RxPG News : Intelligence

How brain pacemakers erase diseased messages

Fri, 01 Jun 2007 15:59:37 PST

( from http://www.rxpgnews.com ) Brain pacemakers that have helped ease symptoms in people with Parkinson's disease and other movement disorders seem to work by drowning out the electrical signals of their diseased brains.

Despite the clinical success of the devices, which have been approved by the Food and Drug Administration and can be found in the heads of about 30,000 Americans, the mechanisms by which deep brain stimulation alleviates disease symptoms aren't well understood.

Biomedical engineers at Duke University's Pratt School of Engineering have found that stimulation administered by rapid-fire electrical pulses deep in the brain produces what they call an informational lesion. By relaying a repetitious and therefore meaningless message, constant pulses overwhelm the erratic bursts of brain activity characteristic of disease.

Periodic bursts in the brains of people with tremor -- which might follow a pattern such as 'pop-pop-pop, silence, pop-pop-pop, silence' -- propagate pathological information within brain circuits, said Warren Grill, the study's lead investigator and an associate professor of biomedical engineering. If you replace that instead with a constant 'pop-pop-pop-pop-pop-pop,' you've erased that pathological information.

Grill said the high-frequency deep brain stimulation acts like a surgical lesion, another acceptable treatment for severe tremor disorders and epilepsies. But the electronic device has the advantage of being adjustable or reversible.

The researchers' report appears in a special June 2007 issue of the journal IEEE Transactions on Neural Systems and Rehabilitation Engineering, edited in part by Grill. The study was conducted by a team that included Alexis Kuncel, a doctoral student in biomedical engineering at Duke, and Scott Cooper, a neurologist at the Cleveland Clinic, with support from the National Institutes of Health.

The FDA approved the use of deep brain stimulation for Parkinson's disease in 1997. The electrical implants are also an approved therapy for other movement disorders and are at various stages of testing for the treatment of epilepsy, depression, obsessive-compulsive disorder and pain, according to Grill.

The complexity of the brain -- in which nerves project in all directions and connect with one another to form multiple, looping networks -- makes studying how deep brain stimulation works a challenge, Grill said.

Grill's team created a mathematical model of a normally functioning brain cell. The researchers then gave the model neuron the pathological pattern of activity seen in people with tremors, assembled a group of these model cells and watched what would happen when the cells were electrically stimulated at various rates and intensities.

In addition to showing how the therapy works, their model of neurons in action also revealed that stimulation delivered at too slow a pace fails to keep bad information at bay. Indeed, slower pulses can actually add to problematic bursts, they showed.

The model's findings closely parallel the clinical responses of patients, who typically experience the greatest relief from symptoms when their devices are tuned by physicians to deliver rapid pulses, Grill said. Patients' symptoms can actually worsen when the devices are dialed to a slower setting.

The intensity of stimulation also plays an important role, the study suggests, by determining the number of brain cells affected by a particular series of pulses.

A better understanding of the processes underlying deep brain stimulation could enable physicians to better fine-tune electrical implants, Grill said. That could be particularly useful for zeroing in on effective settings for implants used to treat diseases, such as epilepsy, in which seizures occur only sporadically, as well as conditions, such as depression, in which symptoms can vary widely from day to day.

In the case of tremor, physicians can alter the setting until they see the symptoms stop, Grill said. You don't have to know how it's really working.

In a condition like epilepsy, however, it's extremely unlikely that a person would have a seizure in the doctor's office, he said. Therefore, it might take months of trial and error to find the optimal setting. Grill's new model promises to streamline the process.

Music thought to enhance intelligence

Sat, 24 Jun 2006 16:05:37 PST

( from http://www.rxpgnews.com ) A recent volume of the Annals of the New York Academy of Sciences takes a closer look at how music evolved and how we respond to it. Contributors to the volume believe that animals such as birds, dolphins and whales make sounds analogous to music out of a desire to imitate each other. This ability to learn and imitate sounds is a trait necessary to acquire language and scientists feel that many of the sounds animals make may be precursors to human music.

Another study in the volume looks at whether music training can make individuals smarter. Scientists found more grey matter in the auditory cortex of the right hemisphere in musicians compared to nonmusicians. They feel these differences are probably not genetic, but instead due to use and practice.

Listening to classical music, particularly Mozart, has recently been thought to enhance performance on cognitive tests. Contributors to this volume take a closer look at this assertion and their findings indicate that listening to any music that is personally enjoyable has positive effects on cognition. In addition, the use of music to enhance memory is explored and research suggests that musical recitation enhances the coding of information by activating neural networks in a more united and thus more optimal fashion.

Other studies in this volume look at music's positive effects on health and immunity, how music is processed in the brain, the interplay between language and music, and the relationship between our emotions and music.

Short term synaptic plasticity play a widespread role in information processing

Fri, 23 Jun 2006 00:32:37 PST

( from http://www.rxpgnews.com ) Animals' neurons, and the synapses that connect them, are constantly changing. This plasticity is thought to underlie learning and memory. Take the rat in the maze. As he learns to navigate a new environment, familiarity with the space is reflected in the neuronal activity of a small almond-shaped brain structure called the hippocampus. Neurons in the hippocampus are generally quiescent. But when the rat meanders into a spot that a specific neuron prefers, called its place field, the neuron responds with high-frequency bursts of spikes. As the rat's familiarity with the maze increases over only a few minutes, so does the reliability by which hippocampal neurons respond to their preferred place. This short-term experience modifies the neurons' responses, and very likely the synapses, although the synaptic mechanisms of short-term plasticity in this context have not been fully described.

A new study takes a step forward in understanding the most basic level of this process: the short-term plasticity at hippocampal synapses that result from processing incoming signals resembling place-field responses. The researchers, Vitaly Klyachko and Charles Stevens, discovered a novel short-term plasticity mechanism by which excitatory and inhibitory synapses can selectively amplify high-frequency bursts.

For the study, the researchers used slices of the rat's hippocampus, focusing on cells from two particular regions, called CA1 and CA3, known for their role in encoding information about the animal's position. The researchers recorded long series of this firing activity, which they then used to stimulate two classes of hippocampal neurons: excitatory neurons, whose function is to spur neurons downstream to fire; and inhibitory neurons, which suppress neurons downstream.

In the hippocampus, these neurons form basic circuit elements, among which a feed-forward loop is one of the most common. In its simplest form, these loops feature an excitatory neuron connected to both an inhibitory neuron and an output neuron, and the inhibitory neuron is also connected to the output neuron. In this simple triangular network, incoming signals trigger both the excitatory and inhibitory neurons at once, and then the inhibitory neuron activates its synapses with a delay of a few milliseconds. From the output neuron's point of view, the incoming excitatory signals are closely followed by the inhibitory ones.

Several previous studies that tried to sort out how these neurons function during processing of incoming signals that resemble natural activity failed to produce coherent outputs from the neurons. These incoherent outputs may have resulted from the fact that the neurons were held at room temperature; as Klyachko and Stevens had shown before, short-term plasticity works differently at room temperature than at body temperature. To avoid the temperature problem in this study, Klyachko and Stevens held the brain slices at near body temperature.

With short-term plasticity, a synapse's response to any one signal depends on the signals it received in the previous few seconds. Synapses can sense when they're receiving a high number of impulses per secondthat is, a high-frequency signal. Klyachko and Stevens found that, as long as the incoming signal was above a certain average rate, around 10 Hz, then the synapses would flip from a baseline state to an active state. The excitatory synapses became more excitatory, amplifying incoming signals. The inhibitory synapses responded oppositely, damping down their activity. Surprisingly, for any signals with higher frequency, these synapses' responses stayed constant even when the incoming signal rose to much higher frequencies, such as 100 Hz. The researchers also found that the excitatory and inhibitory synapses had mirror-image responses: when the excitatory synapses amplified a specific portion of a signal, the inhibitory synapses damped down their response at the same time.

When these two types of cells are wired together in a feed-forward loop, the researchers found that the excitatory and inhibitory synapses acted in concert, filtering out low-frequency signals while amplifying high-frequency signals. Thus, the study shows a function for the hippocampus's feed-forward loops not seen in earlier studies. It also shows a new role for inhibitory synapses: amplifying signals.

In this study, hippocampal neurons used short-term plasticity to filter neuronal signals for high-frequency events that encode important information for the animal. As the authors argue, this plasticity could also play a widespread role in information processing in the brain. Short-term plasticity may provide the mechanism by which animals' quickly changing brains help them navigate and comprehend the world.

Brain Rewards Curiosity with Shot of Natural Opiates

Wed, 21 Jun 2006 00:05:37 PST

( from http://www.rxpgnews.com ) Neuroscientists have proposed a simple explanation for the pleasure of grasping a new concept: The brain is getting its fix.

The "click" of comprehension triggers a biochemical cascade that rewards the brain with a shot of natural opium-like substances, said Irving Biederman of the University of Southern California. He presents his theory in an invited article in the latest issue of American Scientist.

"While you're trying to understand a difficult theorem, it's not fun," said Biederman, professor of neuroscience in the USC College of Letters, Arts and Sciences.

"But once you get it, you just feel fabulous."

The brain's craving for a fix motivates humans to maximize the rate at which they absorb knowledge, he said.

"I think we're exquisitely tuned to this as if we're junkies, second by second."

Biederman hypothesized that knowledge addiction has strong evolutionary value because mate selection correlates closely with perceived intelligence.

Only more pressing material needs, such as hunger, can suspend the quest for knowledge, he added.

The same mechanism is involved in the aesthetic experience, Biederman said, providing a neurological explanation for the pleasure we derive from art.

"This account may provide a plausible and very simple mechanism for aesthetic and perceptual and cognitive curiosity."

Biederman's theory was inspired by a widely ignored 25-year-old finding that mu-opioid receptors binding sites for natural opiates increase in density along the ventral visual pathway, a part of the brain involved in image recognition and processing.

The receptors are tightly packed in the areas of the pathway linked to comprehension and interpretation of images, but sparse in areas where visual stimuli first hit the cortex.

Biederman's theory holds that the greater the neural activity in the areas rich in opioid receptors, the greater the pleasure.

In a series of functional magnetic resonance imaging trials with human volunteers exposed to a wide variety of images, Biederman's research group found that strongly preferred images prompted the greatest fMRI activity in more complex areas of the ventral visual pathway. (The data from the studies are being submitted for publication.)

Biederman also found that repeated viewing of an attractive image lessened both the rating of pleasure and the activity in the opioid-rich areas. In his article, he explains this familiar experience with a neural-network model termed "competitive learning."

In competitive learning (also known as "Neural Darwinism"), the first presentation of an image activates many neurons, some strongly and a greater number only weakly.

With repetition of the image, the connections to the strongly activated neurons grow in strength. But the strongly activated neurons inhibit their weakly activated neighbors, causing a net reduction in activity. This reduction in activity, Biederman's research shows, parallels the decline in the pleasure felt during repeated viewing.

"One advantage of competitive learning is that the inhibited neurons are now free to code for other stimulus patterns," Biederman writes.

This preference for novel concepts also has evolutionary value, he added.

"The system is essentially designed to maximize the rate at which you acquire new but interpretable [understandable] information. Once you have acquired the information, you best spend your time learning something else.

"There's this incredible selectivity that we show in real time. Without thinking about it, we pick out experiences that are richly interpretable but novel."

The theory, while currently tested only in the visual system, likely applies to other senses, Biederman said.

Dysbindin-1 gene (DTNBP1) - The Intelligence Gene

Sun, 30 Apr 2006 23:09:37 PST

( from http://www.rxpgnews.com ) Psychiatric researchers at The Zucker Hillside Hospital campus of The Feinstein Institute for Medical Research have uncovered evidence of a gene that appears to influence intelligence. Working in conjunction with researchers at Harvard Partners Center for Genetics and Genomics in Boston, the Zucker Hillside team examined the genetic blueprints of individuals with schizophrenia, a neuropsychiatric disorder characterized by cognitive impairment, and compared them with healthy volunteers.

They discovered that the dysbindin-1 gene (DTNBP1), which they previously demonstrated to be associated with schizophrenia, may also be linked to general cognitive ability.

"A robust body of evidence suggests that cognitive abilities, particularly intelligence, are significantly influenced by genetic factors. Existing data already suggests that dysbindin may influence cognition," said Katherine Burdick, PhD, the study's primary author. "We looked at several DNA sequence variations within the dysbindin gene and found one of them to be significantly associated with lower general cognitive ability in carriers of the risk variant compared with non-carriers in two independent groups."

The study involved 213 unrelated Caucasian patients with schizophrenia or schizoaffective disorder and 126 unrelated healthy Caucasian volunteers. The researchers measured cognitive performance in all subjects. They then analyzed participants' DNA samples. The researchers specifically examined six DNA sequence variations, also known as single nucleotide polymorphisms (SNPs), in the dysbindin gene and found that one specific pattern of SNPs, known as a haplotype, was associated with general cognitive ability: Cognition was significantly impaired in carriers of the risk variant in both the schizophrenia group and the healthy volunteers as compared with the non-carriers.

"While our data suggests the dysbindin gene influences variation in human cognitive ability and intelligence, it only explained a small proportion of it -- about 3 percent. This supports a model involving multiple genetic and environmental influences on intelligence," said Anil Malhotra, MD, principal investigator of the study.

The specific role of dysbindin in the central nervous system is unknown, but it is highly present in key brain regions linked to cognition, including learning, problem solving, judgment, memory and comprehension. Scientists speculate that dysbindin plays a role in communication between brain cells in these regions and helps promote their survival. An alteration in the genetic blueprint for dysbindin may ultimately interfere with cell communication and fail to protect brain cells from dying, with a resulting negative impact on cognition and intelligence.

Brains of the smarter kids tend to change more dramatically

Thu, 30 Mar 2006 15:02:37 PST

( from http://www.rxpgnews.com ) Brains of the smarter kids tend to change more dramatically as they grow up, say scientists who claim to have discovered why some children have higher IQ levels.

Scientists led by Philip Shaw at the US National Institute of Mental Health and McGill University in Montreal, Canada, studied 307 children and teenagers between the ages of five and 19 using imaging machines to track growth in the part of the brain that helps a person think.

Using the Wechsler intelligence scale, the children were grouped according to superior, high and average intelligence.

The study found that the brains tissue in children with the highest IQ levels starts out thinner, then thickens more quickly and for a longer time than in their peers, the researchers said.

The findings, along with previous research in animals, suggest intelligence is linked to a complex sculpting or fine-tuning of the brain as a child develops, Shaw said.

'From animal studies, there is some suggestion that there is a process of 'use it or lose it' as the brain matures. Perhaps this is happening particularly efficiently in the most intelligent children,' he said.

Scientists need to do more research before they understand what causes that development. 'We have no idea what's happening at the level of the cell that's driving all of the changes.'

Brain size matters for intellectual ability

Fri, 23 Dec 2005 18:52:38 PST

( from http://www.rxpgnews.com ) Brain size matters for intellectual ability and bigger is better, McMaster University researchers have found.

The study, led by neuroscientist Sandra Witelson, a professor in the Michael G. DeGroote School of Medicine, and published in the December issue of the journal Brain, has provided some of the clearest evidence on the underlying basis of differences in intelligence.

The study involved testing of intelligence in 100 neurologically normal, terminally ill volunteers, who agreed that their brains be measured after death.

It found bigger is better, but there are differences between women and men.

In women, verbal intelligence was clearly correlated with brain size, accounting for 36 percent of the verbal IQ score. In men, this was true for right-handers only, indicating that brain asymmetry is a factor in men.

Spatial intelligence was also correlated with brain size in women, but less strongly. In men, spatial ability was not related to overall brain size. These results suggest that women may use verbal strategies in spatial thinking, but that in men, verbal and spatial thinking are more distinct.

It may be that the size or structure of the localized brain regions which underlie spatial skills in men is related to spatial intelligence, as was shown in previous research in Witelson's lab on the brain of Albert Einstein.

In a further sex difference, brain size decreased with age in men over the age span of 25 to 80 years, but age hardly affected brain size in women. It is not known what protective factors, which could be genetic, hormonal or environmental, operate in women.

It remains to be determined what the contribution of nature and nurture are to this cerebral size relationship with intelligence, Witelson said. She added that the results point to the need for responsibility in considering the likely future use of magnetic imaging (or MRIs) of brain structure as a measure of ability in student and workforce settings.

"We're going to need to be careful if, in the future, we use MRI brain scans as a measure of ability in any selection process," she said.