Biology subjects

Amelsvoort, T.

Publications and source records attributed to Amelsvoort, T..

4 recordsLinked to original sources

bioRxiv2023

Exploring Neural Dynamics in Self-Voice Processing and Perception: Implications for Hallucination Proneness.

Altered sensory feedback processing and attention control are assumed to contribute to auditory verbal hallucinations, which are experienced by the general population and patients with psychosis, implying a continuum of hallucination proneness (HP). However, the interaction of altered sensory feedback processing and attention control along this HP continuum remains unclear. Manipulating the level of certainty of sensory feedback by changing self-voice quality (100% neutral, 60-40% neutral-angry, 50-50% neutral-angry, 40-60% neutral-angry, 100% angry) in individuals varying in HP, we tested this interaction using electroencephalography while participants self-generated or passively listened to their voices. Regardless of voice quality, HP modulated the N100 and P200 suppression effects. High HP individuals showed an increased N100 response to the self-generated voices and an increased P200 response for externally-generated voices. This may indicate increased error awareness and attention allocation in high HP individuals for self-voice generation stemming from altered sensory feedback processing, and/or attentional control. The current findings suggest that alterations of the sensory feedback processing in self-voice production are a fundamental characteristic of the continuum of HP, regardless of the clinical status of voice hearers. HighlightsO_LIAltered N100 voice suppression in high HP, regardless of the clinical status. C_LIO_LIHigh HP associated with altered sensory feedback processing and attentional control. C_LIO_LICurrent findings support a neurophysiological continuum of HP. C_LI

neuroscience↗

bioRxiv2023

EEG resting state alpha dynamics predict individual proneness to auditory hallucinations

IntroductionAuditory verbal hallucinations (AVH) are a transdiagnostic phenomenon but also occur in the general population. The disposition to experience AVH is considered a continuous expression from non-clinical to clinical hallucination proneness (HP). Currently, little is known about the neurophysiology of the non-clinical HP part of the continuum. AVH might result from a heightened sensitivity to sensory inputs and a decreased ability to differentiate between externally and internally generated input. Resting state (RS) alpha band activity is associated with perceptual sensitivity, attentional shifts, and cognitive control. Accordingly, spontaneous alpha fluctuations might present as a HP correlate. To investigate the time-varying dynamics of alpha band activity, we deployed a novel method for brain state allocation. MethodsWe recorded RS electroencephalography (EEG) data from 33 individuals with varying levels of HP but without clinically relevant hallucinations and used a Hidden Semi-Markov Model (HsMM) to identify five recurrent alpha states with unique temporal dynamics and topographies. The states mean duration and occupancy were analyzed as a function of HP. The sources of each state were reconstructed to identify the most active brain areas and their correspondence with known resting state networks. ResultsOccupancy and mean duration of a state corresponding to sensorimotor, auditory, and default-mode network (DMN) areas significantly predicted auditory and auditory-verbal HP, but not general HP. The temporal dynamics of all other states did not relate to HP. ConclusionAlpha brain state sources align with prior results on the role of the alpha in the DMN. The temporal dynamics of alpha might reflect individual differences for attentional biases to internally generated sensory events and altered auditory perceptual sensitivity. Thus, changes in the temporal brain state dynamics of RS alpha oscillations could present as a neural marker of increased vulnerability to auditory hallucinatory experiences.

neuroscience↗

bioRxiv2022

Converging pathways found in copy number variation syndromes with high schizophrenia risk

Schizophrenia genetics is complex, and the contribution of common and rare variants are not fully understood. Several specific copy number variations (CNVs) confer increased risk for schizophrenia, and the study of their effects is central to molecular models of mental illness. However, these CNVs - microdeletions or -duplications - are spread across the genome and differ in the number of genes affected and classes of coded proteins. This suggests that, in order to fully understand the contribution of these genetic variants to mental illness, we need to look beyond the deleted or duplicated genes, to their interaction partners and involved molecular pathways. In this study, we developed machine-readable interactive pathways to enable analysis of downstream effects of genes within CNV loci and identify common pathways between CNVs with high schizophrenia risk using the WikiPathways database, and schizophrenia risk gene collections from GWAS studies and a gene-disease association database. For CNVs that are pathogenic for schizophrenia, we found overlapping pathways, including BDNF signaling, cytoskeleton, cell-cell connections, inflammation and MAPK3 signaling. Common schizophrenia risk genes identified by different studies are found in all CNV pathways but not enriched. Our findings suggest that specific pathways - such as BDNF signaling - may be critical contributors to schizophrenia risk conferred by rare CNVs, and common risk variants may operate through distinct mechanisms. Our approach also highlights the importance of not only investigating deleted or duplicated genes within pathogenic CNV loci, but also study their direct interaction partners, which may explain pleiotropic effects of CNVs on schizophrenia risk.

systems biology↗

bioRxiv2021

Asymmetric effects of acute stress on cost and benefit learning

Stressful events trigger a complex physiological reaction - the fight-or-flight response - that can hamper flexible decision-making. Inspired by key neural and peripheral characteristics of the fight-or-flight response, here we ask whether acute stress changes how humans learn about costs and benefits. Participants were randomly exposed to an acute stress or no-stress control condition after which they completed a cost-benefit reinforcement learning task. Acute stress improved learning to maximize benefits (monetary rewards) relative to minimising energy expenditure (grip force). Using computational modelling, we demonstrate that costs and benefits can exert asymmetric effects on decisions when prediction errors that convey information about the reward value and cost of actions receive inappropriate importance; a process associated with distinct alterations in pupil size fluctuations. These results provide new insights into learning strategies under acute stress - which, depending on the context, may be maladaptive or beneficial - and candidate neuromodulatory mechanisms that could underlie such behaviour.

neuroscience↗