Neurodiversity: Unleashing the Advantages of Your Differently Wired Brain

Neurodiversity

This material is based upon Dr Thomas Armstrong's book The Power of Neurodiversity:  Unleashing the Advantages of Your Differently Wired Brain. The Neurodiversity Strengths Checklist for Children.

Neurodiversity:  A Concept Whose Time Has Come

Over the past sixty years, we’ve witnessed a phenomenal growth in the number of new psychiatric illnesses.

The American Psychiatric Association’s Diagnostic and Statistical Manual, first published in 1952, originally listed about 100 categories of illness.

By the year 2000, that number had tripled.  We’ve become accustomed to hearing in the news about “learning disabilities,” “ADHD,” “Asperger’s syndrome,” and other conditions that were virtually unheard of fifty years ago.

A report from the National Institute of Mental Health indicates that about one-fourth of the American population suffers from a psychiatric disorder in any given year, and an article in the Archives of General Psychology suggested that over the course of a lifetime, approximately half of all people may suffer from a mental illness sometime during their lives.

Add to this the observation by Harvard Medical School professor John Ratey that many people have milder versions of psychiatric conditions (he calls them “shadow syndromes”), and we come to the conclusion that when all is said and done, nearly every individual in the country may have a psychiatric illness to one degree or another.

This epidemic in the growth of mental illness suggests that there is a crisis in the making.  How much longer can we continue to add new psychiatric illnesses to the list, before it becomes apparent that we have moved too far in pathologizing a sizeable chunk of the American populace?

There is, however, an answer to this crisis.  The concept of neurodiversity provides a paradigm shift in how we think about mental functioning.

Instead of regarding large portions of the American public as suffering from deficit, disease, or dysfunction in their mental processing, neurodiversity suggests that we instead speak about differences in cognitive functioning.

Just as we talk about differences in bio-diversity and cultural diversity, we need to start using the same kind of thinking in talking about brain differences.

We don’t pathologize a calla lily for not having petals (e.g. petal deficit disorder), nor do we diagnose an individual with brown skin as suffering from a “pigmentation dysfunction.”

Similarly, we ought not to pathologize individuals who have different ways of thinking, relating, attending, and learning

The word neurodiversity was coined in the late 1990’s by two individuals: journalist Harvey Blume, and autism advocate Judy Singer.

Blume wrote in the September 1, 1998 issue of The Atlantic:  “Neurodiversity may be every bit as crucial for the human race as biodiversity is for life in general. Who can say what form of wiring will prove best at any given moment?

Cybernetics and computer culture, for example, may favor a somewhat autistic cast of mind.” Singer in a 1999 book chapter titled:  “Why Can’t You Be Normal For Once in Your Life?” observed:  “For me, the key significance of the ‘Autistic Spectrum’ lies in its call for and anticipation of a politics of Neurological Diversity, or what I want to call ‘Neurodiversity.’

The ‘Neurologically Different’ represent a new addition to the familiar political categories of class/gender/race and will augment the insights of the social model of disability.

”The Wikepedia defines neurodiversity as:  “…an idea which asserts that atypical (neurodivergent) neurological development is a normal human difference that is to be recognized and respected as any other human variation.”  

The online Double-Tongued Dictionary characterizes neurodiversity as:  “the whole of human mental or psychological neurological structures or behaviours, seen as not necessarily problematic, but as alternate, acceptable forms of human biology.”

By using the concept of neurodiversity to account for individual neurological differences, we create a discourse whereby labeled people may be seen in terms of their strengths as well as their weaknesses.

Dyslexics, for example, can be seen in terms of their visual thinking ability and entrepreneurial strengths.  People with ADHD can be regarded as possessing a penchant for novel learning situations.

Individuals along the autistic spectrum can be looked at in terms of their facility with systems such computer programming or mathematical computation.

Those with bipolar disorder can be appreciated for their creative pursuits in the arts.

While proponents of the concept of neurodiversity do not shirk from the realization that people with dyslexia, ADHD, autism, bipolar disorder, and other psychiatric conditions, often suffer great hardships, and that those hardships require a lot of hard work to overcome, they realize that until an individual’s strengths have been recognized, celebrated, and worked with, nothing substantial can be accomplished with regard to their difficulties.

 Eight Principles of Neurodiversity:

The Human Brain Works More Like an Ecosystem than a Machine.  Up until now, the most often used metaphor to refer to the brain has been a computer (or some other type of machine).

However, the human brain isn’t hardware or software, it’s wetware.  The characterization of the brain as an unbelievably intricate network of ecosystems is much closer to the truth than that of a complex machine.

We should devise a discourse that better reflects this new conception of the brain.

Human Brains  Exist Along Continuums of Competence. Rather than regarding disability categories as discrete entities, it’s more appropriate to speak of spectrums or continuums of competence.

Recent research, for example, indicates that dyslexia is part of a spectrum that includes normal reading ability.

Similarly, we use terms such as autistic spectrum disorders, to suggest that there are different gradations of social ability that merge ultimately with normal behavior.

This suggests that we are all somewhere along continuums related to literacy, sociability, attention, learning, and other cognitive abilities, and thus all of us are connected to each other, rather than being separated into "normal" and "those having disabilities."

Human Competence is Defined by the Values of the Culture to Which You Belong.  Categories of disability often deeply reflect the values of a culture.

Dyslexia, for example, is based upon the social value that everyone be able to read.

One hundred and fifty years ago, this wasn’t the case, and dyslexia was unknown.  Similarly, autism may reflect the cultural value that suggests that it’s better to be in relationship than to be alone.

We should recognize that diagnostic categories are not purely scientifically-based but reflect these deeper social biases.

Whether You are Regarded As Disabled or Gifted Depends Largely on When and Where You Were Born.  

In other times and other places, there have been different disability/ability diagnoses depending upon cultural values.

In pre-Civil War America, for example, there was a disorder called “drapetomania” said to afflict blacks.

Its meaning was “an obsession with the urge to flee one’s slave masters” and reflected its racist roots. In India, today, there are people who would be labeled in the West as schizophrenic, but who are regarded as holy beings by the local population.

We should not regard diagnostic labels as absolute and set in stone, but think, instead, of their existence relative to a particular social setting.  

Success in Life is Based on Adapting One’s Brain to the Needs of the Surrounding Environment.   Despite Principles 3 and 4, however, it's true that we don’t live in other places or times, consequently the immediate need is to adapt to our current contemporary culture.

This means that a dyslexic person needs to learn how to read, an autistic individual needs to learn how to relate to others socially, a schizophrenic individual needs to think more rationally and so forth.

Tools such as psychoactive medication or intensive remediation programs can help achieve these aims.

Success in Life Also Depends on Modifying Your Surrounding Environment to Fit the Needs of Your Unique Brain (Niche Construction).

We shouldn’t focus all of our attention on making a neurodiverse person adapt to the environment in which they find themselves, which is a little like making a round peg fit in a square hole.

We should also devise ways of helping an individual change their surrounding environment to fit the needs of their unique brain.

Niche Construction Includes Career and Lifestyle Choices, Assistive Technologies, Human Resources, and Other Life-Enhancing Strategies Tailored to the Specific Needs of a Neurodiverse Individual.

There are many tools, resources, and strategies for altering the environment so that it it meshes with the needs of a neurodiverse brain.

For example, a person with ADHD, can find a career that involves novelty and movement, use an iPhone to help with organizing his day, and hire a coach to assist him with developing better social skills.

Positive Niche Construction Directly Modifies the Brain, Which in Turn Enhances its Ability to Adapt to the Environment. In experiments with mice, neuroscientists have shown that a more enriching environment results in a more complex network of neuronal connections in the brain.

This more complex brain, in turn, has an easier time adapting to the needs of the surrounding environment.

In conclusion, the potential is great for the neurodiversity movement to create significant social transformation.

Already, for example, there are software firms that have recognized the special programming gifts of certain people with Asperger’s syndrome and others on the autistic spectrum, and have hired significant numbers of them to improve their productivity.

Similarly, more people are understanding that ADHD brings with it special abilities as well as difficulties, and that appropriate career selection can be an important part of determining whether one will be successful or unsuccessful in a particular job.

It is hoped that the concept of neurodiversity will help combat “abelism” or the belief that people who are “abnormal” should be discriminated against, condescended to, and ultimately kept out of the basic affairs of society.

Neurodiversity brings with it a sense of hope, that all individuals, regardless of how they read, think, feel, socialize, or attend, will be recognized for their gifts, and accorded the same rights and privileges as any other human being.  

The full article and references here

Learning to read involves tricking the brain

In the experimental sequence, a pair of identical animals (e.g. horses) is preceded on the screen by a pair of mirror-image letters (b and d), or, in the control condition, a pair of non-mirror-image letters (f and t). 

The participant must decide in each case whether the two items (letters or animals) are identical or not. 

Credit: CNRS /Université Paris Descartes, Sorbonne-Paris-Cité /Université de Caen Basse-Normandie

While reading, children and adults alike must avoid confusing mirror-image letters (like b/d or p/q). Why is it difficult to differentiate these letters?

When learning to read, our brain must be able to inhibit the mirror-generalization process, a mechanism that facilitates the recognition of identical objects regardless of their orientation, but also prevents the brain from differentiating letters that are different but symmetrical.

A study conducted by the researchers of the Laboratoire de Psychologie du Développement et de l'Education de l'Enfant (CNRS / Université Paris Descartes / Université de Caen Basse-Normandie) is available on the website of the Psychonomic Bulletin & Review (Online First Articles).

In recent years, many studies on the process of learning to read have been based on the neuronal recycling hypothesis: the reuse of old brain mechanisms in a new adaptive role - a kind of "biological trick."

Specifically, neurons that are originally dedicated to the rapid identification of objects in the environment, through the mirror-generalization process, are "repurposed" during childhood to specialize in the visual recognition of letters and words.

In this study, the researchers showed 80 young adults pairs of images, first two letters and then two animals, asking them to determine whether they were identical.

The readers consistently spent more time determining that two animal images, when preceded by mirror-image letters, were indeed identical.

This increase in response time is called "negative priming": the readers had to inhibit the mirror-generalization process in order to distinguish letters like b/d or p/q. They then needed a little more time to reactivate this strategy when it became useful again to quickly identify animals.

Learning to read involves tricking the brain

The reader must learn to distinguish mirror-image letters (b and d) on the computer screen separated by a target fixation cross (+). 

Credit: CNRS/Université Paris Descartes, Sorbonne-Paris-Cité /Université de Caen Basse-Normandie

These results show that even adults need to inhibit the mirror-generalization process to avoid reading errors.

Children must therefore learn to inhibit this strategy when learning to read. A failure of cognitive inhibition during the recycling of visual neurons in the brain could thus be a factor in dyslexia, a direction worth exploring, in light of these findings.

More information: "The cost of blocking the mirror-generalization process in reading: Evidence for the role of inhibitory control in discriminating letters with lateral mirror-image counterparts." Grégoire Borst, Emmanuel Ahr, Margot Roell, and Olivier Houdé. Psychonomic Bulletin & Review (Online First Articles), 23 May 2014. DOI: 10.3758/s13423-014-0663-9

Children with autism have extra synapses in brain

In a study of brains from children with autism, researchers found that autistic brains did not undergo normal pruning during childhood and adolescence. 

The images show representative neurons from autistic (left) and control (right) brains; the spines on the neurons indicate the location of synapses.

Credit: Guomei Tang, PhD and Mark S. Sonders, PhD/Columbia University Medical Center

Children and adolescents with autism have a surplus of synapses in the brain, and this excess is due to a slowdown in a normal brain "pruning" process during development, according to a study by neuroscientists at Columbia University Medical Center (CUMC).

Because synapses are the points where neurons connect and communicate with each other, the excessive synapses may have profound effects on how the brain functions.

The study was published in the August 21 online issue of the journal Neuron.

A drug that restores normal synaptic pruning can improve autistic-like behaviors in mice, the researchers found, even when the drug is given after the behaviours have appeared.

"This is an important finding that could lead to a novel and much-needed therapeutic strategy for autism," said Jeffrey Lieberman, MD, Lawrence C. Kolb Professor and Chair of Psychiatry at CUMC and director of New York State Psychiatric Institute, who was not involved in the study.

Although the drug, rapamycin, has side effects that may preclude its use in people with autism, "the fact that we can see changes in behaviour suggests that autism may still be treatable after a child is diagnosed, if we can find a better drug," said the study's senior investigator, David Sulzer, PhD, professor of neurobiology in the Departments of Psychiatry, Neurology, and Pharmacology at CUMC.

David Sulzer

During normal brain development, a burst of synapse formation occurs in infancy, particularly in the cortex, a region involved in autistic behaviours; pruning eliminates about half of these cortical synapses by late adolescence.

Synapses are known to be affected by many genes linked to autism, and some researchers have hypothesized that people with autism may have more synapses.

To test this hypothesis, co-author Guomei Tang, PhD, assistant professor of neurology at CUMC, examined brains from children with autism who had died from other causes.

Thirteen brains came from children ages two to 9, and thirteen brains came from children ages 13 to 20. Twenty-two brains from children without autism were also examined for comparison.

Dr. Tang measured synapse density in a small section of tissue in each brain by counting the number of tiny spines that branch from these cortical neurons; each spine connects with another neuron via a synapse.

By late childhood, she found, spine density had dropped by about half in the control brains, but by only 16 percent in the brains from autism patients.

"It's the first time that anyone has looked for, and seen, a lack of pruning during development of children with autism," Dr. Sulzer said, "although lower numbers of synapses in some brain areas have been detected in brains from older patients and in mice with autistic-like behaviours."


Clues to what caused the pruning defect were also found in the patients' brains; the autistic children's brain cells were filled with old and damaged parts and were very deficient in a degradation pathway known as "autophagy."

Cells use autophagy (a term from the Greek for self-eating) to degrade their own components. Using mouse models of autism, the researchers traced the pruning defect to a protein called mTOR.

When mTOR is overactive, they found, brain cells lose much of their "self-eating" ability and without this ability, the brains of the mice were pruned poorly and contained excess synapses.

"While people usually think of learning as requiring formation of new synapses, "Dr. Sulzer says, "the removal of inappropriate synapses may be just as important."

The researchers could restore normal autophagy and synaptic pruning, and reverse autistic-like behaviors in the mice, by administering rapamycin, a drug that inhibits mTOR.

The drug was effective even when administered to the mice after they developed the behaviors, suggesting that such an approach may be used to treat patients even after the disorder has been diagnosed.

Because large amounts of overactive mTOR were also found in almost all of the brains of the autism patients, the same processes may occur in children with autism.

"What's remarkable about the findings," said Dr. Sulzer, "is that hundreds of genes have been linked to autism, but almost all of our human subjects had overactive mTOR and decreased autophagy, and all appear to have a lack of normal synaptic pruning.

This says that many, perhaps the majority, of genes may converge onto this mTOR/autophagy pathway, the same way that many tributaries all lead into the Mississippi River.

Overactive mTOR and reduced autophagy, by blocking normal synaptic pruning that may underlie learning appropriate behaviour, may be a unifying feature of autism."

Alan Packer, PhD, senior scientist at the Simons Foundation, which funded the research, said the study is an important step forward in understanding what's happening in the brains of people with autism.

"The current view is that autism is heterogeneous, with potentially hundreds of genes that can contribute."

"That's a very wide spectrum, so the goal now is to understand how those hundreds of genes cluster together into a smaller number of pathways; that will give us better clues to potential treatments," he said.

"The mTOR pathway certainly looks like one of these pathways. It is possible that screening for mTOR and autophagic activity will provide a means to diagnose some features of autism, and normalizing these pathways might help to treat synaptic dysfunction and treat the disease."

Journal Reference: 
Guomei Tang, Kathryn Gudsnuk, Sheng-Han Kuo, Marisa L. Cotrina, Gorazd Rosoklija, Alexander Sosunov, Mark S. Sonders, Ellen Kanter, Candace Castagna, Ai Yamamoto, Zhenyu Yue, Ottavio Arancio, Bradley S. Peterson, Frances Champagne, Andrew J. Dwork, James Goldman, David Sulzer. "Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits." Neuron, 2014; DOI: 10.1016/j.neuron.2014.07.040

The Woman Who Changed Her Brain: Barbara Arrowsmith-Young - TED Video

Barbara Arrowsmith-Young is the Creator and Director of Arrowsmith School and Arrowsmith Program, and the author of the international best-selling book The Woman Who Changed Her Brain.

She holds a B.A.Sc. in Child Studies from the University of Guelph, and a Master's degree in School Psychology from the University of Toronto (Ontario Institute for Studies in Education).

Arrowsmith-Young is recognized as the creator of one of the first practical applications of the principles of neuroplasticity to the treatment of learning disorders. Her program is implemented in 54 schools internationally.

In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience

Research Team first to Map Autism-Risk Genes by Function

Pity the poor autism researcher. Recent studies have linked hundreds of gene mutations scattered throughout the brain to increased autism risk. Where do you start?

UCLA neuroscientists may have an answer. They are the first to map groups of autism-risk genes by function, and to identify where and when these genes normally play major roles in early brain development.

In addition, they discovered disturbances in neural circuits that define key pathways between parts of the cerebral cortex.

The research suggests that these early disruptions are created by mutations in genes during fetal brain development and are not a result of autism itself.

Published in the Nov. 21 edition of Cell, the findings will help scientists understand how genetic changes cause autism on a molecular level and prioritize targets for future studies.

"Identifying gene variants that boost risk is only the first step of unraveling a disease," explained lead author Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics, professor of neurology at the David Geffen School of Medicine at UCLA and professor of psychiatry at the Semel Institute for Neuroscience and Human Behaviour.

"We need to figure out where genetic changes appear in the brain, at what stages during development and which biological processes they disrupt. Only then will we understand how mutations cause autism."

Using an online atlas called BrainSpan, the authors charted gene activity in the developing brain before birth.

In particular, they examined what happens during gene expression —when genes copy data from DNA to RNA in order to create proteins.

Geschwind and his colleagues found high activity in risk genes during two processes critical to early brain development.

"We found that gene variants are expressed in the developing brain when cells define their future identities and roles in neural circuits," first author Neelroop Parikshak, a graduate student researcher in Geschwind's lab.

"Therefore, changes in the genes influence the brain's wiring by altering the synapse and shaping how neurons transmit signals to each other."

The mutated genes also interfered with how the brain's layers and halves relate to one another, a phenomenon confirmed by previous imaging studies of the autistic brain.

"We discovered gene-related disruption of circuits that connect the autistic brain's layers and hemispheres to each other," explained Geschwind, who is director of the UCLA Neurogenetics Program and the Center for Autism Research and Treatment and co-director of the Center for Neurobehavioral Genetics at UCLA.

 "Our finding suggests that the mutated genes caused the miswiring; it's not a result of having the disease itself."

The UCLA team also demonstrated that while autism and intellectual disability share similar risk genes, the genes behave uniquely, showing for the first time how the two disorders differ.

"People often lump intellectual disability together with autism, because the disorders' risk genes overlap," said Parikshak.

"We showed that these genes have unique expression patterns in different brain regions at varying times during brain development.

"Genes linked to intellectual disability influence many biological processes in the body," he added. "But genes tied to autism tend to affect specific functions, such as the connections between brain regions that are essential to many human-specific behaviours, like speech and language."

The UCLA study will reap immediate benefits in the near future, when neuroscientists sequence the genomes of several thousand people for genetic mutations linked to autism and intellectual disability.

"We've made our analysis publically available to allow other researchers to expand upon our study and explore the data in detail," said Geschwind.

"We believe this will mark an important step forward in understanding the biology behind autism and other neurodevelopmental disorders."

Autism: Research focused on Men, Women are different

Autism affects different parts of the brain in females with autism than males with autism, a new study reveals. The research is published today in the journal Brain as an open-access article.

Scientists at the Autism Research Centre at the University of Cambridge used magnetic resonance imaging to examine whether autism affects the brain of males and females in a similar or different way.

They found that the anatomy of the brain of someone with autism substantially depends on whether an individual is male or female, with brain areas that were atypical in adult females with autism being similar to areas that differ between typically developing males and females. This was not seen in men with autism.

"One of our new findings is that females with autism show neuroanatomical 'masculinization'," said Professor Simon Baron-Cohen, senior author of the paper.

"This may implicate physiological mechanisms that drive sexual dimorphism, such as prenatal sex hormones and sex-linked genetic mechanisms."

Simon Baron-Cohen

Autism affects 1% of the general population and is more prevalent in males. Most studies have therefore focused on male-dominant samples.

As a result, our understanding of the neurobiology of autism is male-biased.

"This is one of the largest brain imaging studies of sex/gender differences yet conducted in autism. Females with autism have long been under-recognized and probably misunderstood," said Dr Meng-Chuan Lai, who led the research project.

"The findings suggest that we should not blindly assume that everything found in males with autism applies to females. This is an important example of the diversity within the 'spectrum'."

Dr Michael Lombardo

Dr Michael Lombardo, who co-led the study, added that although autism manifests itself in many different ways, grouping by gender may help provide a better understanding of this condition.

He said: "Autism as a whole is complex and vastly diverse, or heterogeneous, and this new study indicates that there are ways to subgroup the autism spectrum, such as whether an individual is male or female."

"Reducing heterogeneity via subgrouping will allow research to make significant progress towards understanding the mechanisms that cause autism."

Autism: Voices may not trigger brain's reward centers in children

Brain scans of children with ASD showing weak connections between voice-selective regions and reward pathways. Credit: Daniel A. Abrams, Stanford University.

In autism, brain regions tailored to respond to voices are poorly connected to reward-processing circuits, according to a new study by scientists at the Stanford University School of Medicine.

The research could help explain why children with autism struggle to grasp the social and emotional aspects of human speech.

"Weak brain connectivity may impede children with autism from experiencing speech as pleasurable," said Vinod Menon, PhD, senior author of the study, which will be published online June 17 in Proceedings of the National Academy of Sciences (PNAS).

Menon is a professor of psychiatry and behavioral sciences at Stanford and a member of the Child Health Research Institute at Lucile Packard Children's Hospital.

"The human voice is a very important sound; it not only conveys meaning but also provides critical emotional information to a child," said Daniel Abrams, PhD, a postdoctoral scholar in psychiatry and behavioural sciences who was the study's lead author.

Insensitivity to the human voice is a hallmark of autism, Abrams said, adding, "We are the first to show that this insensitivity may originate from impaired reward circuitry in the brain."

The study focused on children with a high-functioning form of autism. They had IQ scores in the normal range and could speak and read, but had difficulty holding a back-and-forth conversation or understanding emotional cues in another person's voice.

The scientists compared functional magnetic resonance imaging brain scans from 20 of these children with scans from 19 typically developing children, paying particular attention to a portion of the brain that responds selectively to the sound of human voices.

Prior research has shown that adults with autism had low voice-selective cortex activity in response to speech.

But until this study by Menon and his colleagues, no one had looked at connections between the voice-selective cortex and other brain regions in individuals with autism.

The new study found that in children with a high-functioning form of autism, the voice-selective cortex on the left side of the brain was weakly connected to the nucleus accumbens and the ventral tegmental area - brain structures that release dopamine in response to rewards.

The voice-selective cortex on the right side of the brain, which specializes in detecting vocal cues such as intonation and pitch, was weakly connected to the amygdala, which processes emotional cues.

The weaker these connections in children with autism, the worse their communication deficits, the study showed.

The researchers were able to predict the children's scores on the verbal portion of a standard test of autism severity by looking at the degree of impairment in these brain connections.

The findings may help to validate some autism therapies already in use, said co-author Jennifer Phillips, PhD, a clinical associate professor of psychiatry and behavioral sciences at Stanford who also treats children with autism at Packard Children's.

For instance, pivotal-response training aims to increase social use of language in children who can speak some words but who usually do not talk to others.

"Pivotal-response training goes after ways to naturally motivate kids to start using language and other forms of social interaction," Phillips said.

Future studies could test whether brain connections leading from voice to reward centers are strengthened by autism therapies, she added.

The findings also help resolve a long-standing debate about why individuals with autism show less-than-normal interest in human voices.

The team investigated two competing theories to explain the phenomenon: that individuals with autism have a deficit in their social motivation, or, alternatively, that they have sensory-processing deficits which impair their ability to fully hear human voices.

The new study found normal connections between voice-selective cortex and primary auditory brain regions in children with high-functioning autism, suggesting that these children do not have sensory-processing deficits.

The next steps for researchers include studying the consequences of the weak voice-to-reward circuit in autism.

"It is likely that children with autism don't attend to voices because they are not rewarding or emotionally interesting, impacting the development of their language and social communication skills," Menon said.

"We have discovered an aberrant brain circuit underlying a core deficit in autism; our findings may aid the development of new treatments for this disorder."

More information: Underconnectivity between voice-selective cortex and reward circuitry in children with autism, www.pnas.org/cgi/doi/10.1073/pnas.1302982110

Canadian Researchers Discover Two Parents are often Better Than One

A team of researchers at the University of Calgary's Hotchkiss Brain Institute (HBI) have discovered that adult brain cell production might be determined, in part, by the early parental environment.

The study suggests that dual parenting may be more beneficial than single parenting.

Scientists studied mouse pups that were raised by either dual or single parents and found that adult cell production in the brain might be triggered by early life experiences.

The scientists also found that the increased adult brain cell production varied based on gender. Specifically, female pups raised by two parents had enhanced white matter production as adults, increasing motor coordination and sociability.

Male pups raised by dual parents displayed more grey matter production as an adult, which improves learning and memory.

Samuel Weiss

"Our new work adds to a growing body of knowledge, which indicates that early, supportive experiences have long lasting, positive impact on adult brain function," says Samuel Weiss, PhD, senior author of the study and director of the HBI.

Surprisingly, the advantages of dual parenting were also passed along when these two groups reproduced, even if their offspring were raised by one female.

The advantages of dual parenting were thus passed along to the next generation.

To conduct the study, scientists divided mice into three groups

1. pups raised to adulthood by one female 
2. pups raised to adulthood by one female and one male and 
3. pups raised to adulthood by two females. 

Researchers then waited for the offspring to reach adulthood to find out if there was any impact on brain cell production.

Scientists say that this research provides evidence that, in the mouse model, parenting and the environment directly impact adult brain cell production.

While it's not known at this point, it is possible that similar effects could be seen in other mammals, such as humans.

More information: 
The study is published in the May 1 edition of PLOS ONE. dx.plos.org/10.137… pone.0062701

Autism: Difficulty in Recognising Faces Linked to Performance in a Group of Neurons

Neuroscientists at Georgetown University Medical Center (GUMC) have discovered a brain anomaly that explains why some people diagnosed with autism cannot easily recognise faces -- a deficit linked to the impairments in social interactions considered to be the hallmark of the disorder.

They also say that the novel neuro-imaging analysis technique they developed to arrive at this finding is likely to help link behavioural deficits to differences at the neural level in a range of neurological disorders.

The final manuscript published March 15 in the online journal NeuroImage: Clinical, the scientists say that in the brains of many individuals with autism, neurons in the brain area that processes faces (the fusiform face area, or FFA) are too broadly "tuned" to finely discriminate between facial features of different people.

They made this discovery using a form of functional magnetic resonance imaging (fMRI) that scans output from the blueberry-sized FFA, located behind the right ear.

"When your brain is processing faces, you want neurons to respond selectively so that each is picking up a different aspect of individual faces. The neurons need to be finely tuned to understand what is dissimilar from one face to another," says the study's senior investigator, Maximilian Riesenhuber, PhD., an associate professor of neuroscience at GUMC.

"What we found in our 15 adult participants with autism is that in those with more severe behavioral deficits, the neurons are more broadly tuned, so that one face looks more like another, as compared with the fine tuning seen in the FFA of typical adults," he says.

"And we found evidence that reduced selectivity in FFA neurons corresponded to greater behavioral deficits in everyday face recognition in our participants. This makes sense. If your neurons cannot tell different faces apart, it makes it more difficult to tell who is talking to you or understand the facial expressions that are conveyed, which limits social interaction."

Riesenhuber adds that there is huge variation in the ability of individuals diagnosed with autism to discriminate faces, and that some autistic people have no problem with facial recognition.

"But for those that do have this challenge, it can have substantial ramifications -- some researchers believe deficits in face processing are at the root of social dysfunction in autism," he says.

The neural basis for face processing
Neuroscientists have used traditional fMRI studies in the past to probe the neural bases of behavioral differences in people with autism, but these studies have produced conflicting results, says Riesenhuber.

"The fundamental problem with traditional fMRI techniques is that they can tell which parts of the brain become active during face processing, but they are poor at directly measuring neuronal selectivity," he says, "and it is this neuronal selectivity that predicts face processing performance, as shown in our previous studies."

To test their hypothesis that differences in neuronal selectivity in the FFA are foundational to differences in face processing abilities in autism, Riesenhuber and the study's lead author, neuroscientist Xiong Jiang, PhD, developed a novel brain imaging analysis technique, termed local regional heterogeneity, to estimate neuronal selectivity.

Read the full article here 

The above story is reprinted from materials provided by Georgetown University Medical Center

Dyslexia Linked to Brain’s Inconsistency with Encoding Sound

Researchers from Northwestern University report that they have found a biological mechanism that appears to play a vital role in learning to read.

This finding provides significant clues into the workings behind dyslexia — a collection of impairments unrelated to intelligence, hearing or vision that makes learning to read a struggle.

As many as one in 10 children is estimated to suffer from this disorder.

“We discovered a systematic relationship between reading ability and the consistency with which the brain encodes sounds,” said Nina Kraus, Hugh Knowles Professor of Neurobiology, Physiology and Communication.

The report, titled “Unstable Representation of Sound: A Biological Marker of Dyslexia,” is published in the Journal of Neuroscience.

For the study, researchers recorded the automatic brain wave responses of 100 school-aged children to speech sounds.

 They discovered that the very best readers encoded the sound most consistently while the poorest readers encoded it with the most difficulty.

The brain’s response to sound appears to stabilize as children learn to successfully connect sounds with their meanings.

On a positive note, biology is not destiny. In a previous study, the researchers found that the inconsistency with which the poorest readers encoded sound could be “fixed” through training.

In that study, children with reading difficulties were fitted for a year with assistive listening devices that transmitted their teacher’s voice directly into their ears.

After a year, the children made improvements in reading as well as in the consistency with which their brains encoded speech sounds, especially consonants.

“Use of the devices focused youngsters’ brains on the “meaningful” sounds coming from their teacher, diminishing other, extraneous distractions,” said Kraus.

“After a year of use, the students had honed their auditory systems and no longer required the assistive devices to keep their reading and encoding advantage.”

According to Kraus, people rarely have difficulty encoding vowel sounds, which are relatively simple and long.

It is consonant sounds, which are shorter and more acoustically complex, that are more likely to be incorrectly processed by the brain.

“Understanding the biological mechanisms of reading puts us in a better position to both understand how normal reading works and to ameliorate it where it goes awry,” says Kraus.

“Our results suggest that good readers profit from a stable neural representation of sound, and that children with inconsistent neural responses are likely at a disadvantage when learning to read,” Kraus adds.

“The good news is that response consistency can be improved with auditory training.”

Chronic Stress in Pregnancy prevents brain benefits of motherhood

A new study in animals shows that chronic stress during pregnancy prevents brain benefits of motherhood, a finding that researchers suggest could increase understanding of postpartum depression.

Rat mothers showed an increase in brain cell connections in regions associated with learning, memory and mood.

In contrast, the brains of mother rats that were stressed twice a day throughout pregnancy did not show this increase.

The researchers were specifically interested in dendritic spines – hair-like growths on brain cells that are used to exchange information with other neurons.

Previous animal studies conducted by lead author Benedetta Leuner of Ohio State University showed that an increase of dendritic spines in new mothers’ brains was associated with improved cognitive function on a task that requires behavioral flexibility – in essence, enabling more effective multitasking.

The dendritic spines increased by about 20 percent in these brain regions in new mothers, according to her findings.

The stress in this new study negated those brain benefits of motherhood, causing the stressed rats’ brains to match brain characteristics of animals that had no reproductive or maternal experience.

The stressed rats also had less physical interaction with their babies than did unstressed rats, a behaviour observed in human mothers who experience postpartum depression.

“Animal mothers in our research that are unstressed show an increase in the number of connections between neurons. Stressed mothers don’t,” said Leuner, assistant professor of psychology and neuroscience at Ohio State.

“We think that makes the stressed mothers more vulnerable. They don’t have the capacity for brain plasticity that the unstressed mothers do, and somehow that’s contributing to their susceptibility to depression.”


Previous research has suggested that there are a number of risk factors for postpartum depression, including hormone fluctuations, prior history of mental illness and environmental factors such as smoking or low socioeconomic status.

One of the strongest predictors, however, is chronic stress during pregnancy, so Leuner sought to create an animal model that could help explain brain changes linked to postpartum depression.

“It’s devastating not only for the mother, because it affects her well-being, but previous research also has shown that children of depressed mothers have impaired cognitive and social development, may have impaired physical development, and are more likely as adults to have depression or anxiety,” she said.

“A better understanding of postpartum depression is important to help the mother but also to prevent some of the damaging effects that this disorder can have on the child.”

The researchers exposed pregnant rats to stress twice a day by limiting their mobility on some days and on other days placing them in water. For three weeks after the rats gave birth, Leuner and colleagues monitored the rats.

The animals showed classic signs of the effects of stress, including lower than normal weight gain and enlarged adrenal glands, a sign of high stress-hormone production. The mothers stressed during pregnancy also gave birth to smaller pups.

“And they were not very good mothers,” Leuner said. After separation from pups for 30 minutes, unstressed mothers would gather up their babies, put them in the nest and nurse them. Stressed mother rats left the pups scattered around, wandered around the cage and fed the babies less frequently.

The stressed mother rats also exhibited more floating than unstressed rats in a water test; animals that float rather than swim are showing depressive-like symptoms.

“These findings in rats mimic some of the symptoms that are seen in women with postpartum depression,” Leuner said.

An examination of the animals’ brains showed that the rats exposed to chronic stress did not grow the additional dendritic spines in the hippocampus and prefrontal cortex that the unstressed mother rats did.

The stressed rats’ brains more closely resembled the brains of control rats that had never been mothers.

“We don’t yet know what the exact trigger is for the increase in spines in motherhood, but we know that the increase goes away with stress,” Leuner said.

She is continuing the work by investigating whether the beneficial effects of motherhood on cognitive functions are also blocked in mothers who are exposed to pregnancy stress as well as whether hormonal factors play a role.

Brain Potential Institute: Brain-Training Treatment for Learning Disabilities

Several years after launching its online one-on-one brain-training program that treats people with learning disabilties and concentration problems, Brain Potential Institute claims it has affirmative evidence that the program is equally as successful when completed online as at its onsite center.

The Institute believes that Results of the online treatment program indicate a significant increase in IQ, attention, focusing, and memory for those with ADD, ADHD, central auditory processing issues, autism and memory loss.

Jane Davis, P.T., M.S.H.P founded Brain Potential Institute in 2002 as Kid Potential Inc. The company expanded its services to provide brain training to teens, adults and seniors, which required rebranding itself as Brain Potential Institute.

Brain Potential Institute is dedicated to optimizing through cognitive training, the human brain to reach its highest intellectual potential for optimum performance at school and work, and to preserve brain function at all ages. Brain Potential Institute accepts students ages 3 through 90. Screenings are free

Brain Potential Institute claims to be one of the few companies able to increase a persons IQ by significant numbers. Its program is aimed to help with concentration issues, math and reading problems, development disorders and a litany of other cognitive and learning disabilities.

The foundation on which Brain Potential Institute has based its program is neurogenesis the brains ability to create new neuro-pathways.

Jane Davis, P.T., M.S.H.P, CEO and founder, Brain Potential Institute states that many students have gained three grade levels in reading and experienced up to a 30-point IQ increase.

Multiple sclerosis starts in brain’s outer layers

Researchers at the Mayo Clinic and Cleveland Clinic have reversed the traditional understanding of how multiple sclerosis (MS) begins and travels in the brain.

The common view is that the disease starts in the centre of the brain, in the white matter mostly found there, and then moves toward the outer layers, such as the cortex.

But this study, which is unique because it focused on the brain tissues of patients in the very early stages of MS, shows the opposite: that it moves from the outside in.

It begins in the “subarachnoid space,” which surrounds the brain, cushions it and is filled with cerebrospinal fluid. From there it moves into the white matter. This animation shows how the two hypotheses differ.

The findings are also significant because they support the hypothesis that inflammation, not neurodegeneration, is a main driver of the disease.

The authors conclude that it is “overwhelmingly likely” that MS is fundamentally an inflammatory disease, and not a neurodegenerative disease similar to Alzheimer’s.

Researchers are not entirely sure exactly causes MS, but the prevailing theory is that it is an autoimmune disease in which the body’s own immune system attacks and destroys its own myelin, a fatty substance essential to the nervous system. It protects the crucial nerve fibres enable different sections of the brain to communicate.

When myelin is damaged (as in MS), messages between the brain and the body are delayed or blocked, leading to MS symptoms such as blindness, numbness, paralysis, and thinking and memory difficulties.

“Our study shows the cortex is involved early in MS and may even be the initial target of disease,” co-lead author of the study and Mayo Clinic neurologist Dr. Claudia F. Lucchinetti stated.

“Inflammation in the cortex must be considered when investigating the causes and progression of MS”, she says. She and her co-author, Dr. Richard Ransohoff of the Cleveland Clinic, published the results of their study in the New England Journal of Medicine.

Timothy Syndrome: Brain finding sheds light on autism

Cells taken from people with a rare syndrome linked to autism could help explain the origins of the condition, scientists suggest.

The Stanford University team turned skin cells from people with "Timothy syndrome" into fully-fledged brain cells.

The abnormal activity found in these cells could be partially corrected using an experimental drug, Nature Medicine reports.

UK researchers warned the findings might not apply to everyone with autism.

Compared with the hundreds of thousands of people worldwide thought to show characteristics of autism, "Timothy syndrome" is vanishingly rare, affecting an estimated 20 people across the planet.

People who have the syndrome frequently display autistic behaviour, such as problems with social development and communication.

Because it is caused by a single gene defect rather than a combination of small genetic flaws, each making a tiny contribution, it presents a useful target for scientists looking to examine what goes wrong in the developing brain of a child with autism.

Ready for work

The US researchers used a technique developed recently to generate brain cells called neurons from only a sample of the patient's skin.

This allowed them to examine their development in the laboratory, and even use them to test out possible treatments.

They found obvious differences between neurons grown from Timothy syndrome patients, and those from healthy "control" subjects.

The healthy neurons developed into different subtypes, ready for work in different regions of the brain.

In contrast, the proportion of neurons developing into each subtype was different in the Timothy syndrome samples - more were equipped to work in the upper part of the cerebral cortex, and fewer in the lower part.

This meant there were fewer neurons equipped to work in a part of the brain called the corpus callosum, which has the role of helping the left and right "hemispheres" of the brain communicate.

These differences echoed those already observed in mice specially bred with the Timothy syndrome genetic fault.

In addition, the neurons were making too much of a particular body chemical linked to the manufacture of dopamine and norepinephrine, which play a significant role in sensory processing and social behaviour.

Dr Ricardo Dolmetsch, who led the study, said that the abnormalities found tallied with other evidence that autism was due in part to poor communication between different parts of the brain.

The team managed to reduce significantly the number of these malfunctioning neurons by adding a drug as they developed.

This, they said, meant it might be possible one day to treat this defect in a real patient, although the drug used was not currently suitable for children due to side-effects.

The National Autistic Society gave a cautious welcome to findings, but warned that they did not necessarily offer insights into every form of autism.

Researcher Georgina Gomez said: "Timothy syndrome is only one form of autism and so these findings only give a very limited picture of what might cause the condition.

"More work would need to be done to substantiate this particular piece of research."

Speaking and Understanding Speech Share the Same Parts of the Brain

The brain has two big tasks related to speech: making it and understanding it.

Psychologists and others who study the brain have debated whether these are really two separate tasks or whether they both use the same regions of the brain.

Now, a new study, published in the August issue of Psychological Science, a journal of the Association for Psychological Science, finds that speaking and understanding speech share the same parts of the brain, with one difference: we don't need the brain regions that control the movements of lips, teeth, and so on to understand speech.

Most studies of how speech works in the brain focuses on comprehension. That's mostly because it's easier to image the brains of people who are listening quietly; talking makes the head move, which is a problem when you're measuring the brain.

But now, the Donders Institute at the Radboud University Nijmegen, where the study was conducted, has developed technology that allows recording from a moving brain.

Laura Menenti, a Postdoctoral Research Associate at the University of Glasgow, co-wrote the paper along with Peter Hagoort of Radboud University Nijmegen and the Max Planck Institute for Psycholinguistics, Sarah Gierhan and Katrien Segaert.

Menenti was initially interested in how the brain produces grammatical sentences and wanted to track the process of producing a sentence in its entirety; looking not only at its grammatical structure but also at its meaning.

"What made this particularly exciting to us was that no one had managed to perform such a study before, meaning that we could explore an almost completely new topic," says Menenti.

The authors used functional MRI technology to measure brain activity in people who were either listening to sentences or speaking sentences.

The other problem with measuring brain activity in people who are speaking is that you have to get them to say the right kind of sentence.

The authors accomplished this with a picture of an action -- a man strangling a woman, say -- with one person coloured green and one coloured red to indicate their order in the sentence.

This prompted people to say either "The man is strangling the woman" or "The woman is strangled by the man." (The experiments were all carried out in Dutch.)

From this, the researchers were able to tell where in the brain three different speech tasks (computing meaning, coming up with the words, and building a grammatical sentence) -- were taking place.

They found that the same areas were activated for each of these tasks in people who were speaking and people who were listening to sentences.

However, although some studies have suggested that while people are listening to speech, they silently articulate the words in order to understand them, the authors found no involvement of motor regions when people were listening.

According to Menenti, though the study was largely designed to answer a specific theoretical question, it also points towards some useful avenues for treatment of people with language-related problems.

It suggests that while it sometimes seems that people with comprehension problems may have intact production, and vice versa, this may not necessarily be the case. According to Menenti, "Our data suggest that these problems would be expected to always at least partly coincide.

On the other, our data confirm the idea that many different processes in the language system, such as understanding meaning or grammar, can at least partly, be damaged independently of each other."

Filters That Reduce ‘brain Clutter’ Identified

Until now, it has been assumed that people with conditions like ADHD, Tourette syndrome, obsessive compulsive disorder and schizophrenia, all of whom characteristically report symptoms of "brain clutter," may suffer from anomalies in the brain's prefrontal cortex.

Damage to this brain region is often associated with failure to focus on relevant things, loss of inhibitions, impulsivity and various kinds of inappropriate behaviour.

So far, exactly what makes the prefrontal cortex so essential to these aspects of behaviour has remained elusive, hampering attempts to develop tools for diagnosing and treating these patients.

But new research by Julio Martinez-Trujillo, a professor in McGill University's Department of Physiology and Canada Research Chair in Visual Neuroscience, has brought new hope to these patients.

He believes the key to the "brain clutter" and impulsivity shown by individuals with dysfunctional prefrontal cortices lies in a malfunction of a specific type of brain cell. Martinez-Trujilo and his team have identified neurons in the dorsolateral sub-region of the primate prefrontal cortex that selectively filter out important from unimportant visual information.

The key to the normal functioning of these "filter neurons" is their ability to, in the presence of visual clutter, selectively and strongly inhibit the unimportant information, giving the rest of the brain access to what is relevant.

"Contrary to common beliefs, the brain has a limited processing capacity. It can only effectively process about one per cent of the visual information that it takes in," Martinez-Trujilo said. "This means that the neurons responsible for perceiving objects and programming actions must constantly compete with one another to access the important information.

"What we found when we looked at the behaviour of the neurons in the prefrontal cortex, was that an animal's ability to successfully accomplish a single action in the presence of visual clutter, was dictated by how well these units suppressed distracting information."

These results could be highly relevant for identifying the causes and improving the diagnosis and treatments of a wide range of mental disorders including ADHD and schizophrenia.

The research was conducted by Therese Lennert, a PhD student who holds a Vanier Scholarship, and it was funded by the Canada Research Chair program, Canadian Institutes of Health Research (CIHR), EJLB Foundation, and Natural Sciences and Engineering Research Council of Canada (NSERC).

Why Does Brain Development Diverge from Normal in Autism Spectrum Disorders?

Rett syndrome, a neurodevelopmental disorder on the autism spectrum, is marked by relatively normal development in infancy followed by a loss of cognitive, social and language skills starting at 12 to 18 months of age.

It is increasingly seen as a disorder of synapses, the connections between neurons that together form brain circuits. What hasn't been clear is why children start out developing normally, only to become progressively disadvantaged.

New research from Children's Hospital Boston, published in the April 14 issue of Neuron, helps unravel what's going on.

The researchers, led by Chinfei Chen, MD, PhD, of Children's F.M. Kirby Neurobiology Center, studied synapse development in mice with a mutation in the MeCP2 gene, the same gene linked to human Rett syndrome.

They found strong evidence that the loss of functioning MeCP2 prevents synapses and circuits from maturing and refining in response to cues from the environment -- just at the time when babies' brains should be maximally receptive to these cues.

Chen believes her findings may have implications not just for Rett syndrome, but for other autism spectrum disorders. "Many ASDs manifest between 1 and 2 years of age, a period when kids are interacting more with the outside world," says Chen.

"The brain of an autistic child looks normal, but there's a subtle difference in connections that has to do with how they process experiences. If you could diagnose early enough, there might be a way to alter the course of the disease by modifying experience, such as through intense one-to-one therapy."

Chen and colleagues focused on a synaptic circuit in the brain's visual system that is relatively easy to study, known as the retinogeniculate synapse.

It connects the cells receiving input from the eye to the lateral geniculate nucleus, an important relay station in the brain's thalamus. Visual input from the outside world, during a specific "critical period," is crucial for its normal development.

The team tested the functioning of the circuit by stimulating the optic tract and measuring electrical responses in the thalamus to see how the neurons were connected, and how strong the connections were.

In MeCP2-mutant mice, these recordings indicated that the visual circuit formed normally at first, and that during the second week of life, weaker connections were pruned away and others strengthened, just as they should be.

But after day 21 of life -- after mice open their eyes and when the visual circuitry should be further pruned and strengthened based on visual experience -- it became abnormal. The number of inputs and connections actually increased, while the strength of the synapses decreased.

This pattern was similar to that seen when normal mice were kept in the dark after day 21, depriving them of visual stimulation. Together, the findings suggest that MeCP2 is critically important to our ability to refine synaptic circuits based on sensory experience, says Chen. Without MeCP2, the circuit fails to incorporate this experience.

"During this last phase of development, you need sensory input to lock down and stabilize the connections," Chen explains. "But the circuit is not getting the right signal to stabilise, and continues to look around for the right connections."

Dyslexia: MRI Scan 'predicts when dyslexic will read'

The brain disorder makes it difficult for even very bright children to learn how to read and can be a lifelong source of frustration.

But according to research published in the Proceedings of the National Academy of Science (PNAS), brain scans can predict the improvement of teenagers' reading skills, with up to 90 per cent accuracy.

"This study takes an important step toward realising the potential benefits of combining neuroscience and education research by showing how brain scanning measures are sensitive to individual differences that predict educationally relevant outcomes," said Bruce McCandliss, one of the lead authors of the study and a professor at Vanderbilt University.

The research found brain scan results to be significantly more accurate in predicting how well a dyslexic child ultimately reads than standardised reading tests or the child's behaviour.

"This approach opens up a new vantage point on the question of how children with dyslexia differ from one another in ways that translate into meaningful differences two to three years down the line," Prof McCandliss said.

He said the research raises the prospect of a future test that could help match dyslexic students with the most effective treatments.

"Such insights may be crucial for new educational research on how to best meet the individual needs of struggling readers," he said.

The research was primarily conducted by experts at the Stanford University School of Medicine, with help from researchers at the Massachusetts Institute of Technology, the University of Jyvaskyla in Finland. and the University of York in the United Kingdom.

Language and Your Brain - Infographics

For centuries, researchers have studied the brain to find exactly where mechanisms for producing and interpreting language reside. Theories abound on how humans acquire new languages and how our developing brains learn to process languages. We take a look at the mysteries of language and the brain in the infographic below.

Click on the picture to see the whole Infographics on VOXY Blog

New Brain Structure Explains Willful Blindness

The article in today's NYT by Nancy Koehn titled “Why Red Flags Can Go  Unnoticed” was chiefly concerned with the effects of willful blindness  in humans. It did not answer the primary question: WHY do people ignore  clear warnings of impending problems.

Bruce Nappi, in his new novel   LIARS! provides a profound explanation: two human species  coexist on earth today, and one of them is not able to broadly  understand or apply logical reasoning, and no, it's not males and  females!

The new discovery came when he first determined what creates  consciousness in the human brain. Step one was recognising a new  physiological brain model that revises Sigmund Freud's Id, ego and  super-ego brain structure.

The second was sorting out what makes humans  different from animals.  In fact, contrary to common belief, that  difference does not occur at the homo sapiens level but further back  down the evolutionary tree.  Differences in awareness for humans and  animals are described and labeled A2 and A1 respectively, but, the  characteristics listed for humans (A2) raised a big problem: they didn’t  describe all known human abilities.

He categorised the additional  abilities with a new label A3.  The implication was both amazing and  unsettling! Both A3 and A2 had human traits, but they were as distinct  as A2 (humans) and A1 (animals). The solution required that each be  considered a different species - amazing for sure.

However, if the  discovery was true, it would have huge ramifications for human social  structures. He tested the theory against more and more of the great  social questions.  The new A3 model produced so many logical answers  that he is convinced he has stumbled onto a profound discovery.

New Brain Structure Explains Willful Blindness In Humans And Why Red Flags Go Unnoticed