Posts tagged psychology

May 3, 2012

Under some conditions, the brains of embryonic chicks appear to be awake well before those chicks are ready to hatch out of their eggs. That’s according to an imaging study published online on May 3 in Current Biology, a Cell Press publication, in which researchers woke chick embryos inside their eggs by playing loud, meaningful sounds to them. Playing meaningless sounds to the embryos wasn’t enough to rouse their brains.

This image shows an X-ray computed-tomography image of the chicken embryo skeleton inside an egg, which shows the developmental stage, together with a positron emission tomography image showing nervous system activity in the brain. Balaban et al., publishing in Current Biology, report the activity in chicken embryo brains is inversely related to behavioral activity, with different sleep-like states emerging for the first time. Playing meaningful sounds selectively induced patterns of embryonic brain activity similar to awake, post-hatching animals. Image 3D rendering by Carmen García-Villalba. Credit: Balaban et al. Current Biology

The findings may have implications not only for developing chicks and other animals, but also for prematurely born infants, the researchers say. Pediatricians have worried about the effects of stimulating brains that are still under construction, especially as modern medicine continues to push back the gestational age at which preemies can reliably survive.

"This work showed that embryo brains can function in a waking-like manner earlier than previously thought—well before birth," said Evan Balaban of McGill University. "Like adult brains, embryo brains also have neural circuitry that monitors the environment to selectively wake the brain up during important events."

That waking-like brain activity appears in a latent but inducible state during the final 20 percent of embryonic life, the researchers found. At that point, sleep-like brain activity patterns also emerge.

Before that major dividing line in development—for the first 80 percent of embryonic life— “embryos are in a state that is neither like sleep nor waking,” Balaban said. He suggests it may be useful to compare that state to what happens when people are comatose or under the influence of anesthesia.

This entire line of work was made possible by a new generation of molecular brain imagers developed by Balaban’s coauthors Juan-José Vaquero and Manuel Desco at the Universidad Carlos III in Madrid. Those state-of-the art machines can detect very small amounts of tracer molecules and pinpoint them to a tiny region of the brain (about 0.7 mm, or less than 3/100ths of an inch).

The researchers say they were surprised to capture waking-like activity before birth. And there were other surprises, too. The embryo brains they observed showed considerable variation in activity, for one.

Before the emergence of sleep and waking patterns of brain activity, the chick embryos in their study exhibited lots of spontaneous movement, even as their higher-brain regions remained inactive. Once the chicks reached that 80 percent mark in development, higher-brain regions began crackling with activity. At the same time, those physical movements ceased as the embryos entered a sleep-like state.

"The last 30 percent of fetal brain development is a more interesting time than we previously thought, because it’s when complex whole-brain functions that depend on coordination of widely separated brain areas first emerge," Balaban said. "Embryos begin to cycle through a variety of brain states and are even capable of showing waking-like brain activity."

That might explain instances of complex fetal and early neonatal learning. “It also raises questions about the longer-term developmental consequences that such brain activity may have, if it is induced before intrinsic brain wiring is sufficiently completed,” Balaban said, “for example, in babies born very prematurely. We are excited by the possibility that the techniques developed here can now be used to provide answers to these questions.”

Provided by Cell Press

Source: medicalxpress.com

ScienceDaily (May 2, 2012) — Results of a new study reported recently by psychology researcher Lisa Scott and colleagues at the University of Massachusetts Amherst confirm that although infants are born with equal abilities to tell apart people within multiple races, by age 9 months they are better at recognizing faces and emotional expressions of people within groups they interact with most.

For part of the UMass Amherst study of infants and recognition of individuals of other races, a net of recording sensors was placed on the infant’s head to record brain activity while they viewed own-race and other-race emotion faces (happy, sad) that either matched or did not match a corresponding emotion sound (laughing, crying). This measure helps researchers understand how the brain develops in response to experience during the first year of life. Lisa Scott is pictured adjusting the head net on an infant subject. (Credit: UMass Amherst)

The researchers found that by 9 months, infants show a decline in their ability to tell apart two faces within another race and to accurately match emotional sounds with emotional expressions of different-race individuals. This is the first investigation of this effect in infancy and supports other studies suggesting that emotion recognition is less accurate for other-race faces than own-race faces. Scott’s paper was singled out for special mention as the “Editor’s Choice” article in the May issue of Developmental Science.

This research suggests that throughout the first year of life, babies are developing highly specialized perceptual abilities in response to important people in their environment, such as family members. This focus of attention to familiar groups of people compared to unfamiliar groups is hypothesized to be the root of later difficulties some adults have in identifying and recognizing faces of other races.

This is similar to how babies learn language. Early in infancy babies do not know yet which sounds are meaningful in their native language, so they treat all sounds similarly. But as they learn the language spoken around them, their ability to tell apart sounds within other languages declines and their ability to differentiate sounds within their native language improves.

Scott says, “In addition to providing information critical for understanding how infants learn about the surrounding environment, the results of this research may serve as a guide for early education and interventions designed to reduce later racial prejudice and stereotyping” Scott states. “These results suggest that biases in face recognition and perception begin in preverbal infants, well before concepts about race are formed. It is important for us to understand the nature of these biases in order to reduce or eliminate them.”

For this study, each infant came to the lab with a parent for a one-hour session that included showing infants pictures of faces and having them listen to sounds while their looking time and brain activity were recorded. Forty-eight Caucasian infants with little to no previous experience with African-American or black individuals participated in this study.

Infants completed two tasks. The first was designed to assess their ability to tell the difference between two faces within their own race and two faces within another, unfamiliar, race. For the second task, a net of recording sensors was placed on the infant’s head to record brain activity while they viewed own-race and other-race emotion faces (happy, sad) that either matched or did not match a corresponding emotion sound (laughing, crying).

Consistent with previous reports, 5-month-old infants were found to equally tell apart faces from both races, whereas 9-month-old infants were better at telling apart two faces within their own race, Scott and colleagues report.

Further, measures of brain activity revealed differential neural processing of own-race compared to other-race emotional faces at 9 months. However, 5-month olds exhibited similar processing for both own- and other-race faces. In addition, infants were found to shift their processing of face-related emotion information from neural regions in the front of the brain to neural regions in the back of the brain from 5 to 9 months of age. This shift in neural processing helps researchers understand how the brain develops in response to experience during the first year of life.

Source: Science Daily

ScienceDaily (May 2, 2012) — A highly toxic beta-amyloid — a protein that exists in the brains of Alzheimer’s disease victims — has been found to greatly increase the toxicity of other more common and less toxic beta-amyloids, serving as a possible “trigger” for the advent and development of Alzheimer’s, researchers at the University of Virginia and German biotech company Probiodrug have discovered.

Pyroglutanylated beta-amyloid (green) accumulates in the brains of mice genetically engineered to overproduce it. The red cells are astrocytes, which invade brain regions where the amyloid is deposited and neurons die. The blue structures are nuclei of neurons and astrocytes. (Credit: University of Virginia)

The finding, reported in the May 2 online edition of the journal Nature, could lead to more effective treatments for Alzheimer’s. Already, Probiodrug AG, based in Halle, Germany has completed phase 1 clinical trials in Europe with a small molecule that inhibits an enzyme, glutaminyl cyclase, that catalyzes the formation of this hypertoxic version of beta-amyloid.

"This form of beta-amyloid, called pyroglutamylated (or pyroglu) beta-amyloid, is a real bad guy in Alzheimer’s disease," said principal investigator George Bloom, a U.Va. professor of biology and cell biology in the College of Arts & Sciences and School of Medicine, who is collaborating on the study with scientists at Probiodrug. "We’ve confirmed that it converts more abundant beta-amyloids into a form that is up to 100 times more toxic, making this a very dangerous killer of brain cells and an attractive target for drug therapy."

Bloom said the process is similar to various prion diseases, such as mad cow disease or chronic wasting disease, where a toxic protein can “infect” normal proteins that spread through the brain and ultimately destroy it.

In the case of Alzheimer’s, severe dementia occurs over the course of years prior to death.

"You might think of this pyroglu beta-amyloid as a seed that can further contaminate something that’s already bad into something much worse — it’s the trigger," Bloom said. Just as importantly, the hypertoxic mixtures that are seeded by pyroglu beta-amyloid exist as small aggregates, called oligomers, rather than as much larger fibers found in the amyloid plaques that are a signature feature of the Alzheimer’s brain.

And the trigger fires a “bullet,” as Bloom puts it. The bullet is a protein called tau that is stimulated by beta-amyloid to form toxic “tangles” in the brain that play a major role in the onset and development of Alzheimer’s. Using mice bred to have no tau genes, the researchers found that without the interaction of toxic beta-amyloids with tau, the Alzheimer’s cascade cannot begin. The pathway by which pyroglu beta-amyloid induces the tau-dependent death of neurons is now the target of further investigation to understand this important step in the early development of Alzheimer’s disease

"There are two matters of practical importance in our discovery," Bloom said. "One, is the new insights we have as to how Alzheimer’s might actually progress — the mechanisms which are important to understand if we are to try to prevent it from happening; and second, it provides a lead into how to design drugs that might prevent this kind of beta-amyloid from building up in the first place."

Said study co-author Hans-Ulrich Demuth, a biochemist and chief scientific officer at Probiodrug, “This publication further adds significant evidence to our hypothesis about the critical role pyroglu beta-amyloid plays in the initiation of Alzheimer’s Disease. For the first time we have found a clear link in the relationship between pyroglu beta-amyloid, oligomer formation and tau protein in neuronal toxicity.”

Bloom and his collaborators are now looking for other proteins that are needed for pyroglu beta-amyloid to become toxic. Any such proteins they discover are potential targets for the early diagnosis and/or treatment of Alzheimer’s disease.

Source: Science Daily

ScienceDaily (May 2, 2012) — A drug prescribed for Alzheimer’s disease does not ease clinically significant agitation in patients, according to a new study conducted by researchers from the U.K., U.S. and Norway. This is the first randomized controlled trial designed to assess the effectiveness of the drug (generic name memantine) for significant agitation in Alzheimer’s patients.

Previous studies suggested memantine could help reduce agitation and improve cognitive functions such as memory. Led by the University of East Anglia in the U.K., the new research found that while memantine does improve cognitive functioning and neuropsychiatric symptoms such as delusion, mood and anxiety, it is no more effective in reducing significant agitation than a placebo.

"Memantine is quite commonly prescribed for Alzheimer’s disease in the U.S. Despite the negative findings regarding agitation, this trial opens a door of hope," said Regenstrief Institute investigator Malaz Boustani, M.D., MPH, associate professor of medicine at the Indiana University School of Medicine and associate director of the IU Center for Aging Research. "Memantine does appear to help with other behavioral and psychological symptoms of Alzheimer’s disease."

Dr. Boustani, a co-author of the study, is also the medical and research director of the Healthy Aging Brain Center at Wishard Health Services.

"Efficacy of memantine for agitation in Alzheimer’s dementia: a randomized double-blind placebo controlled trial"published in PLoS ONEon May 2. Authors of the study are from Indiana University; the University of East Anglia, University College London, University of Kent, Aston University, Oxleas National Health Service Foundation Trust and Kings College London, all in the U.K.; and the University of Stavanger in Norway.

An estimated 5.4 million Americans have Alzheimer’s disease according to the Alzheimer’s Association. Many are agitated. They may, for example, pace continually, become physically or verbally aggressive or scream persistently. In addition to harming quality of life for the patient, agitation places enormous strain on relationships with family members and care providers, and often results in institutionalization.

"People who have mild symptoms [of agitation] often respond to changes in the environment or psychological treatment, but these methods are impractical in severe agitation," said Chris Fox, M.D., of Norwich Medical School at University of East Anglia, who led the research. "Our findings regarding memantine are disappointing with respect to severe agitation — particularly as the alternative antipsychotic medications can have significant side effects such as increased rates of stroke and death. However, we hope our study will highlight the urgent need for investment in safe and effective new treatments for this growing disease."

The team of researchers studied 153 nursing home residents and hospital inpatients with severe Alzheimer’s from September 2007 to May 2010. All the study participants displayed significant agitation requiring clinical treatment. Half were given memantine, and half received a placebo. The researchers reported signficant improvement in cognitive function and for overall neuropsychiatric symptoms for the group given memantine, but no statistically significant difference in terms of the severe agitation that was the primary focus of the study.

Memantine is approved by the U.S. Food and Drug Administration for Alzheimer’s disease. The trial was sponsored by East Kent Hospitals University National Health Service Foundation Trust in the U.K. The study was funded by Lundbeck, a manufacturer of memantine.

"This research suggests that even though memantine can have real benefits for people in the later stages of Alzheimer’s, it may not have all the answers," said Anne Corbett, research manager at the Alzheimer’s Society of the U.K., which was not involved in the research. "However, prescribers should not see the only alternative as being to hand out antipsychotics. These overprescribed drugs double the risk of death and treble the risk of stroke and should always be a last resort for people with dementia."

Source: Science Daily

ScienceDaily (May 2, 2012) — A new study suggests that eating foods that contain omega-3 fatty acids, such as fish, chicken, salad dressing and nuts, may be associated with lower blood levels of a protein related to Alzheimer’s disease and memory problems. The research is published in the May 2, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.

"While it’s not easy to measure the level of beta-amyloid deposits in the brain in this type of study, it is relatively easy to measure the levels of beta-amyloid in the blood, which, to a certain degree, relates to the level in the brain," said study author Nikolaos Scarmeas, MD, MS, with Columbia University Medical Center in New York and a member of the American Academy of Neurology.

For the study, 1,219 people older than age 65, free of dementia, provided information about their diet for an average of 1.2 years before their blood was tested for the beta-amyloid. Researchers looked specifically at 10 nutrients, including saturated fatty acids, omega-3 and omega-6 polyunsaturated fatty acids, mono-unsaturated fatty acid, vitamin E, vitamin C, beta-carotene, vitamin B12, folate and vitamin D.

The study found that the more omega-3 fatty acids a person took in, the lower their blood beta-amyloid levels. Consuming one gram of omega-3 per day (equal to approximately half a fillet of salmon per week) more than the average omega-3 consumed by people in the study is associated with 20 to 30 percent lower blood beta-amyloid levels.

Other nutrients were not associated with plasma beta-amyloid levels. The results stayed the same after adjusting for age, education, gender, ethnicity, amount of calories consumed and whether a participant had the APOE gene, a risk factor for Alzheimer’s disease.

"Determining through further research whether omega-3 fatty acids or other nutrients relate to spinal fluid or brain beta-amyloid levels or levels of other Alzheimer’s disease related proteins can strengthen our confidence on beneficial effects of parts of our diet in preventing dementia," said Scarmeas.

Source: Science Daily

ScienceDaily (May 2, 2012) — The way we use our hands may determine how emotions are organized in our brains, according to a recent study published inPLoS ONE by psychologists Geoffrey Brookshire and Daniel Casasanto of The New School for Social Research in New York.

Motivation, the drive to approach or withdraw from physical and social stimuli, is a basic building block of human emotion. For decades, scientists have believed that approach motivation is computed mainly in the left hemisphere of the brain, and withdraw motivation in the right hemisphere. Brookshire and Casasanto’s study challenges this idea, showing that a well-established pattern of brain activity, found across dozens of studies in right-handers, completely reverses in left-handers.

The study used electroencepahlography (EEG) to compare activity in participants’ right and left hemispheres during rest. After having their brain waves measured, participants completed a survey measuring their level of approach motivation, a core aspect of our personalities. In right-handers, stronger approach motivation was associated with greater activity in the left hemisphere than the right, consistent with previous studies. Left-handers showed the opposite pattern: approach motivation was associated with greater activity in the right hemisphere than the left.

A New Link Between Motor Action and Emotion

Most cognitive functions do not reverse with handedness. Language, for example, is mainly in the left hemisphere for the majority of right- and left-handers. However, these results were not unexpected.

"We predicted this hemispheric reversal because we observed that people tend to use different hands to perform approach- and avoidance-related actions," says Casasanto. Approach actions are often performed with the dominant hand, and avoidance actions with the non-dominant hand.

"Approach motivation is computed by the hemisphere that controls the right hand in right-handers, and by the hemisphere that controls the left hand in left-handers," says Casasanto. "We don’t think this is a coincidence. Neural circuits for motivation may be functionally related to circuits that control hand actions — emotion may be built upon neural circuits for action, in evolutionary or developmental time."

The authors caution that these data show a correlation between emotional motivation and motor control, and that further studies are needed to establish a causal link.

Implications for the treatment of depression and anxiety disorders

To treat depression and anxiety disorders, brain stimulation is used to increase neural activity in the patient’s left hemisphere, long believed to the ‘approach hemisphere.” “Given what we show here,” says Brookshire, “this treatment, which helps right-handers, may be detrimental to left-handers — the exact opposite of what they need.” The discovery that approach motivation reverses with handedness may lead to safer, more effective neural therapies for left-handers, according to Brookshire, “it’s something we’re investigating now.”

Source: Science Daily

ScienceDaily (May 2, 2012) — Although the two disorders may seem dissimilar, epilepsy and psychosis are associated. Individuals with epilepsy are more likely to have schizophrenia, and a family history of epilepsy is a risk factor for psychosis. It is not known whether the converse is true, i.e., whether a family history of psychosis is a risk factor for epilepsy.

Multiple studies using varied investigative techniques have shown that patients with schizophrenia and patients with epilepsy show some similar structural brain and genetic abnormalities, suggesting they may share a common etiology.

To investigate this possibility, researchers conducted a population-based study of parents and their children born in Helsinki, Finland. Using data available in two Finnish national registers, the study included 9,653 families and 23,404 offspring.

Individuals with epilepsy had a 5.5-fold increase in the risk of having a psychotic disorder, a 6.3-fold increase in the risk of having bipolar disorder, and an 8.5-fold increase in the risk of having schizophrenia.

They also found that the association between epilepsy and psychosis clusters within families. Individuals with a parental history of epilepsy had a 2-fold increase in the risk of developing psychosis, compared to individuals without a parental history of epilepsy. Individuals with a parental history of psychosis had a 2.7-fold increase in the risk of having a diagnosis of epilepsy, compared to individuals without a parental history of psychosis.

There have been multiple theories regarding the link between epilepsy and psychosis, but most have been predicated on the idea that epilepsy has toxic effects on the brain. However, combined with prior genetic and neurodevelopmental evidence, these new findings suggest a much more complex association, which likely includes a shared genetic vulnerability.

"Our evidence that epilepsy and psychotic illness may cluster within some families indicates that these disorders may be more closely linked than previously thought. We hope that this epidemiological evidence may contribute to the on-going efforts to disentangle the complex pathways that lead to these serious illnesses," said Dr. Mary Clarke, first author of the study and lecturer at Royal College of Surgeons in Ireland.

Dr. John Krystal, Editor of Biological Psychiatry, commented: “We have long known that particular types of epilepsy were associated with psychosis. However, the finding that a parental history of psychosis is associated with an increased risk of epilepsy in the offspring strengthens the mechanistic link between the two conditions.”

Source: Science Daily

ScienceDaily (May 2, 2012) — Parkinson’s disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It’s characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson’s symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University’s Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1’s normal function, thereby protecting dopamine- producing neurons. What’s more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson’s patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson’s patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. “We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain,” explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson’s disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Filling an urgent need

According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson’s disease. “Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease,” she says. “Until now, we have lacked tools for neuroprotection.”

The researchers also note the potential for the peptides to be used preventatively. In some cases, Parkinson’s can be diagnosed before motor symptoms begin with the help of brain scans, explains Dr. Lev, and patients who have a genetic link to the disease might opt for early testing. A preventative therapy could help many potential Parkinson’s patients live a normal life.

Source: Science Daily

ScienceDaily (May 1, 2012) — Vision and hearing are so crucial to our daily lives that any impairments usually become obvious to an affected person. Although a number of known genetic mutations can lead to hereditary defects in these senses, little is known about our sense of touch, where defects might be so subtle that they go unnoticed.

There are good reasons to suspect that hearing and touch might have a common genetic basis. Sound-sensing cells in the ear detect vibrations and transform them into electrical impulses. Likewise, nerves that lie just below the surface of the skin detect movement and changes in pressure, and generate impulses. The similarity suggests that the two systems might have a common evolutionary origin—they may depend on an overlapping set of molecules that transform motion into signals that can be transmitted along nerves to the brain. (Credit: © Vladimir Voronin / Fotolia)

People with good hearing also have a keen sense of touch; people with impaired hearing generally have an impaired sense of touch. Extensive data supporting this hypothesis was presented by Dr. Henning Frenzel and Professor Gary R. Lewin of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany. The two researchers showed that both senses — hearing and touch — have a common genetic basis. In patients with Usher syndrome, a hereditary form of deafness accompanied by impaired vision, the researchers discovered a gene mutation that is also causative for the patients’ impaired touch sensitivity.

The examination was preceded by various studies, including studies with healthy identical and non-identical human twins. In total, the researchers assessed sensory function in 518 volunteers.

In all vertebrates, and consequently also in humans, hearing and touch represent two distinct sensory systems that both rely on the transformation of mechanical force into electrical signals. When we hear, sound waves trigger vibrations that stimulate the hair-like nerve endings in the cochlea in the inner ear. These then transform the mechanical stimuli into electrical signals, which are transmitted to the brain via the auditory nerve. When we touch something a similar process takes place: The mechanical stimulus — sliding the fingers over a rough or smooth surface, the perception of vibrations — is taken up via sensors in the skin, converted into an electrical stimulus and transmitted to the brain.

Twin study with 100 pairs of twins

In recent years about 70 genes have been identified in humans, mutations in which trigger hearing loss or deafness. “Surprisingly, no genes have been found that negatively influence the sense of touch,” Professor Lewin said. To see whether the sense of touch also has a hereditary component, the researchers first studied 100 pairs of twins — 66 pairs of monozygotic twins and 34 dizygotic pairs of twins. Monozygotic twins are genetically completely identical; dizygotic twins are genetically identical to 50 percent. The tests showed that the touch sensitivity of the subjects was determined to more than 50 percent by genes. Furthermore, hearing and touch tests showed that there is a correlation between the sense of hearing and touch.

The researchers therefore suspected that genes that influence the sense of hearing may also have an influence on the sense of touch. In a next step, they recruited test subjects at a school in Berlin for students with hearing impairments. There they assessed the touch sensitivity in a cohort of 39 young people who suffered from severe congenital hearing impairment. The researchers compared these findings with the data from their twin study and discovered that not all of the young people with hearing loss had impaired tactile acuity. “Strikingly, however, many of these young people did indeed have poor tactile acuity,” Professor Lewin explained.

The researchers decided it would take too much time to analyze which of the approximately 70 genes that adversely affect the sense of hearing may also negatively affect the sense of touch. Therefore, the researchers focused specifically on patients with the Usher syndrome, a hereditary form of hearing impairment, in which the patients progressively become blind. Usher syndrome patients have varying degrees of hearing impairment, and the disease is genetically very well studied. There are nine known Usher genes carrying mutations which cause the disease.

The researchers examined one cohort of patients in a special consultation at the Charité — Universitätsmedizin Berlin for Usher patients from all over Germany. A second cohort was recruited at the university hospital La Fe in Valencia, Spain. The studies revealed that not all patients with Usher-syndrome have poor tactile acuity and touch sensitivity. The researchers showed that only patients with Usher syndrome who have a mutation in the gene USH2A have poor touch sensitivity. This mutation is also responsible for the impaired hearing of 19 patients. The 29 Usher-syndrome patients in whom the mutation could not be detected had a normal sense of touch. The researchers thus demonstrated that there is a common genetic basis for the sense of hearing and touch. They suspect that even more genes will be discovered in the future that influence both mechanosensory traits.

Women hear better than men and have a finer sense of touch

The researchers discovered another interesting detail during their five-year study. “When women complain that their men are not really listening to them, there is some truth in that,” Professor Lewin said. “The studies with a total of 518 individuals including 295 women have actually shown that women hear better and they also have a finer sense of touch than men; in short woman hear and feel more than men!”

Source: Science Daily

ScienceDaily (May 1, 2012) — Slacker or go-getter? Everyone knows that people vary substantially in how hard they are willing to work, but the origin of these individual differences in the brain remains a mystery.

Slacker or go-getter? Everyone knows that people vary substantially in how hard they are willing to work, but the origin of these individual differences in the brain remained a mystery. Until now. (Credit: © Dana Heinemann / Fotolia)

Now the veil has been pushed back by a new brain imaging study that has found an individual’s willingness to work hard to earn money is strongly influenced by the chemistry in three specific areas of the brain. In addition to shedding new light on how the brain works, the research could have important implications for the treatment of attention-deficit disorder, depression, schizophrenia and other forms of mental illness characterized by decreased motivation.

The study was published May 2 in the Journal of Neuroscience and was performed by a team of Vanderbilt scientists including post-doctoral student Michael Treadway and Professor of Psychology David Zald.

Using a brain mapping technique called positron emission tomography (PETscan), the researchers found that “go-getters” who are willing to work hard for rewards had higher release of the neurotransmitter dopamine in areas of the brain known to play an important role in reward and motivation, the striatum and ventromedial prefrontal cortex. On the other hand, “slackers” who are less willing to work hard for a reward had high dopamine levels in another brain area that plays a role in emotion and risk perception, the anterior insula.

"Past studies in rats have shown that dopamine is crucial for reward motivation," said Treadway, "but this study provides new information about how dopamine determines individual differences in the behavior of human reward-seekers."

The role of dopamine in the anterior insula came as a complete surprise to the researchers. The finding was unexpected because it suggests that more dopamine in the insula is associated with a reduced desire to work, even when it means earning less money. The fact that dopamine can have opposing effects in different parts of the brain complicates the picture regarding the use of psychotropic medications that affect dopamine levels for the treatment of attention-deficit disorder, depression and schizophrenia because it calls into question the general assumption that these dopaminergic drugs have the same effect throughout the brain.

The study was conducted with 25 healthy volunteers (52 percent female) ranging in age from 18 to 29. To determine their willingness to work for a monetary reward, the participants were asked to perform a button-pushing task. First, they were asked to select either an easy or a hard button-pushing task. Easy tasks earned $1 while the reward for hard tasks ranged up to $4. Once they made their selection, they were told they had a high, medium or low probability of getting the reward. Individual tasks lasted for about 30 seconds and participants were asked to perform them repeatedly for about 20 minutes.

"At this point, we don’t have any data proving that this 20-minute snippet of behavior corresponds to an individual’s long-term achievement," said Zald, "but if it does measure a trait variable such as an individual’s willingness to expend effort to obtain long-term goals, it will be extremely valuable."

The research is part of a larger project designed to search for objective measures for depression and other psychological disorders where motivation is reduced. “Right now our diagnoses for these disorders is often fuzzy and based on subjective self-report of symptoms,” said Zald. “Imagine how valuable it would be if we had an objective test that could tell whether a patient was suffering from a deficit or abnormality in an underlying neural system. With objective measures we could treat the underlying conditions instead of the symptoms.”

Further research is needed to examine whether similar individual differences in dopamine levels help explain the altered motivation seen in forms of mental illness such as depression and addiction. Additional research is under way to examine how medications specifically impact these motivational systems.

Source: Science Daily