Brain structural correlates of upward social mobility in ethnic minority individuals

Purpose

Perigenual anterior cingulate cortex (pACC) is a neural convergence site for social stress-related risk factors for mental health, including ethnic minority status. Current social status, a strong predictor of mental and somatic health, has been related to gray matter volume in this region, but the effects of social mobility over the lifespan are unknown and may differ in minorities. Recent studies suggest a diminished health return of upward social mobility for ethnic minority individuals, potentially due to sustained stress-associated experiences and subsequent activation of the neural stress response system.

Methods

To address this issue, we studied an ethnic minority sample with strong upward social mobility. In a cross-sectional design, we examined 64 young adult native German and 76 ethnic minority individuals with comparable sociodemographic attributes using whole-brain structural magnetic resonance imaging.

Results

Results showed a significant group-dependent interaction between perceived upward social mobility and pACC gray matter volume, with a significant negative association in the ethnic minority individuals. Post-hoc analysis showed a significant mediation of the relationship between perceived upward social mobility and pACC volume by perceived chronic stress, a variable that was significantly correlated with perceived discrimination in our ethnic minority group.

Conclusion

Our findings extend prior work by pointing to a biological signature of the “allostatic costs” of socioeconomic attainment in socially disadvantaged upwardly mobile individuals in a key neural node implicated in the regulation of stress and negative affect.

     

From neuroscience to evidence based psychological treatments – The promise and the challenge,ECNP March 2016, Nice,France

This ECNP meeting was designed to build bridges between different constituencies of mental illness treatment researchers from a range of backgrounds with a specific focus on enhancing the development of novel, evidence based, psychological treatments. In particular we wished to explore the potential for basic neuroscience to support the development of more effective psychological treatments, just as this approach is starting to illuminate the actions of drugs. To fulfil this aim, a selection of clinical psychologists, psychiatrists and neuroscientists were invited to sit at the same table. The starting point of the meeting was the proposition that we know certain psychological treatments work, but we have only an approximate understanding of why they work. The first task in developing a coherent mental health science would therefore be to uncover the mechanisms (at all levels of analysis) of effective psychological treatments. Delineating these mechanisms, a task that will require input from both the clinic and the laboratory, will provide a key foundation for the rational optimisation of psychological treatments. As reviewed in this paper, the speakers at the meeting reviewed recent advances in the understanding of clinical and cognitive psychology, neuroscience, experimental psychopathology, and treatment delivery technology focussed primarily on anxiety disorders and depression. We started by asking three rhetorical questions: What has psychology done for treatment? What has technology done for psychology? What has neuroscience done for psychology? We then addressed how research in five broad research areas could inform the future development of better treatments: Attention, Conditioning, Compulsions and addiction, Emotional Memory, and Reward and emotional bias. Research in all these areas (and more) can be harnessed to neuroscience since psychological therapies are a learning process with a biological basis in the brain. Because current treatment approaches are not fully satisfactory, there is an imperative to understand why not. And when psychological therapies do work we need to understand why this is the case, and how we can improve them. We may be able to improve accessibility to treatment without understanding mechanisms. But for treatment innovation and improvement, mechanistic insights may actually help. Applying neuroscience in this way will become an additional mission for ECNP.     

Altered activation patterns within the olfactory network in Parkinson's disease

Olfactory impairment is a consistent premotor symptom in sporadic Parkinson's disease (PD), presumably caused by pathological processes in the olfactory bulb and olfactory structures within mesolimbic brain areas. The objective of the present study was to obtain an in-depth insight into olfactory network dysfunction in PD patients. Event-related functional magnetic resonance imaging (3 T) was conducted with 16 early-stage PD patients and 16 matched controls during an odor detection task. Activation within the olfactory network was analyzed both in terms of strength of activation (whole-brain random effects, regions of interest [ROI] analysis based on the hemodynamic response function) as well as time-course characteristics (finite impulse response-based ROI analysis). Olfactory-induced activation in patients with PD in comparison to a standard activation pattern obtained from controls revealed profound hyperactivation in piriform and orbitofrontal cortices. However, whereas orbitofrontal areas seem to be unable to discriminate between signal and noise, primary olfactory cortex shows preserved discriminatory ability. These results support a complex network dysfunction that exceeds structural pathology observed in the olfactory bulb and mesolimbic cortices and thus demonstrate the important contribution of functional data to describe network dynamics occurring in the degenerating brain.     

The Electrophysiological Signature of Motivational Salience in Mice and Implications for Schizophrenia

According to the aberrant-salience hypothesis, attribution of motivational salience is severely disrupted in patients with schizophrenia. To provide a translational approach for investigating underlying mechanisms, neural correlates of salience attribution were examined in normal mice and in a MK-801 model of schizophrenia. Electrophysiological responses to standard and deviant tones were assessed in the medial prefrontal cortex (mPFC) using an auditory oddball paradigm. Motivational salience was induced by aversive conditioning to the deviant tone. Analysis of the auditory evoked potential (AEP) showed selective modulation of the late frontal negativity (LFN) by motivational salience, which persisted throughout a 4-week delay. MK-801, an N-methyl-𝒟-aspartic acid receptor antagonist, abolished this differential response to motivational salience in conditioned mice. In contrast, a pronounced LFN response was observed towards the deviant, ie, perceptually salient tone, in nonconditioned mice. The finding of a selective modulation of a late frontal slow wave suggests increased top–down processing and emotional evaluation of motivationally salient stimuli. In particular, the LFN is discussed as the mouse analog to the human stimulus preceding negativity, which reflects preparatory processes in anticipation of reward or punishment. MK-801 led to a disruption of the normal response in conditioned and nonconditioned mice, including an aberrantly increased LFN in nonconditioned mice. This pattern of ‘false-negative'' and ‘false-positive'' responses suggests a degradation of salience attribution, which points to mPFC responses to be relevant for translational research on cognitive alterations in schizophrenia.     

On utilizing uncertainty information in template‐based EEG‐fMRI ballistocardiogram artifact removal

The correction of ballistocardiogram artifacts in simultaneous EEG‐fMRI often yields unsatisfactory results. To improve the signal‐to‐noise ratio (SNR) of results, we inferred EEG signal uncertainty from postcorrection artifact residuals and computed the uncertainty‐weighted mean of ERPs. Using an uncertainty‐weighted mean significantly and consistently reduced both inter‐ and intrasubject SEM in the analysis of auditory evoked responses (AER, indicated by the N1‐P2 complex) and in the effects of an auditory oddball paradigm (N1‐P3 complex, standard‐deviant difference). SNR increased by 3% on average for the AER amplitude (intrasubject) and 17% on average for the auditory oddball ERP (intersubject). This demonstrates that weighting by uncertainty complements existing artifact correction algorithms to increase SNR in ERPs. More specifically, it is an efficient method to utilize seemingly corrupt (difficult‐to‐correct) EEG data that might otherwise be discarded.     

Neural responses to social evaluative threat in the absence of negative investigator feedback and provoked performance failures

Functional neuroimaging of social stress induction has considerably furthered our understanding of the neural risk architecture of stress‐related mental disorders. However, broad application of existing neuroimaging stress paradigms is challenging, among others due to the relatively high intensity of the employed stressors, which limits applications in patients and longitudinal study designs. Here, we introduce a less intense neuroimaging stress paradigm in which subjects anticipate, prepare, and give speeches under simulated social evaluation without harsh investigator feedback or provoked performance failures (IMaging Paradigm for Evaluative Social Stress, IMPRESS). We show that IMPRESS significantly increases perceived arousal as well as adrenergic (heart rate, pupil diameter, and blood pressure) and hormonal (cortisol) responses. Amygdala and perigenual anterior cingulate cortex (pACC), two key regions of the emotion and stress regulatory circuitry, are significantly engaged by IMPRESS. We further report associations of amygdala and pACC responses with measures of adrenergic arousal (heart rate, pupil diameter) and social environmental risk factors (adverse childhood experiences, urban living). Our data indicate that IMPRESS induces benchmark psychological and endocrinological responses to social evaluative stress, taps into core neural circuits related to stress processing and mental health risk, and is promising for application in mental illness and in longitudinal study designs.     

Differential responses of the dorsomedial prefrontal cortex and right posterior superior temporal sulcus to spontaneous mentalizing

Previous research suggests a role of the dorsomedial prefrontal cortex (dmPFC) in metacognitive representation of social information, while the right posterior superior temporal sulcus (pSTS) has been linked to social perception. This study targeted these functional roles in the context of spontaneous mentalizing. An animated shapes task was presented to 46 subjects during functional magnetic resonance imaging. Stimuli consisted of video clips depicting animated shapes whose movement patterns prompt spontaneous mentalizing or simple intention attribution. Based on their differential response during spontaneous mentalizing, both regions were characterized with respect to their task‐dependent connectivity profiles and their associations with autistic traits. Functional network analyses revealed highly localized coupling of the right pSTS with visual areas in the lateral occipital cortex, while the dmPFC showed extensive coupling with instances of large‐scale control networks and temporal areas including the right pSTS. Autistic traits were related to mentalizing‐specific activation of the dmPFC and to the strength of connectivity between the dmPFC and posterior temporal regions. These results are in good agreement with the hypothesized roles of the dmPFC and right pSTS for metacognitive representation and perception‐based processing of social information, respectively, and further inform their implication in social behavior linked to autism. Hum Brain Mapp 38:3791–3803, 2017. © 2017 Wiley Periodicals, Inc.