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The microtubule-associated protein tau gene (MAPT) codes for a protein that plays an integral role in stabilisation of microtubules and axonal transport in neurons. As well as its role in susceptibility to neurodegeneration, previous studies have found an association between the MAPT haplotype and intracranial volume and regional grey matter volumes in healthy adults. The glycogen synthase kinase-3β gene (GSK3B) codes for a serine/threonine kinase that phosphorylates various proteins, including tau, and has also been associated with risk for neurodegenerative disorders and schizophrenia. We examined the effects of MAPT and two functional promoter polymorphisms in GSK3B (rs3755557 and rs334558) on total grey matter and intracranial volume in three independent cohorts totaling 776 neurologically healthy individuals. In vitro analyses revealed a significant effect of rs3755557 on gene expression, and altered binding of at least two transcription factors, Octamer transcription factor 1 (Oct-1) and Pre-B-cell leukemia transcription factor 1 (Pbx-1), to the GSK3B promoter. Meta-analysis across the three cohorts revealed a significant effect of rs3755557 on total grey matter volume (summary B = 0.082, 95% confidence interval = 0.037–0.128) and intracranial volume (summary B = 0.113, 95% confidence interval = 0.082–0.144). No significant effect was observed for MAPT H1/H2 diplotype or GSK3B rs334558 on total grey matter or intracranial volume. Our genetic and biochemical analyses have identified a role for GSK3B in brain development, which could have important aetiological implications for neurodegenerative and neurodevelopmental disorders. [ABSTRACT FROM AUTHOR]

White matter (WM) has been shown to be affected in elderly patients with major depressive disorders (MDD). There is only limited evidence of WM structural abnormalities in nongeriatric MDD patients. This study investigates WM microstructural integrity in nongeriatric MDD patients recruited as part of the International Study to Predict Optimized Treatment in Depression clinical trial and establishes the validity of diffusion tensor imaging measures for the investigation of depression. Baseline diffusion tensor imaging data from 29 nongeriatric MDD participants (11 with melancholia) and 39 healthy control participants were used in this analysis. We performed tract-based spatial statistics analyses to evaluate WM microstructural integrity (1) between all healthy controls and all MDD participants, (2) between melancholic and nonmelancholic MDD participants, and (3) between each subgroup (melancholic and nonmelancholic) and controls. Significant WM integrity deficits were seen only for the melancholic MDD participants compared with controls. Compared with controls, melancholic participants showed an average reduction of 7.8% in fractional anisotropy over WM regions associated with the limbic system, dorsolateral prefrontal cortex, thalamic projection fibers, corpus callosum, and other association fibers. These fractional anisotropy deficits were also associated with decreased axial and increased radial diffusivity in these WM regions, suggesting a pattern of decreased myelination or other degeneration change. Our findings of WM structural abnormalities associated with the limbic system, the frontal cortex, and the thalamus support the prevailing theory of limbic-dorsolateral prefrontal cortex-thalamic dysfunction in depression. Our results also suggest that these deficits are most prominent in the melancholic subtype of MDD. Hum Brain Mapp, 2011. © 2010 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objective: To examine resting awake EEG in adolescent AN participants before and after refeeding to determine if EEG abnormalities in Anorexia Nervosa (AN) are reversible. Method: In 37 adolescent first admission AN patients and 45 healthy controls, EEG was recorded during short duration ‘‘eyes open’’ and ‘‘eyes closed’’ awake resting conditions. Repeat testing occurred in 28 AN participants after refeeding and subsequent weight gain. Results: In ‘‘eyes open,’’ underweight AN participants exhibit reduced relative alpha power and increased beta power in frontal brain regions. A significant increase in alpha, and decrease in beta and delta power was observed within participants after refeeding. In ‘‘eyes closed’’, underweight AN participants had elevated theta in parietal-occipital regions which remained after refeeding. Discussion: EEG abnormalities (reduced alpha/increased beta power) in AN normalizes with refeeding, while increased theta power persists in parietal-occipital regions in an eyes closed context. [ABSTRACT FROM AUTHOR]

Background: The risk for mental illnesses such as depression is increasingly conceptualized as the product of gene–environment interactions and their impact on brain structure and function. The role of serotonin 3A receptor gene (HTR3A -42C>T polymorphism) and its interaction with early life stress (ELS) was investigated in view of the receptor's localization to brain regions central to emotion processing. Methods: Fronto-limbic grey matter (GM) loss was measured using magnetic resonance imaging and assessed using voxel-based morphometry analysis in 397 nonclinical individuals from the Brain Resource International Database. Negative mood symptoms were also assessed. Results: The HTR3A CC genotype group, compared to the T carriers, demonstrated comparative loss to GM in hippocampal structures, which extended to the frontal cortices for those CC genotype individuals also exposed to ELS. Elevations in depressed mood were also evident. Conclusions: These findings suggest that the HTR3A CC genotype may be associated with alterations in brain structures central to emotion processing, particularly when exposed to stress, and further highlight the potential role of the serotonin system in the pathophysiology of affective disorders. In contrast, those individuals with the T allele, in particular the TT genotype, may be more protected from such alterations combined with minimal exposure to ELS events. Depression and Anxiety, 2010. © 2010 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Background: Identification of the biological markers of anorexia nervosa (AN) is crucial for the development of new treatments. We aimed to determine whether AN is associated with disturbances in the nonconscious neural processing of innate signals of emotion and whether these disturbances persist after weight gain. Methods: In a retest design, 28 adolescent females with AN were tested at first admission to hospital and again after they had gained weight. Matched healthy control participants were tested at the same times. We assessed emotion-elicited event-related potentials (ERPs) during overt and covert presentation of emotion expressions, scores on an emotion-identification behavioural task, and symptom measures. We performed between and within group analyses. Results: Individuals with AN had a marked alteration in ERPs relative to healthy controls. Irrespective of the form of stimulus, early and late ERP components were significantly reduced in AN patients at baseline (when underweight) and on retest (after weight gain), especially in the temporo-occipital regions, suggesting a persistent disruption of the early automatic appraisal of salient emotional signals. Limitations: This study could have been improved with a longer standardized retest interval. Conclusion: There is likely a core, generic disturbance in AN in the early "automatic" neural processing of emotion irrespective of weight or nutritional status. New innovative emotion-based psychologic or pharmacologic treatments targeting these nonconscious processes may prove beneficial. [ABSTRACT FROM AUTHOR]

This study tested the extent to which coached participants can simulate the neural responses of participants with posttraumatic stress disorder (PTSD) when they are presented with signals of fear. Functional magnetic resonance imaging (fMRI) was used to study blood oxygenation level-dependent signal during the presentations of fearful and neutral faces under both conscious and nonconscious (masked) conditions. Participants comprised 12 patients with PTSD and 12 trauma-exposed controls who were instructed to simulate PTSD. During conscious fear processing, simulators showed greater activation in the left amygdala and medial prefrontal cortex (MPFC) than PTSD participants. By contrast, during nonconscious processing, PTSD participants had greater MPFC activation than simulators. These findings suggest that coached simulators produce a profile of ‘over-responding’ to fear when controlled conscious processing is possible, but are not able to simulate the exaggerated medial prefrontal responses observed in PTSD participants under conditions of nonconscious processing. [ABSTRACT FROM AUTHOR]

With the explosion of knowledge in multiple areas of neuroscience, there is an increasing need to find ways to integrate this knowledge for meaningful implementation in clinical practice. We present an integrative neuroscience model for bringing together key findings in schizophrenia. The ''INTEGRATE model'' identifies four fundamental and highly interconnected domains of processing: emotion, thinking, feeling, and self-regulation. These processes operate along different time scales from very rapid response measured in milliseconds to longer and more lasting responses measured in seconds and minutes. Further, each of these processes preferentially engages different, although overlapping, subcortical-cortical brain systems. These four processes may be studied from molecular (genetic), whole brain (neuroanatomical, neurofunctional, neurophysiological, and neurochemical), and cognitive behavioral perspectives. In this four-component integrative model, schizophrenia is considered a disorder of neural ''dis-integration'' apparent across the entire system of emotion, thinking, feeling, and self-regulation. We highlight the potential for measures of neural synchrony to provide a quantitative marker that captures the real time neural ''dis-integration'' in schizophrenia, and relationships with clinical outcomes. [ABSTRACT FROM AUTHOR]

Objective: To determine the nature and severity of cognitive functioning impairment in adolescent anorexia nervosa (AN) when underweight and following weight gain. Method: In 37 first admission adolescent (12–18 years) AN patients and 45 matched controls, general cognitive functions were assessed at baseline and follow-up using the IntegNeuro-computerized battery. AN participants were tested between days 3 and 10 of their admission when underweight, with retesting conducted after weight restoration. Results: When underweight, AN participants performed more poorly than controls on sensori-motor speed tasks and exhibited a susceptibility to interference, but had superior working memory. Once the weight is restored, individuals significantly improved relative to their own performance. Relative to controls, they were significantly faster on attention and executive function tasks, exhibited superior verbal fluency, working memory, and a significantly superior ability to inhibit well-learnt responses. Discussion: Cognitive impairments in adolescent AN appear to normalize with refeeding and weight gain. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010 [ABSTRACT FROM AUTHOR]

Background: Schizophrenia may be understood as a disorder of neural synchrony. There is also increasing evidence that emotional and social cognitive impairments are central to this disorder. In patients with first-episode schizophrenia, we examined whether emotion perception is associated with disruptions to high-frequency (40 Hz) gamma synchrony and whether these disruptions predict selfregulatory adaptive compensations reflected in social cognitive behaviours. Methods: We obtained electroencephalography recordings from 28 patients with first-episode schizophrenia and matched healthy controls during perception of facial emotion under both conscious and nonconscious conditions. We extracted gamma-band synchrony from the electroencephalogram. We also used behavioural measures of emotion identification, emotional intelligence, negativity bias and social function, along with ratings of first-episode schizophrenia symptoms. We analyzed group differences and predicted social cognition to assess the potential contribution of medication. Results: Within 200 ms poststimulus, patients with first-episode schizophrenia showed alterations in gamma synchrony during both conscious and nonconscious emotion perception. Stimulus-locked synchrony was reduced in patients, particularly over the temporal cortex, whereas complementary enhancements in absolute gamma synchrony (independent of stimuli) were more distributed over temporal and left parieto-occipital regions. This pattern of altered synchrony predicted poor performance on each measure of social cognition among these patients. Medication dosage did not correlate significantly with either gamma synchrony or behavioural measures in this group. Limitations: Limitations to our study include the lack of comparison between medicated and unmedicated patients or between types of medication. Conclusion: These findings suggest that disruptions in integrative processing of motivationally important stimuli show promise as a potential biological marker of social cognitive impairments, present from the first episode of schizophrenia, and their outcomes. [ABSTRACT FROM AUTHOR]

Altered hippocampal volume, the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism, and neuroticism have each been implicated in the etiology of psychiatric disorders, especially depression. However, the relationship between these variables is not well understood. Here, we determined the effects of the BDNF Val66met polymorphism on the five-factor personality dimensions (assessed using the NEO-FFI), trait depression (assessed with the DASS-21) in a cross-sectional cohort of 467 healthy volunteers. A large matched subset of this cohort was also assessed for grey matter volume of the hippocampus and contiguous temporal cortical regions using magnetic resonance imaging. In Met carriers, elevations in neuroticism and trait depression and stress were associated with lower mean hippocampal volume, but there were no such associations in Val homozygotes. Trait depression, in particular, was found to moderate the effects of BDNF genotypes on hippocampal volume. Met carriers with high trait depression showed a reduction in grey matter volume of the mean hippocampus compared with Val homozygotes. These findings suggest that even in otherwise healthy subjects, trait depression may contribute to the susceptibility of Met carriers to hippocampal grey matter loss. Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Attentional impairment in depression is a cardinal feature of depression and has been proposed as a candidate endophenotype for major depressive disorder. Event-related potentials (ERPs) elicited by oddball signal detection tasks provide objective markers of selective stimulus processing, and are pertinent endophenotypic markers for depression. While previous studies have sought to determine objective markers for attentional impairment in depression, evidence is inconsistent and may involve heterogeneity in relatively small samples. Here, we brought together oddball ERP recording with source localization of neural correlates of selective attention in outpatients with major depressive disorder (MDD; n = 78) and participants with depressed mood (PDM; n = 127) relative to healthy controls (CTL; n = 116). The key finding was a dimensional exaggeration of the P200 (140-270 ms) to both target (signal) and non-target (noise) stimuli, most pronounced in MDD, followed by PDM, relative to CTL. This exaggeration was coupled with slower and more variable response times, suggesting that neural systems are attempting to compensate for a difficulty in discriminating signal from noise. P200 alterations were localised to limbic (hippocampal), temporal and ventral prefrontal regions, key components of the signal detection network. A subsequent reduction and delay in the P300 was also revealed for MDD indicating that the pronounced lack of discrimination in clinical depression may also lead to impaired stimulus evaluation. This P200 increase in depression could provide a potential mechanism for the attentional impairment frequently observed in depression and consequent alterations in the P300 may differentiate clinically significant depression. Hum Brain Mapp, 2009. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Psychiatry & Neuroscience is the property of CMA Impact Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Psychiatry & Neuroscience is the property of CMA Impact Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Biological models of posttraumatic stress disorder (PTSD) suggest that patients will display heightened amygdala but decreased medial prefrontal activity during processing of fear stimuli. However, a rapid and automatic alerting mechanism for responding to nonconscious signals of fear suggests that PTSD may display heightened rather than decreased MPFC under nonconscious processing of fear stimuli. This study used functional magnetic resonance imaging to examine blood oxygenation level-dependent signal changes during nonconscious presentation (16.7 ms, masked) of fearful and neutral faces in 15 participants with PTSD and 15 age and sex-matched healthy control participants. Results indicate that PTSD participants display increased amygdala and MPFC activity during nonconscious processing of fearful faces. These data extend existing models by suggesting that the impaired MPFC activation in PTSD may be limited to conscious fear processing. Hum Brain Mapp, 2008. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Previous studies have shown that exposure to early life stress (ELS) is associated with reduced volume of brain regions critical for information processing, memory and emotional function. Further, recent studies from our lab utilizing diffusion tensor imaging (DTI) have found alterations in the microstructural integrity of white matter pathways among adults exposed to ELS. However, it is not clear if these relationships extend to children and adolescents, and it is also unclear if these DTI abnormalities are associated with cognitive performance. The present study examined the relationship between ELS and the microstructural integrity of the corpus callosum among a sample of otherwise healthy controls between the ages of 8 and 73. The participants were subdivided into four age groups (8–12, 13–18, 19–50, 51–73). Individuals with three or more ELS events were compared to individuals with fewer than 3 ELS events on fractional anisotropy (FA) in the genu of the corpus callosum. Separate analyses examined the two groups on tests of verbal memory, information processing speed, psychomotor speed and cognitive flexibility. Results revealed that the youngest group and the oldest group of individuals with ELS exhibited significantly lower FA in the genu compared to individuals without ELS. However, there were no group differences on any of the cognitive tasks. Our results indicate that ELS is related to subtle alterations in brain structure, but not function. The effects found with regard to DTI occurred during periods of critical age-related developmental windows. [ABSTRACT FROM AUTHOR]

Results from recent studies suggest that chronic cigarette smoking is associated with increased white matter volume in the brain as determined by in vivo neuroimaging. We used diffusion tensor imaging to examine the microstructural integrity of the white matter in 10 chronic smokers and 10 nonsmokers. All individuals were healthy, without histories of medical or psychiatric illness. Fractional anisotropy (FA) and trace were measured in the genu, body, and splenium of the corpus callosum. FA provides a measure of directional versus nondirectional water diffusion, whereas trace provides a measure of nondirectional water diffusion. Lower FA and higher trace values are considered to reflect less brain integrity. Voxel-based morphometry was used to define volumes in each of these regions of the corpus callosum. Chronic smokers exhibited significantly higher FA in the body and whole corpus callosum and a strong trend for higher FA in the splenium compared with nonsmokers. FA did not differ between groups in the genu, and neither trace nor white matter volumes differed between groups in any of the regions of interest. When subdivided by Fagerström score (low vs. high), the low Fagerström group exhibited significantly higher FA in the body of the corpus callosum compared with the high Fagerström group and the nonsmokers. These results suggest that, among healthy adults, lower exposure to cigarette smoking is associated with increased microstructural integrity of the white matter compared with either no exposure or higher exposure. Additional studies are needed to further explore differences in white matter integrity between smokers and nonsmokers. [ABSTRACT FROM AUTHOR]

Assessment of neurocognitive functioning is a critical task in many clinical, educational, service, and industrial settings. We report on descriptive and validation data of a new, World-Wide-Web-based, comprehensive battery of neurocognitive functioning, WebNeuro, that can be used in both applied and research contexts. Fifty healthy control participants completed both WebNeuro, and an established non-Internet-based computerized cognitive assessment battery, IntegNeuro, that uses a touchscreen platform. Results indicated comparability across the two batteries, in terms of critical single test scores, factor analysis derived indices, overall performance scores, and sex differences. These results support the validity of WebNeuro as a neurocognitive assessment measure. Advantages of its use in applied and research settings are discussed. [ABSTRACT FROM AUTHOR]

Models of emotion processing have commonly been formulated as dichotomies such as approach versus avoidance. These models and associated research on evolutionary adaptation, awareness, motivational arousal, and cortical-subcortical brain systems are reviewed. A continuum model of emotional-significance processing is proposed to integrate current dichotomies and reflect the highly interconnected nature of brain systems. This model highlights a spectrum from "mismatches," signifying potential danger, to "matches," signifying safety and the expectation of reward. Subcortical-cortical interactions and autonomic arousal modulation support mismatch and match processing across a temporal continuum from milliseconds (in which processing is automatic and arguably nonconscious) to tenths of a second (in which responses are facilitated and contextual evaluation commences) to minutes and hours (when memory consolidation and neural plasticity occur). Variations at distinct points along this continuum, with contributions from constitutional and genetic factors, may contribute to individual differences in emotional stability and instability in neuropsychiatric disorders. [ABSTRACT FROM AUTHOR]

Objective: While schizophrenia has long been considered a disorder of brain connectivity, few studies have investigated white matter abnormalities in patients with first-episode schizophrenia, and even fewer studies have investigated whether there is progressive white matter pathology in the disease. Method: The authors obtained a Tiweighted structural magnetic resonance imaging (MRI) scan on 41 patients with first-episode schizophrenia. These first-episode schizophrenia patients were analyzed relative to 47 age- and sex-matched healthy comparison subjects who also underwent an MRI scan. Of the baseline participants, 25 first-episode schizophrenia patients and 26 comparison subjects returned 2 to 3 years later for a follow-up scan. To identify regional volumetric white matter differences between the two groups at baseline, voxel-based morphometry in statistical parametric mapping-2 (SPM2) was used, while tensorbased morphometry was used to identify the longitudinal changes over the follow-up interval. Results: The first-episode schizophrenia patients exhibited volumetric deficits in the white matter of the frontal and temporal lobes at baseline, as well as volumetric increases in the white matter of the frontoparietal junction bilaterally. Furthermore, these first-episode schizophrenia patients lost considerably more white matter over the follow-up interval relative to comparison subjects in the middle and inferior temporal cortex bilaterally. Conclusions: These results indicate that patients with schizophrenia exhibit white matter abnormalities at the time of their first presentation of psychotic symptoms to mental health services and that these abnormalities degenerate further over the initial years of illness. Given the role that white matter plays in neural communication, the authors suggest that these white matter abnormalities may be a cause of the dysfunctional neural connectivity that has been proposed to underlie the symptoms of schizophrenia. [ABSTRACT FROM AUTHOR]

The harsh reality is that many medical treatments do not work as expected in a significant percentage of patients, and occasionally there are serious side effects. A new paradigm of personalized medicine is emerging, which proactively tailors treatment to each individual's biological and psychological profile. The first proof-of-concept phase of personalized medicine has now been achieved. However, it has thus far focused on the use of genomic markers and on disorders of the body. The complexity of the brain is likely to require a shift from a single genetic marker focus to a more integrated approach in which additional brain-related information (neuromarkers) is taken into account. Codevelopment of genomic neuromarkers with new compounds in a personalized medicine approach will lead to increased drug R&D and treatment benefits. The emerging genomic neuromarker potential has begun to be incorporated into the template for the next version of the Diagnostic and Statistical Manual (DSM-V). The statistical power of large subject numbers in databases in general (and standardized databases in particular) provides an ideal source for elucidating the best genomic-neuromarker profiles (explaining most of the main-effects variance), which will empower a brain-related personalized medicine into mainstream clinical practice. [ABSTRACT FROM AUTHOR]

Adolescence to early adulthood is a period of dramatic transformation in the healthy human brain. However, the relationship between the concurrent structural and functional changes remains unclear. We investigated the impact of age on both neuroanatomy and neurophysiology in the same healthy subjects (n = 138) aged 10 to 30 years using magnetic resonance imaging (MRI) and resting electroencephalography (EEG) recordings. MRI data were segmented into gray and white matter images and parcellated into large-scale regions of interest. Absolute EEG power was quantified for each lobe for the slow-wave, alpha and beta frequency bands. Gray matter volume was found to decrease across the age bracket in the frontal and parietal cortices, with the greatest change occurring in adolescence. EEG activity, particularly in the slow-wave band, showed a similar curvilinear decline to gray matter volume in corresponding cortical regions. An inverse pattern of curvilinearly increasing white matter volume was observed in the parietal lobe. We suggest that the reduction in gray matter primarily reflects a reduction of neuropil, and that the corresponding elimination of active synapses is responsible for the observed reduction in EEG power. Hum Brain Mapp, 2007. © 2006 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Abstract: There is growing evidence that obesity is linked to adverse neurocognitive outcome, including reduced cognitive functioning and Alzheimer disease. However, no study to date has determined whether the relationship between body mass index (BMI) and cognitive performance varies as a function of age. We examined attention and executive function in a cross-section of 408 healthy persons across the adult life span (20-82 years). Bivariate correlation showed that BMI was inversely related to performance on all cognitive tests. After controlling for possible confounding factors, overweight and obese adults (BMI > 25) exhibited poorer executive function test performance than normal weight adults (BMI, 18.5-24.9). No differences emerged in attention test performance, and there was no evidence of a BMI × age interaction for either cognitive domain. These results provide further evidence for the relationship between elevated BMI and reduced cognitive performance and suggest that this relationship does not vary with age. Further research is needed to identify the etiology of these deficits and whether they resolve after weight loss. [Copyright &y& Elsevier]

Abstract: Cohen''s [Cohen, R. (1993). The Neuropsychology of Attention. New York: Plenum Publishing] model of attention proposes four interrelated processes, namely Sensory Selective Attention, Response Selection/Control, Focus/Capacity, and Sustained Attention. Though this model has been supported in patient samples, it has not been examined in a healthy adult cohort. Using Principal Components Analysis, we examined the explanatory power of this model in 342 adults screened for significant medical and psychiatric history. The four derived components accounted for 58.7% of the total variance. Results were generally supportive of Cohen''s [Cohen, R. (1993). The Neuropsychology of Attention. New York: Plenum Publishing] model, though further clarification of the relationship between processing speed and more complex aspects of attention (e.g. working memory, set shifting) is needed. These findings support the notion that attention is not a unitary process, but instead comprised of distinct components. Future studies including both neuropsychological testing and functional neuroimaging may provide important insight into the underpinnings of attentional processes. [Copyright &y& Elsevier]

Facial expressions of fear are universally recognized signals of potential threat. Humans may have evolved specialized neural systems for responding to fear in the absence of conscious stimulus detection. We used functional neuroimaging to establish whether the amygdala and the medial prefrontal regions to which it projects are engaged by subliminal fearful faces and whether responses to subliminal fear are distinguished from those to supraliminal fear. We also examined the time course of amygdala-medial prefrontal responses to supraliminal and subliminal fear. Stimuli were fearful and neutral baseline faces, presented under subliminal (16.7 ms and masked) or supraliminal (500 ms) conditions. Skin conductance responses (SCRs) were recorded simultaneously as an objective index of fear perception. SPM2 was used to undertake search region-of-interest (ROI) analyses for the amygdala and medial prefrontal (including anterior cingulate) cortex, and complementary whole-brain analyses. Time series data were extracted from ROIs to examine activity across early versus late phases of the experiment. SCRs and amygdala activity were enhanced in response to both subliminal and supraliminal fear perception. Time series analysis showed a trend toward greater right amygdala responses to subliminal fear, but left-sided responses to supraliminal fear. Cortically, subliminal fear was distinguished by right ventral anterior cingulate activity and supraliminal fear by dorsal anterior cingulate and medial prefrontal activity. Although subcortical amygdala activity was relatively persistent for subliminal fear, supraliminal fear showed more sustained cortical activity. The findings suggest that preverbal processing of fear may occur via a direct rostral-ventral amygdala pathway without the need for conscious surveillance, whereas elaboration of consciously attended signals of fear may rely on higher-order processing within a dorsal cortico-amygdala pathway. Hum Brain Mapp, 2005. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Abstract: This study examined the effects of age, gender and education on subjects spanning nine decades on a new cognitive battery of 12 tests. One thousand and seven participants between 6 and 82 completed the battery under standardized conditions using an automated, computerized touchscreen. Sensitive indicators of change were obtained on measures of attention and working memory, learning and memory retrieval, and language, visuospatial function, sensori-motor and executive function. Improvement tended to occur through to the third and fourth decade of life, followed by gradual decrement and/or stabilized performance thereafter. Gender differences were obtained on measures of sustained attention, verbal learning and memory, visuospatial processing and dexterity. Years of education in adults was reflected in performance on measures of verbal function. Overall, the test battery provided sensitive indicators on a range of cognitive functions suitable for the assessment of abnormal cognition, the evaluation of treatment effects and for longitudinal case management. [Copyright &y& Elsevier]

Cognitive decline in speeded abilities, executive function, and memory is believed to typify normal aging. However, there is significant variability in cognitive function with advanced age and some reports of relatively intact cognitive function among a subset of older individuals. The present study consists of a cluster analysis to examine the patterns of cognitive function in middle-aged and older individuals. Analyses revealed 3 clusters of middle-aged adults, including an intact group, persons with poor motor speed, and a group with reduced executive function. Three clusters were also identified for older adults, including a group with poor executive function, persons with reduced speed performance (attention, executive function, motor), and a group with global cognitive decline. No evidence emerged for a cluster of older adults with intact performance in all domains or with isolated memory deficits. Findings generally support the frontal aging hypothesis and may provide important information about healthy cognitive aging. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies that have examined the impact of cigarette smoking on cognition have revealed mixed results; some studies report no impact and others report detrimental effects, especially in older individuals. Few studies, however, have examined the effects of cigarette smoking on both young and old healthy individuals using highly robust and standardized methods of cognitive assessment. This study draws on an international database to contrast cognitive differences between younger and older individuals who regularly smoke cigarettes and non-smokers. Data were sampled from 1000 highly screened healthy individuals free of medical or psychiatric health complications. A cohort of 62 regular smokers (n =45<45 years of age; n =17⩾45 years) with a Fagerstrom nicotine dependency score of 1 or more were identified and matched to a cohort of 62 healthy nonsmokers (n =43<45 years; n =19⩾45 years) on demographic variables and estimated intelligence. Performances on cognitive measures of attention, reaction time, cognitive flexibility, psychomotor speed, and memory were considered for analysis. As a group, smokers performed more poorly than nonsmokers on one measure of executive function. A significant age and smoking status interaction was identified with older smokers performing more poorly than older nonsmokers and younger smokers on a measure of long-delayed recall of new information. Cigarette smoking is associated with isolated and subtle cognitive difficulties among very healthy individuals. [Copyright &y& Elsevier]

Copyright of Journal of Psychiatry & Neuroscience is the property of CMA Impact Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)