have emerged at a conference. Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third. The results are being met with cautious optimism, with a separate trial due to report next year. The death of brain cells in Alzheimer's is currently inexorable. Solanezumab may be able to keep them alive. Current medication, such as Aricept, can only manage the symptoms of dementia by helping the dying brain cells function. But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer's. It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death. Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012. But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease. So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years. And the results from this extension of the original trial have now been presented, at the Alzheimer's Association International Conference. Dr Eric Siemers, from the Lilly Research Laboratories, in Indiana, told the BBC: "It's another piece of evidence that solanezumab does have an effect on the underlying disease pathology. "We think there is a chance that solanezumab will be the first disease-modifying medication to be available." The company also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug. © 2015 BBC.
Link ID: 21203 - Posted: 07.22.2015
By BENEDICT CAREY Women who develop slight but detectable deficits in memory and mental acuity late in life tend to decline faster than men with mild impairment, researchers reported on Tuesday. Some two-thirds of the five million Americans with Alzheimer’s disease are women, in part because women live longer. Researchers have searched in vain for decades to determine other reasons for the disparity. The authors of the new study, who presented their work at the Alzheimer’s Association International Conference in Washington, said their findings indicated nothing about possible causes of gender differences and had no immediate implications for treatment. “All we can say at this point is that there appears to be a faster trajectory for women than men” toward dementia, said Dr. P. Murali Doraiswamy, a professor of psychiatry at the Duke Institute for Brain Sciences and the study’s senior author. Katherine Amy Lin, a student of Dr. Doraiswamy’s and a co-author, presented the study. Previous research had found a steeper decline in women with mild deficits over a period of about a year. The new study extends that finding to up to eight years. “It’s a very interesting finding, but it’s also still early, so we’re limited in what conclusions we can draw,” said Dr. Edward D. Huey, a geriatric psychiatrist at Columbia University, who was not involved in the study. “I think of this as an excellent hypothesis generator. It’s something we need to investigate more deeply.” In the study, the Duke researchers analyzed scores on standard cognitive tests taken by 398 men and women, most in their 70s, being followed as part of a large, continuing Alzheimer’s trial. The participants have been taking the cognitive tests — as well as other tests, like PET scans — on average for four years, and as long as eight years. Controlling for factors that influence memory and mental acuity, like age, education and genetic predisposition, the research team found that women’s scores slipped by an average of about two points a year, compared with one point for men. The team also looked at a standard measure of life quality, rating how well people functioned socially: at home, at work and with family. That, too, slipped faster for women than for men, at about the same rate. © 2015 The New York Times Company
Kashmira Gander Performing well at school and going on to have a complex job could lower the risk of dementia, scientists have found. On the contrary, loneliness, watching too much TV and a sedentary lifestyle can make a person’s cognitive abilities decline more quickly, according to new research being presented to experts at the international Alzheimer's Association International Conference in Washington DC. Researchers are also due to show attendees the results from trials Solanezumab – believed to be the first drug to halt the progression of the disease if a patient is diagnosed early enough. One study involving 7,500 people aged 65 and above in Sweden over a 20-year period showed that dementia rates were 21 per cent higher in those whose grades were in the bottom fifth of the population. Meanwhile, participants with complex jobs involving data and numbers saw their chance of developing the disease cut by 23 per cent. Read more: Why fish oil pills may not be so healthy after all Proof that dementia risk can be reduced by improving lifestyle Charity warns of a 'worrying' lack of support for dementia patients Dementia research: Drug firms despair of finding cure and withdraw funding after a catalogue of failures For separate study in Sweden, scientists followed the lives of 440 people aged 75 or over for nine years, and discovered that those in the bottom fifth for school grades were found to have a 50 per cent increase in the risk of developing dementia. © independent.co.uk
By Hanae Armitage Playing an instrument is good for your brain. Compared to nonmusicians, young children who strum a guitar or blow a trombone become better readers with better vocabularies. A new study shows that the benefits extend to teenagers as well. Neuroscientists compared two groups of high school students over 3 years: One began learning their first instrument in band class, whereas the other focused on physical fitness in Junior Reserve Officers’ Training Corps (JROTC). At the end of 3 years, those students who had played instruments were better at detecting speech sounds, like syllables and words that rhyme, than their JROTC peers, the team reports online today in the Proceedings of the National Academy of Sciences. Researchers know that as children grow up, their ability to soak up new information, especially language, starts to diminish. These findings suggest that musical training could keep that window open longer. But the benefits of music aren’t just for musicians; taking up piano could be the difference between an A and a B in Spanish class. © 2015 American Association for the Advancement of Science
Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.
by Sarah Schwartz Brainlike cell bundles grown in a lab may expose some of the biological differences of autistic brains. Researchers chemically reprogrammed human stem cells into small bundles of functional brain cells that mimic the developing brain. These “organoids” appear to be different when built with cells from autistic patients compared with when they are built with cells from the patients’ non-autistic family members, researchers report July 16 in Cell. The brainlike structures created from cells taken from autistic children showed increased activity in genes that control brain-cell growth and development. Too much activity in one of these genes led to an overproduction of a certain type of brain cell that suppresses the activity of other brain cells. At an early stage of development, the miniature organs grown from autistic patients’ stem cells also showed faster cell division rates than those grown from the cells of non-autistic relatives. Though the study was small, using cells from only four autistic patients and eight family members, the results may indicate common factors underlying autism, the scientists say. © Society for Science & the Public 2000 - 2015.
Link ID: 21186 - Posted: 07.18.2015
By Fredrick Kunkle A new study suggests that Alzheimer’s disease may affect the brain differently in black people compared with whites. The research, conducted by Lisa L. Barnes at the Rush University Medical Center, suggests that African Americans are less likely than Caucasians to have Alzheimer’s disease alone and more likely to have other pathologies associated with dementia. These include the presence of Lewy bodies, which are abnormal proteins found in the brain, and lesions arising from the hardening of tiny arteries in the brain, which is caused mainly by high blood pressure and other vascular conditions. The findings suggest that researchers should seek different strategies to prevent and treat Alzheimer’s disease in blacks. While many therapeutic strategies focus on removing or modifying beta amyloid – a key ingredient whose accumulation leads to the chain of event triggering the neurodegenerative disease – the study suggests that possible treatments should pursue additional targets, particularly for African Americans. But the study also points up the critical need to enroll more black people in clinical trials. Although Barnes said the research was the largest sample of its kind, she also acknowledged that the sample is still small. And that’s at least partially because blacks, for a variety of cultural and historical reasons, are less likely to participate in scientific research.
Link ID: 21176 - Posted: 07.16.2015
Nikki Stevenson Autism may represent the last great prejudice we, as a society, must overcome. History is riddled with examples of intolerance directed at the atypical. We can sometime fear that which diverges from the “norm”, and sometimes that fear leads us to frame those who are different as being in some way lesser beings than ourselves. Intolerances take generations to overcome. Racism is an obvious, ugly example. Other horrifying examples are easy to find: take, for instance the intolerance faced by the gay community. Countless gay people were diagnosed with “sociopathic personality disturbance” based upon their natural sexuality. Many were criminalised and forced into institutions, the “treatments” to which they were subject akin to torture. How many believed they were sociopathic and hated themselves, wishing to be free from the label they had been given? How many wished to be “cured” so that they could live their lives in peace? The greatest crime was the damage perpetuated by the image projected upon them by those claiming to be professionals. Autism is framed as a disability, with mainstream theories presenting autism via deficit models. Popular theory is often passed off as fact with no mention of the morphic nature of research and scientific process. Most mainstream theory is silent regarding autistic strengths and atypical ability; indeed, what is in print often presents a damning image of autism as an “epidemic”. Hurtful words such as risk, disease, disorder, impairment, deficit, pedantic, obsession are frequently utilised. © 2015 Guardian News and Media Limited
Link ID: 21175 - Posted: 07.16.2015
By Lauran Neergaard, New research suggests it may be possible to predict which preschoolers will struggle to read — and it has to do with how the brain deciphers speech when it's noisy. Scientists are looking for ways to tell, as young as possible, when children are at risk for later learning difficulties so they can get early interventions. There are some simple pre-reading assessments for preschoolers. But Northwestern University researchers went further and analyzed brain waves of children as young as three. How well youngsters' brains recognize specific sounds — consonants — amid background noise can help identify who is more likely to have trouble with reading development, the team reported Tuesday in the journal PLOS Biology. If the approach pans out, it may provide "a biological looking glass," said study senior author Nina Kraus, director of Northwestern's Auditory Neuroscience Laboratory. "If you know you have a three-year-old at risk, you can as soon as possible begin to enrich their life in sound so that you don't lose those crucial early developmental years." Connecting sound to meaning is a key foundation for reading. For example, preschoolers who can match sounds to letters earlier go on to read more easily. Auditory processing is part of that pre-reading development: If your brain is slower to distinguish a "D" from a "B" sound, for example, then recognizing words and piecing together sentences could be affected, too. What does noise have to do with it? It stresses the system, as the brain has to tune out competing sounds to selectively focus, in just fractions of milliseconds. And consonants are more vulnerable to noise than vowels, which tend to be louder and longer, Kraus explained. ©2015 CBC/Radio-Canada
By Ferris Jabr Newborns are hardly blank slates devoid of knowledge and experience, contrary to historical notions about the infant mind. Sensory awareness and learning start in the womb, as the recently reinvigorated study of fetal perception has made clearer than ever. In the past few years lifelike images and videos created by 3-D and 4-D ultrasound have divulged much more about physiology and behavior than the blurry 2-D silhouettes of typical ultrasound. And noninvasive devices can now measure electrical activity in the developing brain of a fetus or newborn. Recent insights gleaned from such tools provide a rich portrait of how a fetus uses its budding brain and senses to learn about itself and the outside world well before birth. Such research has improved care for preterm babies, suggesting the benefits of dim lights, familiar and quiet voices, and lots of comforting skin contact between mother and child. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 21161 - Posted: 07.13.2015
Patricia Neighmond Some antidepressants may increase the risk of birth defects if taken early in pregnancy, while others don't seem to pose the same risks, a study finds. The question of whether antidepressants can cause birth defects has been debated for years, and studies have been all over the map. That makes it hard for women and their doctors to make decisions on managing depression during pregnancy. To try to untangle the question, researchers at the Centers for Disease Control and Prevention analyzed federal data on more than 38,000 women who gave birth between 1997 and 2009. They looked at the number of birth defects among babies and asked women whether they took any antidepressants in the month before getting pregnant or during the first three months of pregnancy. The study, published Wednesday in The BMJ, found no association between the most commonly used antidepressant, sertraline (Zoloft), and birth defects. Forty percent of the women who took antidepressants took sertraline. They also found no increased risk of birth defects with the antidepressants citalopram (Celexa) and escitalopram (Lexapro). But the analysis did find an association between birth defects and the antidepressants fluoxetine (Prozac) or paroxetine (Paxil). That included heart defects, abdominal wall defects, and missing brain and skull defects with paroxetine, and heart wall defects and irregular skull shape with fluoxetine. The relative risk increased 2 to 3.5 times, depending on the defect and the medication. That may sound like a lot, but Jennita Reefhuis, an epidemiologist and lead researcher in the study, says "the overall risk is still small." © 2015 NPR
By Sarah C. P. Williams The next time you forget where you left your car keys, you might be able blame an immune protein that builds up in your blood as you age. The protein impairs the formation of new brain cells and contributes to age-related memory loss—at least in mice, according to a new study. Blocking it could help prevent run-of-the-mill memory decline or treat cognitive disorders, the researchers say. “The findings are really exciting,” says neurologist Dena Dubal of the University of California, San Francisco (UCSF), who was not involved in the study. “The importance of this work cannot be underestimated as the world’s population is aging rapidly.” Multiple groups of scientists have shown that adding the blood of older mice to younger animals’ bodies makes them sluggish, weaker, and more forgetful. Likewise, young blood can restore the memory and energy of older mice. Neuroscientist Saul Villeda of UCSF homed in on one actor he thought might be responsible for some of that effect: β2 microglobulin (B2M), an immune protein normally involved in distinguishing one’s own cells from invading pathogens. B2M has also been found at increased levels in patients with Alzheimer’s disease and other cognitive disorders. Villeda and his colleagues first measured B2M levels in the blood of both people and mice of different ages; they found that those levels increased with age. When the researchers injected B2M into 3-month-old mice, the young animals suddenly had trouble remembering how to complete a water maze, making more than twice as many errors after they’d already been trained to navigate the maze. Moreover, their brains had fewer new neurons than other mice. Thirty days later, however, when the protein had been cleared from their bodies, the animals' memory troubles were gone as well, and the number of newly formed brain cells was back to normal. © 2015 American Association for the Advancement of Science
By Adrian Cho Whether they're from humans, whales, or elephants, the brains of many mammals are covered with elaborate folds. Now, a new study shows that the degree of this folding follows a simple mathematical relationship—called a scaling law—that also explains the crumpling of paper. That observation suggests that the myriad forms of mammalian brains arise not from subtle developmental processes that vary from species to species, but rather from the same simple physical process. In biology, it rare to find a mathematical relationship that so tightly fits all the data, say Georg Striedter, a neuroscientist at the University of California, Irvine. "They've captured something," he says. Still, Striedter argues that the scaling law describes a pattern among fully developed brains and doesn't explain how the folding in a developing brain happens. The folding in the mammalian brain serves to increase the total area of the cortex, the outer layer of gray matter where the neurons reside. Not all mammals have folded cortices. For example, mice and rats have smooth-surfaced brains and are "lissencephalic." In contrast, primates, whales, dogs, and cats have folded brains and are "gyrencephalic." For decades, scientists have struggled to relate the amount of folding in a species' brain to some other characteristic. For example, although animals with tiny brains tend to have smooth ones, there is no clean relationship between the amount of folding—measured by the ratio of the total area of the cortex to the exposed outer surface of the brain—and brain mass. Make a plot of folding versus brain mass for various species and the data points fall all over and not on a unified curve. Similarly, there is no clean relationship between the amount of folding and the number of neurons, the total area of the cortex, or the thickness of the cortex. © 2015 American Association for the Advancement of Science