Omission responses have been proposed as neural signatures of predictive coding mechanisms that arise when expected sensory events fail to occur. These responses support the view that the brain actively generates and updates internal models to anticipate future events, rather than passively processing incoming sensory input. Importantly, omission responses offer a direct index of prediction error and prediction. They are modulated by the behavioral relevance and predictability of the omitted stimulus. Emerging studies have shown that omission responses occur across a range of auditory paradigms and involve complex interactions between excitatory and inhibitory neurons, particularly via feedforward inhibition of pyramidal cells by specific interneuron populations. When an anticipated stimulus is omitted, the resulting disinhibition of pyramidal neurons generates a prediction error signal; crucial for updating internal models and driving synaptic plasticity. This mechanism shares key features with mismatch negativity and corollary discharge, suggesting that overlapping cortical circuits are engaged in predictive processing. Taken together, these findings highlight the value of omission responses as electrophysiological markers of the brain's active prediction and prediction error signaling in auditory perception.

Addiction is often framed as a disorder of synaptic plasticity and circuit rewiring. We propose a complementary cellular mechanism: that persistent relapse vulnerability arises when the postsynaptic density (PSD) undergoes pathological "maturation" into a maladaptive biomolecular condensate-a membraneless, phase-separated assembly-we term the "Addivosome." Across repeated cycles of intoxication, withdrawal, and abstinence, drug exposure co-activates dopamine and glutamate pathways and progressively shifts the PSD toward a more rigid, self-maintaining state. This state enforces aberrant pathway cross-talk, biases gene regulation, and resists dispersal, creating a durable cellular mnemonic. We outline discriminative tests to evaluate this model: (i) define state-specific proteomic and post-translational signatures using proximity labeling; (ii) use optogenetic tools that acutely cluster or disperse selected synaptic proteins to establish causality; (iii) screen for compounds that restore liquid-like molecular mobility (reliquefaction) measured by fluorescence recovery after photobleaching; and (iv) pursue selective clearance with autophagy-tethering chimeras directed at drug-induced signatures. A central challenge-separating pathological from physiological condensates-can be addressed by targeting these state-specific features rather than core scaffold proteins. Framing addiction as a condensate disorder integrates synaptic biology, phase separation, and addiction neuroscience into a falsifiable, translational model that suggests new therapeutic avenues focused on restoring dynamics or clearing the pathological condensate.

There is an asymmetry in the ability to process visual information in the left and right visual fields. Extensive literature has consistently shown that young, healthy human adults exhibit a visuospatial bias towards the left hemifield (pseudoneglect). This leftward bias has traditionally been demonstrated through horizontal line bisection tasks in 2D experimental settings. However, as research progressed into 3D space, where lines are presented far from the observer, the dissipation of the classical leftward bias tended to reverse into a rightward bias. The precise distances at which the leftward bias, a neutral point, and rightward biases occur remain unclear. Here, we present a meta-analysis to model how bisection performance changes across 3D space quantitatively. We identified the boundary conditions where leftward biases reverse into rightward biases and at what distances this change can be predicted using line bisection. A total of 30 samples (25 studies, 142 bisection-error effects, n=720) were included. Overall, the analysis revealed a significant leftward bias within near space, followed by a rightward bias in far space. Three critical ranges for visuospatial asymmetries across depth were revealed in young, healthy adults: (1) significant leftward biases up to 48cm, (2) no reliable leftward/rightward biases from 49-87cm, and (3) significant rightward biases beyond 88cm. In addition, we revealed significant moderating effects of participant age (50+ years old), the use of tools to perform bisection, and the control of retinal size across depth. The findings establish important benchmarks when investigating visuospatial asymmetries and could inform clinical assessment.

This scoping review aimed to comprehensively examine methods for measuring changes in fetal movement in response to maternal activity and synthesize evidence on objective measurement techniques.

The impact of simultaneously performing two tasks, and its potentially detrimental effect, have been extensively investigated. Carrying out two tasks might require more resources than performing them in isolation, resulting in worsened performance for either or both tasks. Growing evidence from dual-task paradigms highlights considerable advancements in experimental designs, which, however, reflect in a variety of distinct parameters to assess cognitive-motor interference (CMI). Such heterogeneity hampers comparing results from single studies, and thus the identification of the most suitable paradigms to assess CMI in experimental and clinical settings. To address this issue, we performed a meta-analysis of published studies addressing CMI during overground walking in healthy participants. We aimed to assess the direction and strength of CMI and the impact of different cognitive tasks on gait performance. We retrieved twenty-five studies that allowed performing five distinct meta-analyses focusing on spatial, temporal and spatiotemporal gait measures, alongside cognitive performance. We additionally performed moderator analyses considering age and type of cognitive task. The results confirmed an overall CMI effect on gait measures, as well as on task accuracy, but not on reaction times. Moderator analyses highlighted significant results for gait speed, while no effect of age group was found. Overall, these results reflect the considerable heterogeneity of measurements and tasks employed to assess CMI and its modulating factors. Future research in this field should therefore promote the use of more standardized paradigms, both in healthy participants and clinical populations, particularly when aiming at developing targeted interventions such as training for neuro-motor rehabilitation.

Microdosing - the practice of consuming extremely low doses of classical psychedelic substances that do not elicit overt psychedelic effects - has gained significant attention as a potential method for enhancing cognitive performance. However, findings from controlled studies remain mixed and inconclusive. This preregistered meta-analysis examined the cognitive effects of classical psychedelic microdosing in 14 different studies (N = 1614), analyzing 59 effect sizes across multiple cognitive domains, spanning both acute (on-drug) and post-acute (off-drug) assessments. Results show a significant decrease in cognitive control, with no detectable effects on other cognitive domains or in general. Neither substance type (psilocybin or LSD), dosage (0.1-0.5 g psilocybin; 6.5-20 µg LSD), nor microdosing duration (1-42 days) emerged as significant moderators. Assessment timing (on- vs. off-drug) likewise did not moderate the effects. These findings suggest that microdosing may disrupt top-down cognitive control processes, aligning with cognitive and neural models of how classical psychedelics alter information processing in the brain to reduce rigidity and enable more fluid states of consciousness. However, better distinguishing between on-drug and off-drug effects is essential for clarifying whether microdosing exerts only transient pharmacological influences or promotes lasting cognitive change. Given the methodological heterogeneity across studies, future research using standardized protocols and mechanistic approaches is needed to fully characterize the cognitive and neural effects of microdosing classical psychedelics.

The ability to copy others is rooted in biology, from invertebrates to non-human primates and Homo sapiens, including Müllerian-Batesian mimicry of permanent traits and automatic mimicry of transient behaviours. The latter is grouped with behavioural contagion under basic behavioural matching, but they differ phenomenologically along the dimensions of accuracy (fixed/modal components), latency (response delay), latency variability (delay range), and interactional properties (dyadic-to-supra-dyadic). Drawing on primate research and other scientific domains, I propose an eco-ethological model considering these dimensions, where the core is type of releasing stimulus. Signals (evolved to elicit responses in specific receivers) act as mirroring social releasers triggering automatic mimicry, which is accurate, fast, with reduced latency variability, and contingent on dyadic interaction. Cues (passively released sensory information) act as matching social releasers promoting behavioural contagion, which involves the replication of the same behaviour type (more than the same behaviour) and is slower, variably delayed, and primarily supra-dyadic. This distinction affects modelling, involving different levels of stochasticity and linear-to-nonlinear approaches. Because some signals can serve as cues - and some cues are signal-like - grey areas emerge, including mimicry-like behavioural contagion. When motor replication is coupled with emotional contagion (e.g. via the perception-action link), automatic mimicry may drive fine-grained, near-instantaneous/instantaneous, contingent, and dyadic emotional mirroring, whereas behavioural contagion may support coarse-grained, imminent/upcoming, temporally flexible, and collective emotional matching. As signal and cue processing has been shaped by natural selection over millions of years, the related emotional contagion is also tightly linked to human evolutionary history.

The largely accepted view of the brain function is corticocentric: the cerebral cortex monitors the world to provide optimal behavioural decisions given current external and internal demands. However, this overlooks a crucial fact: the cerebral cortex has very little direct input from the outside world, and hence is not in a position to monitor it. In fact, the cortex receives the majority of its information from the thalamus. As such, the cortex monitors the thalamus, while the thalamus monitors the external environment. Interactions between the two are controlled by inhibition from the thalamic reticular nucleus (TRN), which dynamically modifies the information transmitted by the thalamus to the cortex and vice versa. The thalamus is an evolutionarily conserved structure, present in all vertebrates. While it is increasingly clear that the thalamus is not a simple sensory relay, the exact purpose of this structure and of the thalamocortical architecture which separates the computational power of the cerebral cortex from direct access to information about the external world is not clear. Theoretical considerations regarding self-monitoring of brain function and observations of the behavioural impact of resective surgery elevate the thalamus in control terms from anatomically sub-cortical to functionally supra-cortical. They suggest that the final output of the system is determined, dynamically, at the thalamic level, driven by the integration of the cortical and sensory inputs with the current thalamic state. Investigating this idea to understand the role of the thalamus will require a concerted effort across electrophysiology, neuroimaging and computational approaches.

The degree of interaction between language and consciousness is a theoretically significant yet poorly understood question. In this review, we examine neuroimaging, cognitive, and neuropsychological studies that address this issue by distinguishing between different aspects or dimensions of language and consciousness. The reviewed studies indicate that high-level semantic and sentence integration occur only in higher consciousness state and under conscious processing conditions, while lower-level phonetic, phonological or lexico-semantic processes appear to remain functional even in the absence of consciousness. We also highlight parallel recovery trajectories between aspects of language and states of consciousness, along with experimental and clinical evidence suggesting that language processing may, in some cases, influence consciousness content or even precede the reemergence of a consciousness state. Evidence of associations between language processing and higher-order conscious thought is further described. Finally, we discuss the theoretical implications and methodological challenges involved in studying and interpreting the interaction between language and consciousness, with particular attention to causal direction and to the possibility that observed associations reflect broader disruptions of integration rather than language-specific mechanisms only.

The acquisition of disgust through Pavlovian conditioning is thought to be a crucial mechanism underlying the development of mental disorders such as obsessive-compulsive disorder and eating disorders. The present systematic review and meta-analysis aims to enhance our understanding of disgust conditioning by examining research using psychophysiological (autonomic) and self-report measures (disgust, valence, expectancy). Furthermore, the role of characteristics of the unconditioned stimulus (UCS), i.e., modality and number of different stimuli paired with a single conditioned stimulus, was analyzed based on 44 studies (total N = 3832). In addition, findings from studies using facial electromyography, electroencephalography, and functional magnetic resonance imaging as well as research in clinical samples were systematically reviewed. Regarding differential conditioned responses, our results indicate medium effect sizes for valence and disgust ratings and very large effect sizes for expectancy ratings, whereas effect sizes for psychophysiological measures were small. We found no evidence for a moderator effect of UCS modality or UCS number on self-report indices, despite high between-study heterogeneity. In contrast, larger effect sizes for psychophysiological outcomes emerged for (audio-)visual UCS (as compared to olfactory UCS) and with increasing number of disgust-related UCS. Evidence for publication bias was low. In conclusion, there is robust evidence for disgust acquisition through Pavlovian conditioning based on self-report and psychophysiology. However, potential factors influencing the depth and speed of acquisition remain to be examined. Furthermore, additional research using psychophysiological and neural measures, in healthy and clinical samples, is required to gain a deeper understanding of disgust conditioning and its underlying neurobiological processes.

As life expectancy increases, cognitive impairments such as Alzheimer's disease (AD) create serious problems for older adults. Women regardless of ethnicity and age group, are disproportionately affected, accounting for two-thirds of AD cases, with post-menopausal women representing over 60 % of those affected. Sarcopenia, defined by gradual reduction of skeletal muscle mass, strength, and activities, is increasingly correlated with an elevated risk of cognitive decline in post-menopausal women. Menopause-related hormonal decline (particularly estrogen loss) and aging contribute to sarcopenia, characterized by muscle mitochondrial dysfunction, oxidative stress, and insulin resistance. This sarcopenia-driven reduction in muscle mass and functional capacity further reduces the production of myokines (e.g., BDNF, irisin), impairing neuronal proliferation, adult neurogenesis, and spatial learning/memory. These pathophysiological changes show a contributing link between sarcopenia and AD progression in post-menopausal women. This review is unique in that it discusses the triangular interplay between menopause, sarcopenia, and AD, offering an integrated mechanistic framework that links hormonal decline, muscle loss, and neurodegeneration. We aim to clarify the pathophysiological causes behind the muscle-brain axis and suggest viable treatment approaches to slow down sarcopenia and cognitive deterioration in postmenopausal women based on current evidence. The formulation of targeted strategies for enhancing the quality of life and lessening healthcare expenditures in this expanding population depends on the advancement of understanding this complex interconnection between menopause, sarcopenia and cognition.

Oxytocin (OT) is a hypothalamic neurohormone extensively studied for its role in affiliative behavior, yet its influence on epistemic trust, or trust in communicated knowledge, has received less attention. We synthesized evidence from human experiments on epistemic trust and rodent experiments using the social transmission of food preference (STFP) paradigm. During STFP, rodents learn about food safety through interaction with a conspecific, a learning process that may engage cognitive processes functionally parallel to elements of human epistemic trust. We combined effect sizes from five human studies (N = 414) and three rodent studies (N = 330), revealing no significant overall effect of OT administration on epistemic trust in humans (g = 0.25, 95 % CI: -0.25 to 0.75, p = .23) or STFP acquisition in rodents (g = -0.02, 95 % CI: -0.60 to 0.56, p = .84), with substantial heterogeneity across samples. Narrative syntheses suggest that OT may dynamically modulate epistemic trust and STFP acquisition based on informant and recipient characteristics, as well as contextual factors. By integrating these complementary lines of evidence, the current study advances a translational framework to test the allostatic model of OT and probe underlying neural mechanisms. Our findings may therefore guide future research, addressing more precise questions regarding OT effects, and ultimately improve clinical outcomes.

New concepts build on research on the rodent hippocampus, but go beyond that to understand how the hippocampal system operates in primates including humans. First, in rodents place cells and entorhinal cortex grid cells represent the place where the individual is located, but in primates including humans, many hippocampal system neurons respond to spatial view, to where the individual looks in space. Second, rodent navigation is described from place to place, but in primates including humans, the highly developed foveal visual system and hippocampal spatial view cells allow use of visual landmarks for completely different navigational strategies. Third, research in primates including humans emphasises functions of the hippocampus in episodic memory, rather than a cognitive map. Fourth, in humans the ventromedial cortical visual pathway for scenes, the ventrolateral cortical visual pathway for faces and objects, and the orbitofrontal cortex for reward provide the hippocampus with its inputs and outputs. Fifth, these discoveries in primates including humans fit with the computational theory of hippocampal CA3 circuitry for episodic memory. Sixth, in humans, the major connectivity from the hippocampal episodic memory system to the anterior temporal lobe semantic cortical regions is stimulating new approaches to how the hippocampus helps to build semantic memories.

Globally, there is increasing legalization, permissiveness and acceptability of medical and recreational cannabis use-including among pregnant people. Yet, we lack a full understanding of cannabis' effects, including during pregnancy and in offspring who experienced prenatal cannabis exposure (PCE), despite decades of research. In particular, the ability of PCE to impact offspring mental health has been investigated in literature. Given the emerging link between mental health and immune system functioning (both centrally and peripherally) and that cannabinoid receptors are abundantly expressed in the immune system, it may be the case that PCE alters offspring mental health by impacting the immune system. In this review, we highlight current research on the effects of PCE and discuss differences among administration methods and across species, with a particular focus on changes in the immune system-focusing both on immune processes in the central nervous system and peripherally-relevant to altered offspring mental health. While the field is too nascent for robust conclusions, some interesting findings have been reported. Particularly in the placenta, in both humans and rodents (using vaporized exposure paradigms), cannabis use during pregnancy is associated with a reduction in pro-inflammatory cytokine levels, which is linked, in humans, to increased offspring anxiety, aggression and hyperactivity behaviors. Whereas data with regards to microglia is limited, PCE seems to impact T cell dynamics in various organs. However, the link between offspring immune cell changes and offspring mental health requires further establishment. We conclude by discussing important future directions and a focus on harm reduction.

Significant advances in the scientific investigation of the neurobiology of consciousness have been slow to be translated into clinical settings, limited by a lack of generally agreed working definition (e.g., what is consciousness?) and methodology (e.g., how to identify reliable biomarkers/indicators of consciousness? How to improve sensitivity and specificity of the technological identification of consciousness?). In the present paper we aim at proposing potential strategies for reducing the gap between research, clinical practice, and patients' and their caregivers' needs regarding disorders of consciousness. By implementing a multidisciplinary (i.e., involving different disciplines) and multiperspective (i.e., involving different stakeholders) approach, the paper focuses on disorders of consciousness: it starts from the review of some of the most promising measures of consciousness from brain activity (i.e., electrophysiology and spectral measures, measures of functional connectivity, complexity-based measures). Next the paper introduces brain responses to illusions as a possible new indicator of consciousness (i.e., a feature that facilitates the attribution of consciousness), and illustrates a possible clinical operationalization of the indicators of consciousness through the case of virtual reality. Finally, the paper analyses a set of urgent ethical issues and describes a model for assessing and dealing with those issues, concluding by elaborating key recommendations for improving the clinical treatment of patients with disorders of consciousness through a better translation of research into clinics.

The ability to recognize sick and potentially contagious conspecifics is crucial for survival, particularly in social species where close contact increases the risk for disease transmission. This creates an evolutionary trade-off between avoiding infection and maintaining care for sick group members. This narrative review summarizes research using bacterial endotoxin (lipopolysaccharide, LPS) to experimentally induce sickness, focusing on its effects on social behavior in animals and humans. LPS-treated animals generally show reduced social exploration of healthy conspecifics, while healthy conspecifics tend to avoid them. Such avoidance behavior is influenced by environmental factors such as housing conditions, health status, and social hierarchy. Some species, when sick, show a preference for familiar individuals, and exhibit more affiliative, less aggressive behaviors. In humans, LPS-induced sickness leads to heightened sensitivity to both positive and negative social cues, which may reflect an adaptive response to increased vulnerability. Individuals under LPS also demonstrate an enhanced ability to regulate emotional responses and reduced empathy for others' psychological pain, suggesting a shift towards a more self-focused, energy-conserving state. Sick individuals additionally tend to seek care from those with a history of supportive behavior. Humans can detect sickness in others through olfactory and visual cues, such as odor, facial expressions and posture. As observed during the COVID-19 pandemic, prolonged social isolation negatively affects both infected individuals and their caregivers. Future research should therefore investigate the impact of sickness on higher level social cognitive functioning, as well as the role of modulating variables such as familiarity, sickness severity and sample demographics.

Post-traumatic stress disorder (PTSD) is a complex neuropsychiatric condition characterised by persistent fear-related memories, dysregulated stress responses, metabolic and appetite disturbances. The mechanistic target of rapamycin (mTOR) has emerged as a central hub linking these pathways involved in synaptic plasticity, memory consolidation, metabolic and satiety adaptation. This review explores the multifaceted role of mTOR in PTSD, highlighting its involvement in fear memory persistence, neurotransmission, neuroinflammation, and satiety. Dysregulated mTOR signalling has been linked to aberrant fear extinction, heightened synaptic plasticity, and altered brain metabolism, contributing to PTSD symptoms. mTOR's role in regulating protein synthesis, neuronal excitability, and glucose metabolism underscores its importance as a therapeutic target. Pharmacological modulation of mTOR, through inhibitors such as rapamycin, has shown promise in clinical and animal models for mitigating PTSD-like behaviours and promoting adaptive fear extinction and warrants further translation research for human trials. Additionally, PTSD is associated with widespread metabolic dysfunction, including insulin resistance, altered lipid metabolism, and dopaminergic dysregulation. Given mTOR's role in energy homeostasis, mTOR dysregulation may exacerbate metabolic disturbances observed in PTSD. Therefore, understanding the interplay between mTOR-driven neurobiological and metabolic pathways offers novel insights into prospective treatment strategies for PTSD. This review highlights the potential of mTOR as a key therapeutic target in PTSD, emphasising the need for further research to elucidate the precise molecular mechanisms governing its role in trauma-related disorders. Future studies exploring mTOR and Mitogen-activated protein kinase (MAPK) modulation could be used to restore metabolic balance, normalise appetite regulation, and improve cognitive resilience in individuals with PTSD.

Identifying what aspects of brain activity are responsible for conscious perception remains one of the most challenging problems in science. While progress has been made through psychophysical studies employing EEG and fMRI, research would greatly benefit from improved methods for stimulating the brain in healthy human subjects. Traditional techniques for neural stimulation through the skull, including electrical or magnetic stimulation, suffer from coarse spatial resolution and have limited ability to target deep brain structures with high spatial selectivity. Over the past decade, a new tool has emerged known as transcranial focused ultrasound (tFUS), which enables the human brain to be stimulated safely and non-invasively through the skull with millimeter-scale spatial resolution, including cortical as well as deep brain structures. This tool offers an exciting opportunity for breakthroughs in consciousness research. Given the extensive preparation and regulatory approvals associated with tFUS testing, careful experimental planning is essential. Therefore, our goal here is to provide a roadmap for using tFUS in humans for exploring the neural substrate of conscious perception.

Individuals with autism spectrum disorder (ASD) and co-occurring global developmental delay or intellectual disability (GDD-ID) are highly vulnerable to stress, but a very small amount of research is being conducted at the physiological level. This review aims to identify and synthesize studies examining autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis biomarkers in such populations.