Biology subjects

Hermans, E. J.

Publications and source records attributed to Hermans, E. J..

7 recordsLinked to original sources

bioRxiv2023

Changes in large-scale neural networks under stress are linked to affective reactivity to stress in real life

Controlled laboratory stress induction procedures are very effective in inducing physiological and subjective stress. However, whether such stress responses are representative for stress reactivity in real life is not clear. Using a combined within-subject functional MRI laboratory stress and ecological momentary assessment stress paradigm, we investigated dynamic shifts in large-scale neural network configurations under stress and how these relate to affective reactivity to stress in real life. Laboratory stress induction resulted in significantly increased cortisol levels, and shifts in task-driven neural activity including increased salience network (SN) activation in an oddball task and decreased default mode network activity in a memory retrieval task. Crucially, individuals showing increased SN reactivity specifically in the early phase of the acute stress response also expressed increased affective reactivity in real life. Our findings provide (correlational) evidence that real-life affective stress reactivity is driven primarily by vigilant attentional reorienting mechanisms associated with SN.

neuroscience↗

bioRxiv2023

A Comparison of fMRI Data-Derived and Physiological Data-Derived Methods for Physiological Noise Correction

Physiological noise substantially affects fMRI data quality, particularly in areas near fluid-filled cavities and arteries such as the brainstem. Peripheral physiological signals can be recorded alongside fMRI and incorporated into general linear models to remove variance associated with cardiac and respiratory cycles using methods such as Retrospective Image Correction (RETROICOR). In contrast, data-driven noise reduction methods such as anatomical component correction (aCompCor) and independent component analysis based automatic removal of motion artifacts (ICA-AROMA) do not rely on additional peripheral physiological recordings. These methods have shown efficacy in correcting for motion, scanner as well as physiological artifacts. This raises the question of whether logistically demanding peripheral recordings offer added value. We therefore used nuisance regression methods based on peripherally recorded physiology (RETROICOR, heart rate, respiratory volume) as well as fMRI data itself (ICA-AROMA, aCompCor) to account for noise in a resting-state data set. Subsequently, we compared variance explained by the respective methods and improvements in temporal signal-to-noise ratio throughout different regions of interest in the brain. Consistent with prior research, RETROICOR, heart rate and respiratory volume explain significant variance throughout the brain with peaks around areas of strong cardiac pulsations. ICA-AROMA and aCompCor account for a substantial proportion of the variance explained by the methods using peripheral physiology. Nonetheless, the methods based on peripheral physiological recordings retain unique explanatory power. Analysis revealed a pattern of unreliability of ICA-AROMA to consistently identify and remove physiological noise across recordings in each participant, which is compensated by RETROICOR, heart rate and respiratory volume. This unreliability partially results from misclassifications in the noise selection models of ICA-AROMA. Our results suggest that it is advisable to additionally apply cleaning based on peripheral physiological recordings, especially when assessing inter-individual differences and areas with regionally high levels of physiological noise.

neuroscience↗

bioRxiv2022

Cortical distribution of neurofilaments associates with pathological hallmarks and MRI measures of atrophy and diffusivity in Parkinson's disease

Increased neurofilament levels in biofluids, commonly used as a proxy for axonal degeneration in the brain, have been found in Parkinsons disease (PD), PD with dementia (PDD) and dementia with Lewy bodies (DLB), and correlate with MRI biomarkers. The aim of the current study was to unravel the regional distribution of cortical neurofilaments and their association with pathology load and MRI measures of atrophy and diffusivity in the post-mortem brain. Using a within-subject post-mortem MRI-pathology approach, we included 9 PD, 12 PDD/DLB and 18 age-matched control donors. Cortical thickness and mean diffusivity (MD) metrics were extracted respectively from 3DT1 and DTI at 3T in-situ MRI. After autopsy, pSer129 alpha-synuclein (pSer129-Syn), p-tau, and amyloid-beta, together with neurofilament light-chain (NfL) and phosphorylated neurofilament medium- and heavy-chain (p-NfM/H) immunoreactivity were quantified in 7 cortical regions, and studied in detail with confocal-laser scanning microscopy. The correlations between MRI and pathological measures were studied using linear mixed models. Compared to controls, p-NfM/H immunoreactivity was increased in all cortical regions in PD and PDD/DLB, whereas NfL immunoreactivity was mainly increased in the parahippocampal and entorhinal cortex in PDD/DLB. NfL-positive neurons showed degenerative morphological features and axonal fragmentation. Increased p-NfM/H correlated with p-tau load, and NfL correlated with pSer129-Syn but more strongly with p-tau load in PDD/DLB. Lastly, neurofilament immunoreactivity correlated with cortical thinning in PD and with increased cortical MD in PDD/DLB. Taken together, increased neurofilament immunoreactivity suggests underlying axonal injury and neurofilament accumulation in morphologically altered neurons with increasing pathological burden. Importantly, we demonstrate that such neurofilament markers at least partly explain MRI measures that are associated with the neurodegenerative process.

neuroscience↗

bioRxiv2022

The role of preterm birth and postnatal stress in neonatal structural brain development

Preterm birth disrupts the emerging foundations of the brains architecture, and the continuum of early-life stress-provoked alterations reaches from a healthy adaptation with resilience to severe vulnerability and maladjustment with psychopathology. The current study examined how structural brain development is affected by a stressful extra-uterine environment and whether changes in topological architecture at term-equivalent age could explain the increased vulnerability for behavioral symptoms during early childhood. Longitudinal changes in structural brain connectivity were quantified using diffusion-weighted imaging (DWI) and tractography in preterm born infants (gestational age <28 weeks), imaged at 30 and/or 40 weeks of gestation (N=145, 43.5% female). A global index of postnatal stress was based on invasive procedures during hospitalization (e.g., heel lance). Infants were classified as vulnerable and resilient based on having more or less internalizing symptoms at 2-5 years of age (n=71). Findings were replicated in an independent validation sample (N=123, 39.8% female, n=91 with follow-up). Higher stress levels impaired structural connectivity growth in the amygdala, insula, hippocampus, and posterior cingulate cortex. The hippocampus, amygdala, and subthalamic nucleus showed lower global connectivity in vulnerable relative to resilient individuals. The distinct characteristics of the resilient brain allowed for a good predictive accuracy of group membership using local network measures (80%, p<10-5, {kappa}=0.61). These findings emphasize the detrimental impact of postnatal stress and, more importantly, the relative plasticity of the preterm brain. Resilience following postnatal stress appertains to a potential compensatory or innate ability to propagate global information flow. Significance StatementThe underdeveloped preterm brain is exposed to various external stimuli following birth. Although the importance of early adversity has been widely recognized, the essential understanding of the effects of early chronic stress on neonatal brain networks as well as the remarkable degree of resilience is not well understood. We aim to provide an increased understanding of the impact of postnatal stress on brain development between 30 and 40 weeks of gestation and describe the topological architecture of a resilient brain. We observed global alteration in neonatal brain networks following postnatal stress and identified key contributive regions conferring resilience to the development of future internalizing symptoms.

neuroscience↗

bioRxiv2020

Meta-analytic evidence for downregulation of the amygdala during working memory maintenance

The amygdala is a region critically implicated in affective processes. Downregulation of the amygdala is therefore one of the hallmarks of successful emotion regulation. Downregulation is thought to be established through top-down control of the executive control network over the amygdala. Such a reciprocal relationship, however, is not exclusive to cognitive regulation of emotion. It has recently been noted that any cognitively demanding task may downregulate the amygdala, including a standard working memory task. Here, using a coordinate-based meta-analysis based on an activation likelihood estimation (ALE), we examined whether a standard working memory task (i.e., a 2-back task) downregulates the amygdala similarly to a cognitive reappraisal task. Following the PRISMA guidelines, we included a total of 66 studies using a 2-back working memory task and 65 studies using a cognitive reappraisal task. We found that a standard 2-back working memory task indeed systematically downregulates the amygdala, and that deactivated clusters strongly overlap with those observed during a cognitive reappraisal task. This finding has important consequences for the interpretation of the underlying mechanism of the effects of cognitive reappraisal on amygdala activity: downregulation of amygdala during cognitive reappraisal might be due to the cognitively demanding nature of the task and not per se by the act of the reappraisal itself. Moreover, it raises the possibility of applying working memory tasks in a clinical setting as an alternative emotion regulation strategy.

neuroscience↗

bioRxiv2019

The role of hippocampal spatial representations in contextualization and generalization of fear

Using contextual information to predict aversive events is a critical ability that protects from generalizing fear responses to safe contexts. Animal models have demonstrated the importance of spatial context representations within the hippocampal formation in contextualization of fear learning. The ventromedial prefrontal cortex (vmPFC) is known to play an important role in safety learning, possibly also through the incorporation of context information. However, if contextual representations are related to context-dependent expression of fear memory in humans remains unclear. Twenty-one healthy participants underwent functional MRI combined with a cue-context conditioning paradigm within a self-navigated virtual reality environment. The environment included two buildings (Threat and Safe context), which had distinct features outside but were identical inside. Within each context, participants saw two cues (CS+, CS-). The CS+ was consistently (100% reinforcement rate) paired with an electric shock in the Threat context, but never in the Safe context. The CS- was never paired with a shock. We found robust differential skin conductance responses (SCRs; CS+ > CS-) in the Threat context, but also within the Safe context, indicating fear generalization. Within the Safe context, vmPFC responses to the CS+ were larger than those in the Threat context. We furthermore found environment-specific representantions for the two contexts in the training paradigm (i.e., before conditioning took place) in the hippocampus to be related to fear expression and generalization. Namely, participants with a weak context representation (z-score < 1.65) showed stronger fear generalization compared to participants with a strong context representation (z-score > 1.65). Thus, a low neural representation of spatial context may explain overgeneralization of memory to safe contexts. In addition, our findings demonstrate that context-dependent regulation of fear expression engages ventromedial prefrontal pathways suggesting this involves a similar mechanism that is known to be involved in retrieval of extinction memory.

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bioRxiv2018

Eye-movement intervention enhances extinction via amygdala deactivation

Improving extinction learning is essential to optimize psychotherapy for persistent fear-related disorders. In two independent studies (both n=24), we found that goal-directed eye movements activate a dorsal fronto-parietal network and transiently deactivate the amygdala. Connectivity analyses revealed this down-regulation engages a ventromedial prefrontal pathway known to be involved in cognitive regulation of emotion. Critically, when eye movements followed memory reactivation during extinction learning, this reduced spontaneous fear recovery 24 hours later. Stronger amygdala deactivation furthermore predicted a stronger reduction in subsequent fear recovery after reinstatement. In conclusion, we show that extinction learning can be improved with a non-invasive eye-movement intervention that triggers a transient suppression of the amygdala. Our finding that another task which taxes working memory leads to a similar amygdala suppression furthermore indicates that this effect is likely not specific to eye movements, which is in line with a large body of behavioral studies. This study contributes to the understanding of a widely used treatment for traumatic symptoms by providing a parsimonious account for how working memory tasks and goal-directed eye movements can enhance extinction-based psychotherapy, namely through neural circuits similar to those that support cognitive control of emotion.\n\nSignificant statementFear-related disorders represent a significant burden on individual sufferers and society. There is a high need to optimize treatment, in particular via non-invasive means. One potentially effective intervention is execution of eye movements following trauma recall. However, a neurobiological understanding of how eye movements can reduce traumatic symptoms is lacking. We demonstrate that goal-directed eye-movements, like working memory tasks, deactivate the amygdala, the core neural substrate of fear learning. Effective connectivity analyses revealed amygdala deactivation engaged dorsolateral and ventromedial prefrontal pathways. When applied during safety learning, this deactivation predicts a reduction in later fear recovery. These findings provide a parsimonious and mechanistic account of how behavioral manipulations taxing working memory and suppress amygdala activity can alter retention of emotional memories.

neuroscience↗