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Posts Tagged ‘brain

Get Rhythm – Intelligence And Rhythmic Accuracy Go Hand In Hand

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People who score high on intelligence tests are also good at keeping time, new Swedish research shows. The team that carried out the study also suspect that accuracy in timing is important to the brain processes responsible for problem solving and reasoning.

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Researchers at the medical university Karolinska Institutet and Umeå University have now demonstrated a correlation between general intelligence and the ability to tap out a simple regular rhythm. They stress that the task subjects performed had nothing to do with any musical rhythmic sense but simply measured the capacity for rhythmic accuracy. Those who scored highest on intelligence tests also had least variation in the regular rhythm they tapped out in the experiment.

“It’s interesting as the task didn’t involve any kind of problem solving,” says Fredrik Ullén at Karolinska Institutet, who led the study with Guy Madison at Umeå University. “Irregularity of timing probably arises at a more fundamental biological level owing to a kind of noise in brain activity.”

According to Fredrik Ullén, the results suggest that the rhythmic accuracy in brain activity observable when the person just maintains a steady beat is also important to the problem-solving capacity that is measured with intelligence tests.

“We know that accuracy at millisecond level in neuronal activity is critical to information processing and learning processes,” he says.

They also demonstrated a correlation between high intelligence, a good ability to keep time, and a high volume of white matter in the parts of the brain’s frontal lobes involved in problem solving, planning and managing time.

“All in all, this suggests that a factor of what we call intelligence has a biological basis in the number of nerve fibres in the prefrontal lobe and the stability of neuronal activity that this provides,” says Fredrik Ullén.

J Neurosci. 2008 Apr 16;28(16):4238-43.
Intelligence and variability in a simple timing task share neural substrates in the prefrontal white matter.

Neuropediatric Research Unit Q2:07, Department of Woman and Child Health, Karolinska Institutet, SE-171 77 Stockholm, Sweden. fredrik.ullen@ki.se

General intelligence is correlated with the mean and variability of reaction time in elementary cognitive tasks, as well as with performance on temporal judgment and discrimination tasks. This suggests a link between the temporal accuracy of neural activity and intelligence. However, it has remained unclear whether this link reflects top-down mechanisms such as attentional control and cognitive strategies or basic neural properties that influence both abilities. Here, we investigated whether millisecond variability in a simple, automatic timing task, isochronous tapping, correlates with intellectual performance and, using voxel-based morphometry, whether these two tasks share neuroanatomical substrates. Stability of tapping and intelligence were correlated and related to regional volume in overlapping right prefrontal white matter regions. These results suggest a bottom-up explanation of the link between temporal stability and intellectual performance, in which more extensive prefrontal connectivity underlies individual differences in both variables.

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Written by huehueteotl

April 21, 2008 at 8:45 am

Genetic Factor In Stress Response Variability Discovered

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Inherited variations in the amount of an innate anxiety-reducing molecule help explain why some people can withstand stress better than others, according to a new study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH).

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“Stress response is an important variable in vulnerability to alcohol dependence and other addictions, as well as other psychiatric disorders,” noted NIAAA Director Ting-Kai Li, M.D. “This finding could help us understand individuals’ initial vulnerability to these disorders.”

Scientists led by David Goldman, M. D., chief of the NIAAA Laboratory of Neurogenetics, identified gene variants that affect the expression of a signaling molecule called neuropeptide Y (NPY). Found in brain and many other tissues, NPY regulates diverse functions, including appetite, weight, and emotional responses.

“NPY is induced by stress and its release reduces anxiety,” said Dr. Goldman. “Previous studies have shown that genetic factors play an important role in mood and anxiety disorders. In this study, we sought to determine if genetic variants of NPY might contribute to the maladaptive stress responses that often underlie these disorders.” A report of the findings appears online today in Nature.

Analyses of human tissue samples led by researchers at NIAAA identified several NPY gene variants. Collaborations with NIH-supported scientists at the University of Michigan, University of Pittsburgh, University of Helsinki, University of Miami, University of Maryland, the University of California at San Diego, and Yale University, showed that these variants result in a range of different effects including altered levels of NPY in brain and other tissues, and differences in emotion and emotion-induced responses of the brain.

The researchers evaluated the NPY gene variants’ effects on brain responses to stress and emotion. Using functional brain imaging, they found that individuals with the variant that yielded the lowest level of NPY reacted with heightened emotionality to images of threatening facial expressions. “Metabolic activity in brain regions involved in emotional processing increased when these individuals were presented with the threatening images,” explained Dr. Goldman.

In another brain imaging experiment, people with the low level NPY variant were found to have a diminished ability to tolerate moderate levels of sustained muscular pain. Previous studies had shown that NPY’s behavioral effects are mediated through interactions with opioid compounds produced by the body to help suppress pain, stress, and anxiety. “As shown by brain imaging of opioid function, these individuals released less opioid neurotransmitter in response to muscle discomfort than did individuals with higher levels of NPY,” said Dr. Goldman. “Their emotional response to pain was also higher, showing the close tie between emotionality and resilience to pain and other negative stimuli.”

In a preliminary finding, the low level NPY gene variant was found to be more common than other variants among a small sample of individuals with anxiety disorders. The researchers also found that low level NPY expression was linked to high levels of trait anxiety. “Trait anxiety is an indication of an individual’s level of emotionality or worry under ordinary circumstances,” explained Dr. Goldman.

The researchers conclude that these converging findings are consistent with NPY’s role as an anxiety-reducing peptide and help explain inter-individual variation in resiliency to stress. “This inherited functional variation could also open up new avenues of research for other human characteristics, such as appetite and metabolism, which are also modulated by NPY,” said Dr. Goldman.

Nature. 2008 Apr 2 [Epub ahead of print]
Genetic variation in human NPY expression affects stress response and emotion.

[1] Laboratory of Neurogenetics, NIAAA, NIH, Bethesda, Maryland 20892, USA [2] These authors contributed equally to this work.

Understanding inter-individual differences in stress response requires the explanation of genetic influences at multiple phenotypic levels, including complex behaviours and the metabolic responses of brain regions to emotional stimuli. Neuropeptide Y (NPY) is anxiolytic and its release is induced by stress. NPY is abundantly expressed in regions of the limbic system that are implicated in arousal and in the assignment of emotional valences to stimuli and memories. Here we show that haplotype-driven NPY expression predicts brain responses to emotional and stress challenges and also inversely correlates with trait anxiety. NPY haplotypes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY. Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency as assessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain regions. A single nucleotide polymorphism (SNP rs16147) located in the promoter region alters NPY expression in vitro and seems to account for more than half of the variation in expression in vivo. These convergent findings are consistent with the function of NPY as an anxiolytic peptide and help to explain inter-individual variation in resiliency to stress, a risk factor for many diseases.

Written by huehueteotl

April 7, 2008 at 2:51 pm

Damaged Brain Can Be Repaired, Study Suggests

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Scientists in the Laboratoire de Neurobiologie des Processus Adaptatifs (CNRS/Université Pierre et Marie Curie) have shown that it is possible to repair an injured brain by creating a small number of new, specifically-targeted innervations, rather than a larger number of non-specific connections. Behavioral tests have demonstrated that such reinnervation can thus restore damaged cerebral functions.

A new afference/connection (in red) which has formed contacts on a target Purkinje cell (in blue), permitting functional restoration. (Credit: Copyright Dixon Kirsty)
Brain injury in adults can cause irreparable, long-term physical and cognitive damage. However, motor and spatial functions can be recovered if undamaged neurons are stimulated to create new innervation. This type of innervation develops spontaneously after a brain injury in very young children.

Researchers had previously shown – based on injury to the neuronal pathway linking the stem to the cerebellum(1) – it was possible to induce reinnervation in young adults similar to that observed in newborn infants. This repair was rendered possible by treating the damaged cerebellum with a peptide(2) called Brain Derived Neurotrophic Factor (BDNF) which plays a role in the development and satisfactory functioning of this neuronal pathway.

In the present case, the researchers have extended the use of this model and showed that the terminals of new axons interact with the network of undamaged neuronal cells to restore their associated functions, such as synchronized movement and spatial orientation. These results demonstrate a correlation between an improvement in behavior and the degree of reinnervation in the cerebellum. Thus a small amount of correctly-targeted reinnervation makes it possible to recover fine functions such as motor and cognitive skills.

These results open promising new perspectives and make it possible to envisage using BDNF – already employed during clinical trials on the treatment of neurodegenerative conditions such as Parkinson’s disease – to repair the human brain after a cerebral lesion.

Notes:

1) This neuronal pathway is referred to as the cerebellum to Purkinje cell climbing fiber pathway and it is implicated in the coordination of movements.

2) A protein that is normally present in the brain and is involved in its development and functioning.

Brain. 2008 Apr;131(Pt 4):1099-112. Epub 2008 Feb 25.
BDNF increases homotypic olivocerebellar reinnervation and associated fine motor and cognitive skill.
Université Pierre et Marie Curie-Paris 6, Unité Mixte de Recherche (UMR) 7102-Neurobiologie des Processus Adaptatifs (NPA), Centre National de la Recherche Scientifique (CNRS), UMR 7102-NPA, F-75005 Paris, France.

Recovery of complex neural function after injury to the adult CNS is limited by minimal spontaneous axonal regeneration and/or sprouting from remaining pathways. In contrast, the developing CNS displays spontaneous reorganization following lesion, in which uninjured axons can develop new projections to appropriate target neurons and provide partial recovery of complex behaviours. Similar pathways can be induced in the mature CNS, providing models to optimize post-injury recovery of complex neural functions. After unilateral transection of a developing olivocerebellar path (pedunculotomy), remaining inferior olivary axons topographically reinnervate the denervated hemicerebellum and compensate functional deficits. Brain-derived neurotrophic factor (BDNF) partly recreates such reinnervation in the mature cerebellum. However the function of this incomplete reinnervation and any unwanted behavioural effects of BDNF remain unknown. We measured olivocerebellar reinnervation and tested rotarod and navigation skills in Wistar rats treated with BDNF/vehicle and pedunculotomized on day 3 (Px3; with reinnervation) or 11 (Px11; without spontaneous reinnervation). BDNF treatment did not affect motor or spatial behaviour in normal (control) animals. Px11-BDNF animals equalled controls on the rotarod, outperforming Px11-vehicle animals. Moreover, Px3-BDNF and Px11-BDNF animals achieved spatial learning and memory tasks as well as controls, with Px11-BDNF animals showing better spatial orientation than Px11-vehicle counterparts. BDNF slightly increased olivocerebellar reinnervation in Px3 animals and induced sparse (22% Purkinje cells) yet widespread reinnervation in Px11 animals. As reinnervation correlated with spatial function, these data imply that after injury even a small amount of reinnervation that is homotypic to correct target neurons compensates deficits in appropriate complex motor and spatial skills. As there was no effect in control animals, BDNF effectively induces this axon collateralisation without interfering with normal neuronal circuits.

Written by huehueteotl

April 7, 2008 at 8:52 am

Neural Basis Of ‘Number Sense’ In Young Infants

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Behavioral experiments indicate that infants aged 4½ months or older possess an early “number sense” that allows them to detect changes in the number of objects.
Distinct cerebral pathways for object identity and number have been identified in the brain of human infants. (Credit: Izard V, Dehaene-Lambertz G, Dehaene S)

However, the neural basis of this ability was previously unknown.

In new research, Véronique Izard, Ghislaine Dehaene-Lambertz, and Stanislas Dehaene provide brain imaging evidence showing that very young infants are sensitive to both the number and identity of objects, and these pieces of information are processed by distinct neural pathways.

The authors recorded the electrical activity evoked by the brain on the surface of the scalp as 3-months-old infants were watching images of objects. The number or identity of objects occasionally changed.

The authors found that the infant brain responds to both changes, but in different brain regions, which map onto the same regions that activate in adults. These results show that very young infants are sensitive to small changes in number, and the brain organization that underlies the perception of object number and identity are established early during development.

PLoS Biology Vol. 6, No. 2, e11 doi:10.1371/journal.pbio.0060011

Distinct Cerebral Pathways for Object Identity and Number in Human Infants

Izard V, Dehaene-Lambertz G, Dehaene S 

All humans, regardless of their culture and education, possess an intuitive understanding of number. Behavioural evidence suggests that numerical competence may be present early on in infancy. Here, we present brain-imaging evidence for distinct cerebral coding of number and object identity in 3-mo-old infants. We compared the visual event-related potentials evoked by unforeseen changes either in the identity of objects forming a set, or in the cardinal of this set. In adults and 4-y-old children, number sense relies on a dorsal system of bilateral intraparietal areas, different from the ventral occipitotemporal system sensitive to object identity. Scalp voltage topographies and cortical source modelling revealed a similar distinction in 3-mo-olds, with changes in object identity activating ventral temporal areas, whereas changes in number involved an additional right parietoprefrontal network. These results underscore the developmental continuity of number sense by pointing to early functional biases in brain organization that may channel subsequent learning to restricted brain areas.

Written by huehueteotl

February 11, 2008 at 9:39 am

Brain Less Coordinated With Age, Even In The Absence Of Disease

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Some brain systems become less coordinated with age even in the absence of Alzheimer’s disease, according to a new study from Harvard University. The results help to explain why advanced age is often accompanied by a loss of mental agility, even in an otherwise healthy individual.

The study was led by Jessica Andrews-Hanna, a doctoral candidate in the Department of Psychology in the Faculty of Arts and Sciences at Harvard.

“This research helps us to understand how and why our minds change as we get older, and why some individuals remain sharp into their 90s, while others’ mental abilities decline as they age,” says Andrews-Hanna. “One of the reasons for loss of mental ability may be that these systems in the brain are no longer in sync with one another.”

Previous studies have focused on the specific structures and functions within the brain, and how their deterioration might lead to decreased cognitive abilities. However, this study examined the way that large-scale brain systems that support higher-level cognition correlate and communicate across the brain, and found that in older adults these systems are not in sync. In particular, widely separated systems from the front to the back of the brain were less correlated.

The human brain can be divided into major functional regions, each responsible for different kinds of “applications,” such as memory, sensory input and processing, executive function or even one’s own internal musing. The functional regions of the brain are linked by a network of white matter conduits. These communication channels help the brain coordinate and share information from the brain’s different regions. White matter is the tissue through which messages pass from different regions of the brain.

Scientists have known that white matter degrades with age, but they did not understand how that decline contributes to the degradation of the large-scale systems that govern cognition.

“The crosstalk between the different parts of the brain is like a conference call,” said Jessica Andrews-Hanna, a graduate student in Buckner’s lab and the lead author of the study. “We were eavesdropping on this crosstalk and we looked at how activity in one region of the brain correlates with another.”

The researchers studied 55 older adults, approximately age 60 and over, and 38 younger adults, approximately age 35 and younger. They used a neuroimaging technique called fMRI to obtain a picture of activity in the brain. The results showed that among the younger people, brain systems were largely in sync with one another, while this was not the case with the older individuals.

Among the older individuals, some of the subjects’ brains systems were correlated, and older individuals that performed better on psychometric tests were more likely to have brain systems that were in sync. These psychometric tests, administered in addition to the fMRI scanning, measured memory ability, processing speed and executive function.

Among older individuals whose brain systems did not correlate, all of the systems were not affected in the same way. Different systems process different kinds of information, including the attention system, used to pay attention, and the default system, used when the mind is wandering. The default system was most severely disrupted with age. Some systems do remain intact; for example, the visual system was very well preserved. The study also showed that the white matter of the brain, which connects the different regions of the brain, begins to lose integrity with age.

One of the challenges to studying the aging brain is that the early signs of Alzheimer’s disease are very subtle, and it is difficult to distinguish between the early stages of Alzheimer’s disease and normal aging. In order to ensure that the researchers were only looking at healthy aging brains, the researchers used a PET scanning process to identify the presence of amyloid, a chemical present in individuals with Alzheimer’s. When the presence of this chemical was detected, individuals were not included in the study. In this way, the researchers ensured that they were looking at a healthy aging brain.

“Understanding why we lose cognitive function as we age may help us to prolong our mental abilities later in life,” says Buckner. “The results of this study help us to understand how the aging brain differs from the brain of a younger individual.”

This research was published in the Dec. 6 issue of Neuron. Other researchers involved in this study include Justin Vincent, a graduate student in the Department of Psychology at Harvard and Randy Buckner, Harvard professor of psychology and an investigator with the Howard Hughes Medical Institute. Co-authors also include Andrew Snyder, Denise Head and Marcus Raichle of Washington University in St. Louis and Cindy Lustig of the University of Michigan.

The research was funded by the National Institutes of Health, the Alzheimer’s Association, and the Howard Hughes Medical Institute.

Neuron. 2007 Dec 6;56(5):924-35.

Disruption of large-scale brain systems in advanced aging.

Andrews-Hanna JR, Snyder AZ, Vincent JL, Lustig C, Head D, Raichle ME, Buckner RL.

Department of Psychology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA; Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA 02129, USA.

Cognitive decline is commonly observed in advanced aging even in the absence of disease. Here we explore the possibility that normal aging is accompanied by disruptive alterations in the coordination of large-scale brain systems that support high-level cognition. In 93 adults aged 18 to 93, we demonstrate that aging is characterized by marked reductions in normally present functional correlations within two higher-order brain systems. Anterior to posterior components within the default network were most severely disrupted with age. Furthermore, correlation reductions were severe in older adults free from Alzheimer’s disease (AD) pathology as determined by amyloid imaging, suggesting that functional disruptions were not the result of AD. Instead, reduced correlations were associated with disruptions in white matter integrity and poor cognitive performance across a range of domains. These results suggest that cognitive decline in normal aging arises from functional disruption in the coordination of large-scale brain systems that support cognition.

Written by huehueteotl

December 7, 2007 at 1:52 pm