Gaze fixations predict brain activation during the voluntary regulation of picture-induced negative affect

Recent studies have identified a distributed network of brain regions thought to support cognitive reappraisal processes underlying emotion regulation in response to affective images, including parieto-temporal regions and lateral/medial regions of prefrontal cortex (PFC). A number of these commonly activated regions are also known to underlie visuospatial attention and oculomotor control, which raises the possibility that people use attentional redeployment rather than, or in addition to, reappraisal as a strategy to regulate emotion. We predicted that a significant portion of the observed variance in brain activation during emotion regulation tasks would be associated with differences in how participants visually scan the images while regulating their emotions. We recorded brain activation using fMRI and quantified patterns of gaze fixation while participants increased or decreased their affective response to a set of affective images. fMRI results replicated previous findings on emotion regulation with regulation differences reflected in regions of PFC and the amygdala. In addition, our gaze fixation data revealed that when regulating, individuals changed their gaze patterns relative to a control condition. Furthermore, this variation in gaze fixation accounted for substantial amounts of variance in brain activation. These data point to the importance of controlling for gaze fixation in studies of emotion regulation that use visual stimuli.

Watching the infant brain learn words: Effects of vocabulary size and experience

Previous investigations comparing auditory event-related potentials (ERPs) to words whose meanings infants did or did not comprehend, found bilateral differences in brain activity to known versus unknown words in 13-month-old infants, in contrast with unilateral, left hemisphere, differences in activity in 20-month-old infants. We explore two alternative explanations for these findings. Changes in hemispheric specialization may result from a qualitative shift in the way infants process known words between 13 and 20 months. Alternatively, hemispheric specialization may arise from increased familiarity with the individual words tested. We contrasted these two explanations by measuring ERPs from 20-month-old infants with high and low production scores, for novel words they had just learned. A bilateral distribution of ERP differences was observed in both groups of infants, though the difference was larger in the left hemisphere for the high producers. These findings suggest that word familiarity is an important factor in determining the distribution of brain regions involved in word learning. An emerging left hemispheric specialization may reflect increased efficiency in the manner in which infants process familiar and novel words. (c) 2004 Elsevier Inc. All rights reserved.

Gaming and social interactions in the rehabilitation of brain injuries: a pilot study

Physical rehabilitation of brain injuries and strokes is a time consuming and costly process. Over the past decade several studies have emerged looking at the use of highly sophisticated technologies, such as robotics and virtual reality to tap into the needs of clinicians and patients. While such technologies can be a valuable tool to facilitate intensive movement practice in a motivating and engaging environment, success of therapy also depends on self-administered therapy beyond hospital stay. With the emergence of low-cost gaming consoles such as the Nintendo Wii, new opportunities arise for home-therapy paradigms centred on social interactions and values, which could reduce the sense of isolation and other depression related complications. In this paper we examine the potential, user acceptance and usability of an unmodified Nintendo Wii gaming console as a low-cost treatment alternative to complement current rehabilitation programmes.

Reduced capacity to sustain positive emotion in major depression reflects diminished maintenance of fronto-striatal brain activation

Anhedonia, the loss of pleasure or interest in previously rewarding stimuli, is a core feature of major depression. While theorists have argued that anhedonia reflects a reduced capacity to experience pleasure, evidence is mixed as to whether anhedonia is caused by a reduction in hedonic capacity. An alternative explanation is that anhedonia is due to the inability to sustain positive affect across time. Using positive images, we used an emotion regulation task to test whether individuals with depression are unable to sustain activation in neural circuits underlying positive affect and reward. While up-regulating positive affect, depressed individuals failed to sustain nucleus accumbens activity over time compared with controls. This decreased capacity was related to individual differences in self-reported positive affect. Connectivity analyses further implicated the fronto-striatal network in anhedonia. These findings support the hypothesis that anhedonia in depressed patients reflects the inability to sustain engagement of structures involved in positive affect and reward.

A shift to randomness of brain oscillations in people with autism

BACKGROUND: Resting-state functional magnetic resonance imaging (fMRI) enables investigation of the intrinsic functional organization of the brain. Fractal parameters such as the Hurst exponent, H, describe the complexity of endogenous low-frequency fMRI time series on a continuum from random (H = .5) to ordered (H = 1). Shifts in fractal scaling of physiological time series have been associated with neurological and cardiac conditions. METHODS: Resting-state fMRI time series were recorded in 30 male adults with an autism spectrum condition (ASC) and 33 age- and IQ-matched male volunteers. The Hurst exponent was estimated in the wavelet domain and between-group differences were investigated at global and voxel level and in regions known to be involved in autism. RESULTS: Complex fractal scaling of fMRI time series was found in both groups but globally there was a significant shift to randomness in the ASC (mean H = .758, SD = .045) compared with neurotypical volunteers (mean H = .788, SD = .047). Between-group differences in H, which was always reduced in the ASC group, were seen in most regions previously reported to be involved in autism, including cortical midline structures, medial temporal structures, lateral temporal and parietal structures, insula, amygdala, basal ganglia, thalamus, and inferior frontal gyrus. Severity of autistic symptoms was negatively correlated with H in retrosplenial and right anterior insular cortex. CONCLUSIONS: Autism is associated with a small but significant shift to randomness of endogenous brain oscillations. Complexity measures may provide physiological indicators for autism as they have done for other medical conditions.

Controlling a mobile robot with a biological brain

The intelligent controlling mechanism of a typical mobile robot is usually a computer system. Some recent research is ongoing in which biological neurons are being cultured and trained to act as the brain of an interactive real world robot�thereby either completely replacing, or operating in a cooperative fashion with, a computer system. Studying such hybrid systems can provide distinct insights into the operation of biological neural structures, and therefore, such research has immediate medical implications as well as enormous potential in robotics. The main aim of the research is to assess the computational and learning capacity of dissociated cultured neuronal networks. A hybrid system incorporating closed-loop control of a mobile robot by a dissociated culture of neurons has been created. The system is flexible and allows for closed-loop operation, either with hardware robot or its software simulation. The paper provides an overview of the problem area, gives an idea of the breadth of present ongoing research, establises a new system architecture and, as an example, reports on the results of conducted experiments with real-life robots.

Flavonoids and brain health: multiple effects underpinned by common mechanisms

The neuroprotective actions of dietary flavonoids involve a number of effects within the brain, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation, and the potential to promote memory, learning and cognitive function. This multiplicity of effects appears to be underpinned by two processes. Firstly, they interact with important neuronal signalling cascades leading to an inhibition of apoptosis triggered by neurotoxic species and to a promotion of neuronal survival and differentiation. These interactions include selective actions on a number of protein kinase and lipid kinase signalling cascades, most notably the PI3K/Akt and MAP kinase pathways which regulate pro-survival transcription factors and gene expression. Secondly, they induce peripheral and cerebral vascular blood flow in a manner which may lead to the induction of angiogenesis, and new nerve cell growth in the hippocampus. Therefore, the consumption of flavonoid-rich foods, such as berries and cocoa, throughout life holds a potential to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance.

Effect of apoE genotype and vitamin E on biomarkers of oxidative stress in cultured neuronal cells and the brain of targeted replacement mice

The aetiology of apoE4 genotype-Alzheimer's disease (AD) association are complex. The current study emphasizes the impact of apoE genotype and potential beneficial effects of vitamin E (VE) in relation to oxidative stress. Agonist induced neuronal cell death was examined 1) in the presence of conditioned media containing equal amounts of apoE3 or apoE4 obtained from stably transfected macrophages, and 2) after pretreatment with alpha- and gamma-tocopherol, and -tocotrienol. ApoE3 and apoE4 transgenic mice were fed a diet poor or rich in VE to study the interplay of both apoE genotype and VE status, on membrane lipid peroxidation, antioxidative enzyme activity and glutathione levels in the brain. Cytotoxicity of hydrogen peroxide and glutamate was higher in neuronal cells cultured with apoE4 than apoE3 conditioned media. VE pre-treatment of neurons counteracted the cytotoxicity of a peroxide challenge but not of nitric oxide. No significant effects of apoE genotype or VE supplementation were observed on lipid peroxidation or antioxidative status in the brain of apoE3 and apoE4 mice. VE protects against oxidative insults in vitro, however, no differences in brain oxidative status were observed in mice. Unlike in cultured cells, apoE4 may not contribute to higher neuronal oxidative stress in the brain of young targeted replacement mice.

Age-associated changes in protein oxidation and proteasome activities in rat brain: modulation by antioxidants

The free radical theory of ageing postulates that age-associated neurodegeneration is caused by an imbalance between pro-oxidants and antioxidants resulting in oxidative stress. The current study showed regional variation in brain susceptibility to age-associated oxidative stress as shown by increased lipofuscin deposition and protein carbonyl levels in male rats of age 15-16 months compared to control ones (3-5 months). The hippocampus is the area most vulnerable to change compared to the cortex and cerebellum. However, proteasomal enzyme activity was not affected by age in any of the brain regions studied. Treatment with melatonin or coenzyme Q10 for 4 weeks reduced the lipofuscin content of the hippocampus and carbonyl level. However, both melatonin and coenzyme Q10 treatments inhibited beta-glutamyl peptide hydrolase activity. This suggests that these molecules can alter proteasome function independently of their antioxidant actions. (c) 2005 Elsevier Inc. All rights reserved.

Blueberry-induced changes in spatial working memory correlate with changes in hippocampal CREB phosphorylation and brain-derived neurotrophic factor (BDNF) levels

Phytochemical-rich foods have been shown to be effective at reversing age-related deficits in memory in both animals and humans. We show that a supplementation with a blueberry diet (2% w/w) for 12 weeks improves the performance of aged animals in spatial working memory tasks. This improvement emerged within 3 weeks and persisted for the remainder of the testing period. Memory performance correlated well with the activation of cAMP-response element-binding protein (CREB) and increases in both pro- and mature levels of brain-derived neurotrophic factor (BDNF) in the hippocampus. Changes in CREB and BDNF in aged and blueberry-supplemented animals were accompanied by increases in the phosphorylation state of extracellular signal-related kinase (ERK1/2), rather than that of calcium calmodulin kinase (CaMKII and CaMKIV) or protein kinase A. Furthermore, age and blueberry supplementation were linked to changes in the activation state of Akt, mTOR, and the levels of Arc/Arg3.1 in the hippocampus, suggesting that pathways involved in de novo protein synthesis may be involved. Although causal relationships cannot be made among supplementation, behavior, and biochemical parameters, the measurement of anthocyanins and flavanols in the brain following blueberry supplementation may indicate that changes in spatial working memory in aged animals are linked to the effects of flavonoids on the ERK-CREB-BDNF pathway. (c) 2008 Elsevier Inc. All Fights reserved.

Theory of mind in children with traumatic brain injury

Objective: This study was designed to examine the existence of deficits in mentalizing or theory of mind (ToM) in children with traumatic brain injury (TBI). Research design: ToM functioning was assessed in 12 children aged 6-12 years with TBI and documented frontal lobe damage and compared to 12 controls matched for age, sex and verbal ability. Brief measures of attention and memory were also included. Main outcome and results: The TBI group was significantly impaired relative to controls on the advanced ToM measure and a measure of basic emotion recognition. No difference was found in a basic measure of ToM. Conclusion: Traumatic brain damage in childhood may disrupt the developmental acquisition of emotion recognition and advanced ToM skills. The clinical and theoretical importance of these findings is discussed and the implications for the assessment and treatment of children who have experienced TBI are outlined.

Neural response to emotional prosody in schizophrenia and in bipolar affective disorder

Background Evidence suggests a reversal of the normal left-lateralised response to speech in schizophrenia. Aims To test the brain's response to emotional prosody in schizophrenia and bipolar disorder. Method BOLD contrast functional magnetic resonance imaging of subjects while they passively listened or attended to sentences that differed in emotional prosody Results Patients with schizophrenia exhibited normal right-lateralisation of the passive response to 'pure' emotional prosody and relative left-lateralisation of the response to unfiltered emotional prosody When attending to emotional prosody, patients with schizophrenia activated the left insula more than healthy controls. When listening passively, patients with bipolar disorder demonstrated less activation of the bilateral superior temporal gyri in response to pure emotional prosody, and greater activation of the left superior temporal gyrus in response to unfiltered emotional prosody In both passive experiments, the patient groups activated different lateral temporal lobe regions. Conclusions Patients with schizophrenia and bipolar disorder may display some left-lateralisation of the normal right-lateralised temporal lobe response to emotional prosody. Declaration of interest R.M. received a studentship from Neuraxis,, and funding from the Neuroscience and Psychiatry Unit, University of Manchester.