Neuroscience

Articles and news from the latest research reports.

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Fear study reveals mental processes

July 25, 2012

A University study has shown how our minds unconsciously respond to threats.

Researchers studying how our minds develop fears in response to danger found that people can quickly learn to recognise a threat even when they are unaware of it.

However, they also found that this learning is swiftly forgotten. In contrast, when people are aware of the threat, they take longer to learn to be afraid of it, but retain the fear in the long term.

Scientists from the University of Edinburgh and New York University, who carried out the study, say the finding may be a key insight into the differences between conscious and nonconscious mental processes.

Fear study

Researchers measured physiological fear responses - the amount of sweat on the fingertips - in groups of people who looked at pictures and were given mild electric shocks whenever one of these pictures was shown.

All the people who participated in the study saw the pictures with just one eye. But whereas some of them were allowed to see the pictures clearly, the researchers suppressed the pictures from other subjects’ awareness by showing colourful, dynamic images to the other eye.

The study found that subjects who were prevented from consciously seeing the pictures learned to be afraid of the image associated with a shock more quickly than those who were allowed to see them without suppression.

However, these subjects quickly forgot this association between the images and the electric shocks as the experiment continued.

In contrast, those subjects who were allowed to see the image clearly formed a stronger association over time.

How the brain reacts to threats is key to understanding how human beings function. This study shows that we are capable of learning very rapidly that something is a threat even when we don’t perceive it consciously. Such learning, however, is fleeting.
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David Carmel, Researcher, Department of Psychology

Source: The University of Edinburgh

Filed under science neuroscience brain psychology emotions fear mental processes conscious nonconscious research learning

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Building a human on a chip, organ by organ

Human “organs on chips” could be linked to make the ideal guinea pig, revolutionising the way drugs are tested and cancer is treated

Such organs on chips can be used to model how human organs function and respond to drugs, says Ingber. He thinks that they even have the potential to eliminate the use of animals in drug testing. “Animal testing is expensive and time-consuming, and animals are not always representative of humans.”

Still, Ingber points out that the chips can perform some roles that animal studies cannot. For instance, they could be personalised by building them from an individual’s own cells. In theory, a doctor could send tissue samples to a lab to test a potentially harmful therapy on such a chip before handing out a prescription. This would be especially useful for people with cancer, as the various therapies available can have very different effects on different people, Ingber says. “You could get a quick yes-or-no answer to whether a drug would work or not,” he says.

Personalised chips might also speed up clinical trials. “Someday it might be possible to shortcut clinical trials by using chips containing cells from different human populations that are known to respond differently to specific drug classes,” Ingber says.

Filed under cancer chips drugs human organs medicine neuroscience pharmacology research science animal studies

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Shortened telomere length tied to dementia, mortality risk

July 25, 2012

(HealthDay) — Shortened telomere length (TL) is associated with risks for dementia and mortality in a population of older adults, according to a study published online July 23 in the Archives of Neurology.

Lawrence S. Honig, M.D., Ph.D., from the Columbia University College of Physicians and Surgeons in New York City, and colleagues used real-time polymerase chain reaction analysis to determine TL in stored leukocyte DNA from 1,983 participants in a community-based study of aging. Participants were 65 years or older and blood was drawn at a mean age of 78.3 years. Participants were followed for a median of 9.3 years for mortality, and 9.6 percent developed incident dementia.

The researchers found that TL correlated inversely with age and was shorter in men than women. TL was significantly shorter in persons dying during follow-up compared with survivors, even after adjusting for age, sex, education, and apolipoprotein E genotype. TL was significantly shorter in the participants with incident and prevalent dementia, compared with those who remained dementia-free. Shorter TL correlated with earlier onset of dementia but this association was significant in women only.

"Our results show an association between shortened TL and mortality, and more specifically an association of shortened TL with Alzheimer’s disease, and are consistent with but not indicative of the possibility that TL may be a factor indicative of biological age," the authors conclude.

Source: medicalxpress.com

Filed under science neuroscience psychology brain telomere dementia mortality alzheimer alzheimer's disease research

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Californian biotech firm Life Technologies is the first team to register for the $10 million (£6.4m) Archon Genomics X Prize, which will be a race to sequence the genomes of 100 centenarians.
The prize was first announced in 2006, and is a joint effort between the X Prize Foundation and geneticist J Craig Venter. It’s supposed to stimulate the development of less expensive sequencing technologies, and establish a clinical standard for DNA research.
Interested parties have until May 2013 to register. Late that year, in September, each team will have 30 days to sequence the genomes of 100 people, at a cost of $1,000 (£643) or less.
The DNA has been donated by 100 100 year old people from all over the world, to make the competition “scientifically valuable and more meaningful to the general public”. That way, the prize can double up as medical research into the science of healthy aging and longevity.
Life Technologies’ secret weapon is the Ion Proton Sequencer, which it describes as a “semiconductor device that enables chemical signals to be directly translated into digital information for the first time” — a bit like the CMOS imager in an iPhone, which turns photons into electrons.
"It would have cost $100 million and taken 33 years to meet this challenge when the competition was announced in 2006," said Jonathan Rothberg, CEO and founder of Life Technology’s Ion Torrent brand. "The Ion Proton sequencer is designed to sequence a human genome for $1,000 in just a few hours."

Source: Wired

Californian biotech firm Life Technologies is the first team to register for the $10 million (£6.4m) Archon Genomics X Prize, which will be a race to sequence the genomes of 100 centenarians.

The prize was first announced in 2006, and is a joint effort between the X Prize Foundation and geneticist J Craig Venter. It’s supposed to stimulate the development of less expensive sequencing technologies, and establish a clinical standard for DNA research.

Interested parties have until May 2013 to register. Late that year, in September, each team will have 30 days to sequence the genomes of 100 people, at a cost of $1,000 (£643) or less.

The DNA has been donated by 100 100 year old people from all over the world, to make the competition “scientifically valuable and more meaningful to the general public”. That way, the prize can double up as medical research into the science of healthy aging and longevity.

Life Technologies’ secret weapon is the Ion Proton Sequencer, which it describes as a “semiconductor device that enables chemical signals to be directly translated into digital information for the first time” — a bit like the CMOS imager in an iPhone, which turns photons into electrons.

"It would have cost $100 million and taken 33 years to meet this challenge when the competition was announced in 2006," said Jonathan Rothberg, CEO and founder of Life Technology’s Ion Torrent brand. "The Ion Proton sequencer is designed to sequence a human genome for $1,000 in just a few hours."

Source: Wired

Filed under Archon Genomics X prize DNA biology genetics genomics ion proton sequencer medicine neuroscience psychology research science technology X prize foundation ageing

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Multiple sclerosis drug disappoints on disability

July 23, 2012 By David Orenstein

(Medical Xpress) — This week the Journal of the American Medical Association published a study with unfortuate news for the millions of people who suffer from multiple sclerosis. In the large study, a therapy known as interferon beta failed to stave off the progression of the incurable disease. Albert Lo, associate professor of neurology and epidemiology, comments on what the study means for patients, why it was well-designed, and how a new effort to support research on the disease in Rhode Island could help.

The results of this study with nearly 2,700 participants showed that treatment with interferon beta, which is a major class of disease-modifying therapy for multiple sclerosis, did not prevent progression of disability, which is very disappointing from a therapeutic perspective. Currently, there is no cure for MS, and as a lifelong disorder of the nervous system, MS is characterized by episodic relapses of neurological injury such as weakness or blindness. While in most cases, there is a varying degree of recovery after relapses, over time, disability accumulates. The accumulation of deficits and the loss of physical and mental function is a major concern for people with MS and their clinicians.

Currently, there is no medication on the market that is directed explicitly for neuroprotection and the prevention of disability. Many had hoped that the interferons, along with the other disease-modifying agents (which were developed to reduce relapse rates) would also have a significant effect on protecting patients from MS disability.

Although the results from this study were not as we would have hoped, they reflect a marked improvement over prior studies which used known methodologic flaws. The new results from the Tremlett group point to the importance of the research methodology used (prospectively collected longitudinal study data) and a well-controlled design to generate the results – approaches that we are using in our own research at Brown University.

A number of the early studies examining the effect of interferons on disability primarily used patient sample groups of convenience for post-marketing studies. They indicated that interferons were in fact preventing disability. However, using samples of convenience inherently includes a number of biases and problems. Dr. Tremlett’s results were generated from a more systematic longitudinal study in which biases and shortcomings can be better addressed. Therefore, making conclusions and clinical decisions from the results is more reliable. These data both will help in making clinical decisions on treating MS patients during the later course of their disease, when there are virtually no relapses, and will help to point more urgently toward the clinical need of an agent to prevent disability.

Provided by Brown University

Source: medicalxpress.com

Filed under MS disease drug health medication neuroscience psychology science research

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More than 125 years ago, Santiago Ramón y Cajal was able to draft and prove the neuron doctrine, and later, to develop prophetic theories about neural function and plasticity, many of which have been proven by current neuroscience.It was chance that made Cajal, during his doctorate studies, have his first contact with histology and force him to study the then current theories about pathogenesis of inflammation.Thus, he gained knowledge of the vascular hypothesis, by Julius Cohnheim, a German pathologist who, opposing the opinion of his teacher and father of cellular pathology, Rudolf Virchow, made leukocytes the protagonists of inflammation, given their ability to develop ameboid movements directed by chemical signals. Cohnheim’s chemotactic theory deeply influenced Cajal’s conception of biology. So, the basic postulates of chemotaxis can be identified at different moments in Cajal’s research, from the description of the “growth cone” in embryonic neuroblasts, the origin of the neurotrophic theory, to the proposal of the pathophysiological mechanisms of neuronal plasticity.From Cajal’s point of view, the neurons move during their development and also adapt to different external circumstances. Chemical endogenous substances can stimulate this movement in a similar way to leukocytes during the process of inflammation.

Source: Neuroscience, Volume 217, Pages 1-5 (16 August 2012)

More than 125 years ago, Santiago Ramón y Cajal was able to draft and prove the neuron doctrine, and later, to develop prophetic theories about neural function and plasticity, many of which have been proven by current neuroscience.

It was chance that made Cajal, during his doctorate studies, have his first contact with histology and force him to study the then current theories about pathogenesis of inflammation.

Thus, he gained knowledge of the vascular hypothesis, by Julius Cohnheim, a German pathologist who, opposing the opinion of his teacher and father of cellular pathology, Rudolf Virchow, made leukocytes the protagonists of inflammation, given their ability to develop ameboid movements directed by chemical signals. Cohnheim’s chemotactic theory deeply influenced Cajal’s conception of biology. So, the basic postulates of chemotaxis can be identified at different moments in Cajal’s research, from the description of the “growth cone” in embryonic neuroblasts, the origin of the neurotrophic theory, to the proposal of the pathophysiological mechanisms of neuronal plasticity.

From Cajal’s point of view, the neurons move during their development and also adapt to different external circumstances. Chemical endogenous substances can stimulate this movement in a similar way to leukocytes during the process of inflammation.

Source: Neuroscience, Volume 217, Pages 1-5 (16 August 2012)

Filed under science neuroscience brain psychology modern neuroscience Cajal research neuron plasticity histology inflammation leukocytes biology

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Nocebo Effect, Not Placebo Effect: Induced Illness Studied

ScienceDaily (July 12, 2012) — Negative suggestion can induce symptoms of illness. Nocebo effects are the adverse events that occur during sham treatment and/or as a result of negative expectations. While the positive counterpart — the placebo effect — has been intensively studied in recent years, the scientific literature contains few studies on nocebo phenomena. In the latest issue of Deutsches Ärzteblatt International, Winfried Häuser of the Technical University of Munich and his co-authors present the underlying neurobiological mechanisms and highlight the relevance of the nocebo effect in everyday clinical practice.

Nocebo responses can, for instance, be brought about by unintended negative suggestion on the part of doctors or nurses, e.g., when informing the patient about the possible complications of a proposed treatment. It is also assumed that a certain proportion of the undesired effects of drugs can be attributed to nocebo effects. The mechanisms behind this phenomenon are — as with placebo effects — learning by Pavlovian conditioning and reaction to induced expectations.

What are the consequences for clinical practice? Doctors find themselves in an ethical dilemma between their obligation to tell the patient about the possible side effects of a treatment and their duty to minimize the risk of a medical intervention and thus to avoid triggering nocebo effects. As one possible strategy to solve this dilemma, Häuser et al. suggest emphasizing the tolerability of therapeutic measures. Another option, with the patient’s permission, would be to desist from discussing undesired effects during the patient briefing.

Source: Science Daily

Filed under science neuroscience psychology placebo nocebo research

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