A ‘hands-on’ approach could help babies develop spatial awareness

A study from the Department of Psychology published today found:

• Changes in the way the brain processes touch in the first year of life
• Babies start keeping track of their hands are when their arms move around from 8 months
• Crossing the hands confuses the mind in young babies
• The way we perceive touch in the outside world develops in the first year of life

The research, from Goldsmiths’ InfantLab, suggested that babies’ tactile experiences could be important for developing their sense of place in the world around them.

The InfantLab research team carried out their study on 66 babies aged from six to ten months old.

Babies felt harmless ‘buzzes’ on their arms

In the study, babies felt little tactile ‘buzzes’ on their hands first with their arms in an uncrossed position and then in a crossed position, while their brain activity was recorded through an EEG (electroencephalography) sensor net.

This is one of the first pieces of research to focus on the development of ‘touch perception’, which is crucial for investigating how babies learn to perceive how their own bodies fit into the world around them.

Dr Andy Bremner, InfantLab Director, explained: “We discovered that it takes time for babies to build up good mechanisms for perceiving how they fit into the outside world. Specifically, early on they do not appear to perceive the ways in which the body changes when their limbs, in this case their arms, move around.” 

Dr Silvia Rigato, researcher on the project, commented: “The vast majority of previous studies on infant perception has focussed on what babies perceive of a visual environment on a screen and out of reach, giving us a picture of what babies can do and understand when in couch potato mode.”

“Our research has taken this a step further. As adults we need good maps of where our bodies and limbs are in order to be able to act and move around competently. It seems these take time to develop in the first year, and we didn’t know that before.”

The full research paper ‘The neural basis of somatosensory remapping develops in human infancy’ was published in the journal Current Biology.

Citizens help researchers to challenge scientific theory

Science crowdsourcing was used to disprove a widely held theory that “supertasters” owe their special sensitivity to bitter tastes to an usually high density of taste buds on their tongue, according to a study published in the open-access journal Frontiers in Integrative Neuroscience.

Supertasters are people who can detect and are extremely sensitive to phenylthiocarbamide and propylthiouracil, two compounds related to the bitter molecules in certain foods such as broccoli and kale. Supertasting has been used to explain why some people don’t like spicy foods or “hoppy” beers, or why some kids are picky eaters.

The sensitivity to these bitter tastants is partly due to a variation in the taste receptor gene TAS2R38. But some scientists believe that the ability to supertaste is also boosted by a greater-than-average number of “papillae”, bumps on the tongue that contain taste buds. Nicole Garneau, Curator and Chair of the Department of Health Sciences, Denver Museum of Nature & Science, and colleagues tested if this is true.

"There is a long-held belief that if you stick out your tongue and look at the bumps on it, then you can predict how sensitive you are to strong tastes like bitterness in vegetables and strong sensations like spiciness," says Garneau. "The commonly accepted theory has been that the more bumps you have, the more taste buds you have and therefore the more sensitive you are."

Over 3000 visitors to the museum’s Genetics of Taste Lab volunteered to stick their tongue out so that their papillae could be counted and their sensitivity to phenylthiocarbamide and propylthiouracil measured. In total, 394 study subjects were included in the analysis. Cell swabs from volunteers were taken to determine their DNA sequence at TAS2R38. Results confirmed that certain variations in TAS2R38 make it more likely that somebody is sensitive to bitter, but also proved that the number of papillae on the tongue does not affect increased taste sensitivity.

"No matter how we looked at the data, we couldn’t replicate this long held assumption that a high number of papillae equals supertasting," says Garneau.

The authors argue against the continued misuse of the term supertaster, and for the use of the more objective term hypergeusia – abnormally sensitized taste – to describe people who are sensitive to all tastes and sensations from food.

"What we know and understand about how our bodies work improves greatly when we challenge central dogmas of our knowledge. This is the nature of science itself," adds Garneau. "As techniques improve, so too does our ability to do science, and we find that what we accepted as truth 20, 30, or 100 years ago gets replaced with better theories as we gather new data, which advances science. In this case, we’ve proven that with the ‘Denver Papillae Protocol’, our new method for objective analysis for papillae density, we were unable to replicate well-known studies about supertasting."

What make this study unique is that most of the results were collected by citizen scientists including over 130 volunteers who had been specially trained by Garneau and her colleagues. The Genetics of Taste Lab is located in the heart of the museum, uniquely situated to attract volunteers and dedicated citizen scientists who conduct population-based research about human genetics, taste, and health.

Cynical? You May Be Hurting Your Brain Health

People with high levels of cynical distrust may be more likely to develop dementia, according to a study published in the May 28, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Cynical distrust, which is defined as the belief that others are mainly motivated by selfish concerns, has been associated with other health problems, such as heart disease. This is the first study to look at the relationship between cynicism and dementia.

“These results add to the evidence that people’s view on life and personality may have an impact on their health,” said study author Anna-Maija Tolppanen, PhD, of the University of Eastern Finland in Kuopio. “Understanding how a personality trait like cynicism affects risk for dementia might provide us with important insights on how to reduce risks for dementia.”

For the study, 1,449 people with an average age of 71 were given tests for dementia and a questionnaire to measure their level of cynicism. The questionnaire has been shown to be reliable, and people’s scores tend to remain stable over periods of several years. People are asked how much they agree with statements such as “I think most people would lie to get ahead,” “It is safer to trust nobody” and “Most people will use somewhat unfair reasons to gain profit or an advantage rather than lose it.” Based on their scores, participants were grouped in low, moderate and high levels of cynical distrust.

A total of 622 people completed two tests for dementia, with the last one an average of eight years after the study started. During that time, 46 people were diagnosed with dementia. Once researchers adjusted for other factors that could affect dementia risk, such as high blood pressure, high cholesterol and smoking, people with high levels of cynical distrust were three times more likely to develop dementia than people with low levels of cynicism. Of the 164 people with high levels of cynicism, 14 people developed dementia, compared to nine of the 212 people with low levels of cynicism.

The study also looked at whether people with high levels of cynicism were more likely to die sooner than people with low levels of cynicism. A total of 1,146 people were included in this part of the analysis, and 361 people died during the average of 10 years of follow-up. High cynicism was initially associated with earlier death, but after researchers accounted for factors such as socioeconomic status, behaviors such as smoking and health status, there was no longer any link between cynicism and earlier death.

(Image: Shutterstock)

The claustrum’s proposed role in consciousness is supported by the effect and target localization of Salvia divinorum

This article brings together three findings and ideas relevant for the understanding of human consciousness: (I) Crick’s and Koch’s theory that the claustrum is a “conductor of consciousness” crucial for subjective conscious experience. (II) Subjective reports of the consciousness-altering effects the plant Salvia divinorum, whose primary active ingredient is salvinorin A, a κ-opioid receptor agonist. (III) The high density of κ-opioid receptors in the claustrum. Fact III suggests that the consciousness-altering effects of S. divinorum/salvinorin A (II) are due to a κ-opioid receptor mediated inhibition of primarily the claustrum and, additionally, the deep layers of the cortex, mainly in prefrontal areas. Consistent with Crick and Koch’s theory that the claustrum plays a key role in consciousness (I), the subjective effects of S. divinorum indicate that salvia disrupts certain facets of consciousness much more than the largely serotonergic hallucinogen lysergic acid diethylamide (LSD). Based on this data and on the relevant literature, we suggest that the claustrum does indeed serve as a conductor for certain aspects of higher-order integration of brain activity, while integration of auditory and visual signals relies more on coordination by other areas including parietal cortex and the pulvinar.

Full Article

Uncovering Clues to the Genetic Cause of Schizophrenia

The overall number and nature of mutations—rather than the presence of any single mutation—influences an individual’s risk of developing schizophrenia, as well as its severity, according to a discovery by Columbia University Medical Center researchers published in the latest issue of Neuron. The findings could have important implications for the early detection and treatment of schizophrenia.

Maria Karayiorgou, MD, professor of psychiatry and Joseph Gogos, MD, PhD, professor of physiology and cellular biophysics and of neuroscience, and their team sequenced the “exome”—the region of the human genome that codes for proteins—of 231 schizophrenia patients and their unaffected parents. Using this data, they demonstrated that schizophrenia arises from collective damage across several genes.

“This study helps define a specific genetic mechanism that explains some of schizophrenia’s heritability and clinical manifestation,” said Dr. Karayiorgou, who is acting chief of the Division of Psychiatric and Medical Genetics at the New York State Psychiatric Institute. “Accumulation of damaged genes inherited from healthy parents leads to higher risk not only to develop schizophrenia but also to develop more severe forms of the disease.”

Schizophrenia is a severe psychiatric disorder in which patients experience hallucination, delusion, apathy and cognitive difficulties. The disorder is relatively common, affecting around 1 in every 100 people, and the risk of developing schizophrenia is strongly increased if a family member has the disease. Previous research has focused on the search for individual genes that might trigger schizophrenia. The availability of new high-throughput DNA sequencing technology has contributed to a more holistic approach to the disease.

The researchers compared sequencing data to look for genetic differences and identify new loss-of-function mutations—which are rarer, but have a more severe effect on ordinary gene function—in cases of schizophrenia that had not been inherited from the patients’ parents. They found an excess of such mutations in a variety of genes across different chromosomes.

Using the same sequencing data, the researchers also looked at what types of mutations are commonly passed on to schizophrenia patients from their parents. It turns out that many of these are “loss-of-function” types. These mutations were also found to occur more frequently in genes with a low tolerance for genetic variation.

“These mutations are important signposts toward identifying the genes involved in schizophrenia,” said Dr. Karayiorgou.

The researchers then looked more deeply into the sequencing data to try to determine the biological functions of the disrupted genes involved in schizophrenia. They were able to verify two key damaging mutations in a gene called SETD1A, suggesting that this gene contributes significantly to the disease.

SETD1A is involved in a process called chromatin modification. Chromatin is the molecular apparatus that packages DNA into a smaller volume so it can fit into the cell and physically regulates how genes are expressed. Chromatin modification is therefore a crucial cellular activity.

The finding fits with accumulating evidence that damage to chromatin regulatory genes is a common feature of various psychiatric and neurodevelopmental disorders. By combining the mutational data from this and related studies on schizophrenia, the authors found that “chromatin regulation” was the most common description for genes that had damaging mutations.

“A clinical implication of this finding is the possibility of using the number and severity of mutations involved in chromatin regulation as a way to identify children at risk of developing schizophrenia and other neurodevelopmental disorders,” said Dr. Gogos. “Exploring ways to reverse alterations in chromatic modification and restore gene expression may be an effective path toward treatment.”

In further sequencing studies, the researchers hope to identify and characterize more genes that might play a role in schizophrenia and to elucidate common biological functions of the genes.

Learning Early in Life May Help Keep Brain Cells Alive

Using your brain – particularly during adolescence – may help brain cells survive and could impact how the brain functions after puberty.

According to a recently published study in Frontiers in Neuroscience, Rutgers behavioral and systems neuroscientist Tracey Shors, who co-authored the study, found that the newborn brain cells in young rats that were successful at learning survived while the same brain cells in animals that didn’t master the task died quickly.

“In those that didn’t learn, three weeks after the new brain cells were made, nearly one-half of them were no longer there,” said Shors, professor in the Department of Psychology and Center for Collaborative Neuroscience at Rutgers. “But in those that learned, it was hard to count. There were so many that were still alive.”

The study is important, Shors says, because it suggests that the massive proliferation of new brain cells most likely helps young animals leave the protectiveness of their mothers and face dangers, challenges and opportunities of adulthood.

Scientists have known for years that the neurons in adult rats, which are significant but fewer in numbers than during puberty, could be saved with learning, but they did not know if this would be the case for young rats that produce two to four times more neurons than adult animals.

By examining the hippocampus – a portion of the brain associated with the process of learning – after the rats learned to associate a sound with a motor response, scientists found that the new brain cells injected with dye a few weeks earlier were still alive in those that had learned the task while the cells in those who had failed did not survive.

“It’s not that learning makes more cells,” says Shors. “It’s that the process of learning keeps new cells alive that are already present at the time of the learning experience.”

Since the process of producing new brain cells on a cellular level is similar in animals, including humans, Shors says ensuring that adolescent children learn at optimal levels is critical.

“What it has shown me, especially as an educator, is how difficult it is to achieve optimal learning for our students. You don’t want the material to be too easy to learn and yet still have it too difficult where the student doesn’t learn and gives up,” Shors says.

So, what does this mean for the 12-year-old adolescent boy or girl?

While scientists can’t measure individual brain cells in humans, Shors says this study, on the cellular level, provides a look at what is happening in the adolescent brain and provides a window into the amazing ability the brain has to reorganize itself and form new neural connections at such a transformational time in our lives.

“Adolescents are trying to figure out who they are now, who they want to be when they grow up and are at school in a learning environment all day long,” says Shors. “The brain has to have a lot of strength to respond to all those experiences.”