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• This is an overview of the state of tES/TMS applied in drug addictions. • Neuroscience will be translated into tES/TMS tools for clinical practice in addiction. • Heterogeneity of methods and outcome measures in the literature are addressed. • This article provides guidelines for best practices in tES/TMS addiction research. There is growing interest in non-invasive brain stimulation (NIBS) as a novel treatment option for substance-use disorders (SUDs). Recent momentum stems from a foundation of preclinical neuroscience demonstrating links between neural circuits and drug consuming behavior, as well as recent FDA-approval of NIBS treatments for mental health disorders that share overlapping pathology with SUDs. As with any emerging field, enthusiasm must be tempered by reason; lessons learned from the past should be prudently applied to future therapies. Here, an international ensemble of experts provides an overview of the state of transcranial-electrical (tES) and transcranial-magnetic (TMS) stimulation applied in SUDs. This consensus paper provides a systematic literature review on published data – emphasizing the heterogeneity of methods and outcome measures while suggesting strategies to help bridge knowledge gaps. The goal of this effort is to provide the community with guidelines for best practices in tES/TMS SUD research. We hope this will accelerate the speed at which the community translates basic neuroscience into advanced neuromodulation tools for clinical practice in addiction medicine. [ABSTRACT FROM AUTHOR]

Family, twin, and adoption studies have documented a strong genetic basis for ADHD/HKD, but these studies do not identify specific genes linked to the disorder. Molecular genetic studies can identify allelic variations of specific genes that are functionally associated with ADHD/HKD, and dopamine genes have been the initial candidates based on the site of action of the stimulants drugs, which for a half century have provided the primary pharmacological treatment for ADHD/HKD. Two candidate dopamine genes have been investigated and reported to be associated with ADHD/HKD: the dopamine transporter (DAT1) gene [Cook et al., American Journal of Human Genetics 1995;56:993-998, Gill et al., Molecular Psychiatry 1997;2:311-313] and the dopamine receptor D4 (DRD4) gene [LaHoste et al., Molecular Psychiatry 1996;1:121-124: Smalley et al., 1998;3:427-430; Swanson et al., Molecular Psychiatry 1998;3:38-41]. Speculative hypotheses [Swanson and Castellanos, NIH Consensus Development Conference: Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder, November 1998. p. 37-42] have suggested that specific alleles of these dopamine genes may alter dopamine transmission in the neural networks implicated in ADHD/HKD (e.g. that the 10-repeat allele of the DAT1 gene may be associated with hyperactive re-uptake of dopamine or that the 7-repeat allele of the DRD4 gene may be associated with a subsensitive postsynaptic receptor). These and other variants of the dopamine hypothesis of ADHD will be discussed.

The prenatal and neonatal periods are two of the most important developmental stages of the human brain. It is therefore crucial to understand normal brain development and how early connections are established during these periods, in order to advance the state of knowledge on altered brain development and eventually identify early brain markers of neurodevelopmental disorders and diseases. In this systematic review (Prospero ID: CRD42024511365), we compiled resting state functional magnetic resonance imaging (fMRI) studies in healthy fetuses and neonates, in order to outline the main characteristics of typical development of the functional brain connectivity during the prenatal and neonatal periods. A systematic search of five databases identified a total of 12 573 articles. Of those, 28 articles met pre-established selection criteria based determined by the authors after surveying and compiling the major limitations reported within the literature. Inclusion criteria were: (1) resting state studies; (2) presentation of original results; (3) use of fMRI with minimum one Tesla; (4) a population ranging from 20 weeks of GA to term birth (around 37–42 weeks of PMA); (5) singleton pregnancy with normal development (absence of any complications known to alter brain development). Exclusion criteria were: (1) preterm studies; (2) post-mortem studies; (3) clinical or pathological studies; (4) twin studies; (5) papers with a sole focus on methodology (i.e. focused on tool and analysis development); (6) volumetric studies; (7) activation map studies; (8) cortical analysis studies; (9) conference papers. A risk of bias assessment was also done to evaluate each article's methodological rigor. 1877 participants were included across all the reviewed articles. Results consistently revealed a developmental gradient of increasing functional brain connectivity from posterior to anterior regions and from proximal-to-distal regions. A decrease in local small-world organization shortly after birth was also observed; small-world characteristics were present in fetuses and newborns, but appeared weaker in the latter group. Also, the posterior-to-anterior gradient could be associated with earlier development of the sensorimotor networks in the posterior regions while more complex higher-order networks (e.g. attention-related) mature later in the anterior regions. The main limitations of this systematic review stem from the inherent limitations of functional imaging in fetuses, mainly: unevenly distributed populations and limited sample sizes; fetal movements in the womb and other imaging obstacles; and a large voxel resolution when imaging a small brain. Another limitation specific to this review is the relatively small number of included articles compared to very a large search result, which may have led to relevant articles having been overlooked. • Functional connectivity maturation throughout the brain follows a posterior-to-frontal axis and proximal-to-distal axis. • Interhemispheric homologous regions have synchronized growth. • Fetuses show small-world connections at 25 weeks, decreasing with age. • Brain develops from posterior to frontal areas: sensorimotor areas mature earlier than complex frontal regions. [ABSTRACT FROM AUTHOR]

Social gradients in health and aging have been reported in studies across many human populations, and - as the papers included in this special collection highlight – also occur across species. This paper serves as a general introduction to the special collection of Neuroscience and Biobehavioral Reviews entitled "Social dimensions of health and aging: population studies, preclinical research, and comparative research using animal models". Authors of the fourteen reviews are primarily members of a National Institute of Aging-supported High Priority Research Network on "Animal Models for the Social Dimensions of Health and Aging". The collection is introduced by a foreword, commentaries, and opinion pieces by leading experts in related fields. The fourteen reviews are divided into four sections: Section 1: Biodemography and life course studies; Section 2: Social behavior and healthy aging in nonhuman primates; Section 3: Social factors, stress, and hallmarks of aging; Section 4: Neuroscience and social behavior. [ABSTRACT FROM AUTHOR]

Social play has been described in many animals. However, much of this social behaviour among birds, particularly in adults, is still relatively unexplored in terms of the environmental, psychological, and social dynamics of play. This paper provides an overview of what we know about adult social play in birds and addresses areas in which subtleties and distinctions, such as in play initiation and social organisation and its relationship to expressions of play, are considered in detail. The paper considers emotional, social, innovative, and cognitive aspects of play, then the environmental conditions and affiliative bonds, suggesting a surprisingly complex framework of criteria awaiting further research. Adult social play has so far been studied in only a small number of avian species, exclusively in those with a particularly large brain relative to body size without necessarily addressing brain functions and lateralization. When lateralization of brain function is considered, it can further illuminate a possibly significant relevance of play behaviour to the evolution of cognition, to management of emotions, and the development of sociality. [ABSTRACT FROM AUTHOR]

• 19 RCTs were fully evaluated for effectiveness of social robots in autism care. • Roughly 2/3 had positive & 1/3 had negative news for effectiveness of this method. • It seems that robots are mainly used in the experiments as the entertainment agents. • The main limitations of current studies are shortage of RCTs, low power, and bias. • Future studies try same ideas by other robots & arrange dialogue of child and robot. Autism is a neurodevelopmental disorder that affects the everyday life of people who have this lifelong condition. Robots hold great promise for uplifting therapy and care of the affected population. We searched Scopus, Medline, ScienceDirect, Web of Science, and PubMed databases for randomized controlled trials that had evaluated robot use in the therapy of people with autism, to see how effective social robots have been incorporated in autism care. Out of 240 papers initially identified, 19 satisfied the inclusion criteria and were fully evaluated. Overall, 10 different robots were utilized in the trials, out of which, four were non-humanoids. The number of papers with positive results for using robots on the main and secondary parameters was 11 and 5, respectively. Three papers reported that robot groups did not achieve better results than others. Robots in the papers included here were mainly added as the "entertainment agent" to elicit greater engagement from the participants, which is understandable, as robots at this stage might not be ready yet to deliver high-end care. [ABSTRACT FROM AUTHOR]

• Comorbidity of depression and obesity contributes to disability burden worldwide. • The number of papers researching FTO on BMI and FTO on depression is highly imbalanced. • FTO is strongly linked with obesity and has a key role in the central nervous system. • Further research is needed to confirm the role of FTO in depression-obesity comorbidity. • Future genetic studies should include a detailed characterization of depression. Depression and obesity are major global health problems that frequently co-occur. The FTO gene has one of the strongest links with obesity and high body mass index (BMI) in humans. Besides, this gene is highly expressed in the brain, may play a role in the nervous system, and could confer risk for depression, although scarce literature is available in this respect. We perform a systematic review of the relationship between FTO and both conditions. We selected original articles with observational design or reviews, where depression was assessed with ICD-10, DSM-5 or previous versions, published from 2012 (when the first related paper was published) to November 2020, performed in adults, in English or Spanish and having an optimal methodological quality (evaluated with SIGN checklist). Five original studies were finally included. The results regarding the role of FTO in depression-obesity comorbidity were inconclusive. This leads us to endorse further research covering the role of this gene on both conditions, emphasising a more precise characterization of depression, in order to confirm this role. [ABSTRACT FROM AUTHOR]

• A synopsis of recent papers about the reuniens and rhomboid nuclei (ReRh) is proposed. • Recent findings confirm a key role of ReRh nuclei in a multi-structural circuitry supporting numerous cognitive functions. • ReRh gate the information flow and coordinate activity between the medial prefrontal cortex and the hippocampus • ReRh nuclei are affected in diseases or disorders (e.g., Alzheimer's disease, depression, alcohol abuse, A. ALS). Over the past twenty years, the reuniens and rhomboid (ReRh) nuclei, which constitute the ventral midline thalamus, have received constantly growing attention. Since our first review article about the functional contributions of ReRh nuclei (Cassel et al., 2013), numerous (>80) important papers have extended anatomical knowledge, including at a developmental level, introduced new and very original electrophysiological insights on ReRh functions, and brought novel results on cognitive and non-cognitive implications of the ReRh. The current review will cover these recent articles, more on Re than on Rh, and their contribution will be approached according to their affiliation with work before 2013. These neuroanatomical, electrophysiological or behavioral findings appear coherent and point to the ReRh nuclei as two major components of a multistructural system supporting numerous cognitive (and non-cognitive) functions. They gate the flow of information, perhaps especially from the medial prefrontal cortex to the hippocampus and back, and coordinate activity and processing across these two (and possibly other) brain regions of major cognitive relevance. [ABSTRACT FROM AUTHOR]

• HDL, ApoA1 and PON1 are related to inflammation and lipid peroxidation in psychiatry. • Reduced HDL contributes both localised and systemic inflammation. • Homocysteine contributes to inflammation, oxidative stress and mitochondrial dysfunction. Lowered high-density lipoprotein (HDL) cholesterol has been reported in major depressive disorder, bipolar disorder, first episode of psychosis, and schizophrenia. HDL, its major apolipoprotein component, ApoA1, and the antioxidant enzyme paraoxonase (PON)1 (which is normally bound to ApoA1) all have anti-atherogenic, antioxidant, anti-inflammatory, and immunomodulatory roles, which are discussed in this paper. The paper details the pathways mediating the anti-inflammatory effects of HDL, ApoA1 and PON1 and describes the mechanisms leading to compromised HDL and PON1 levels and function in an environment of chronic inflammation. The molecular mechanisms by which changes in HDL, ApoA1 and PON1 might contribute to the pathophysiology of the neuroprogressive disorders are explained. Moreover, the anti-inflammatory actions of ApoM-mediated sphingosine 1-phosphate (S1P) signalling are reviewed as well as the deleterious effects of chronic inflammation and oxidative stress on ApoM/S1P signalling. Finally, therapeutic interventions specifically aimed at improving the levels and function of HDL and PON1 while reducing levels of inflammation and oxidative stress are considered. These include the so-called Mediterranean diet, extra virgin olive oil, polyphenols, flavonoids, isoflavones, pomegranate juice, melatonin and the Mediterranean diet combined with the ketogenic diet. [ABSTRACT FROM AUTHOR]

The neuroscience of volition is an emerging subfield of the brain sciences, with hundreds of papers on the role of consciousness in action formation published each year. This makes the state-of-the-art in the discipline poorly accessible to newcomers and difficult to follow even for experts in the field. Here we provide a comprehensive summary of research in this field since its inception that will be useful to both groups. We also discuss important ideas that have received little coverage in the literature so far. We systematically reviewed a set of 2220 publications, with detailed consideration of almost 500 of the most relevant papers. We provide a thorough introduction to the seminal work of Benjamin Libet from the 1960s to 1980s. We also discuss common criticisms of Libet's method, including temporal introspection, the interpretation of the assumed physiological correlates of volition, and various conceptual issues. We conclude with recent advances and potential future directions in the field, highlighting modern methodological approaches to volition, as well as important recent findings. • We systematically reviewed 2220 papers related to the neuroscience of volition. • We detail Libet's work including the seminal "free will" experiments. • We discuss and categorize the extensive criticisms of Libet's experiments. • We present key philosophical issues relevant to the neuroscience of volition. • We examine contemporary techniques, methods, and findings related to volition. [ABSTRACT FROM AUTHOR]

• We present a universal theory on information processing in living systems that is based on first principles in biophysics. • Organisms are modeled as 'hierarchical Bayesian control systems' involved in perception, goal-setting and action control. • Goal hierarchies imply the existence of 'highest goals', which inspire highly integrated normative (moral) behavior. • Severe stress causes a top-down collapse of goal hierarchies, producing behavior that lacks control by higher goals. • A temporary collapse causes episodic disorders (psychopathology); insufficient maturition causes personality disorders. In this paper, we show that organisms can be modeled as hierarchical Bayesian control systems with small world and information bottleneck (bow-tie) network structure. Such systems combine hierarchical perception with hierarchical goal setting and hierarchical action control. We argue that hierarchical Bayesian control systems produce deep hierarchies of goal states, from which it follows that organisms must have some form of 'highest goals'. For all organisms, these involve internal (self) models, external (social) models and overarching (normative) models. We show that goal hierarchies tend to decompose in a top-down manner under severe and prolonged levels of stress. This produces behavior that favors short-term and self-referential goals over long term, social and/or normative goals. The collapse of goal hierarchies is universally accompanied by an increase in entropy (disorder) in control systems that can serve as an early warning sign for tipping points (disease or death of the organism). In humans, learning goal hierarchies corresponds to personality development (maturation). The failure of goal hierarchies to mature properly corresponds to personality deficits. A top-down collapse of such hierarchies under stress is identified as a common factor in all forms of episodic mental disorders (psychopathology). The paper concludes by discussing ways of testing these hypotheses empirically. [ABSTRACT FROM AUTHOR]

• Neurophysiological correlates of positive emotions contribute to wellbeing. • Brain networks that implement positive emotions are flexible and modifiable. • Developmental, social, and environmental factors impact positive emotions. • Meditation, contemplative practices, and flow cultivate positive emotions. • Linguistic dimensions contribute to advancing the neuroscience of positive emotions. This review paper provides an integrative account regarding neurophysiological correlates of positive emotions and affect that cumulatively contribute to the scaffolding for happiness and wellbeing in humans and other animals. This paper reviews the associations among neurotransmitters, hormones, brain networks, and cognitive functions in the context of positive emotions and affect. Consideration of lifespan developmental perspectives are incorporated, and we also examine the impact of healthy social relationships and environmental contexts on the modulation of positive emotions and affect. The neurophysiological processes that implement positive emotions are dynamic and modifiable, and meditative practices as well as flow states that change patterns of brain function and ultimately support wellbeing are also discussed. This review is part of "The Human Affectome Project" (http://neuroqualia.org/background.php), and in order to advance a primary aim of the Human Affectome Project, we also reviewed relevant linguistic dimensions and terminology that characterizes positive emotions and wellbeing. These linguistic dimensions are discussed within the context of the neuroscience literature with the overarching goal of generating novel recommendations for advancing neuroscience research on positive emotions and wellbeing. [ABSTRACT FROM AUTHOR]

• Behavioural tests using the CPZ model focus mainly on motor, anxiety and cognition but not other common clinical symptoms in MS like pain or fatigue. • Most histological correlations associated with behavioural deficits were found to be inappropriate. • CPZ-feeding alone may be a useful tool to model some behavioural aspects of demyelinating diseases but it should not be regarded as a model of MS per se. The feeding of cuprizone (CPZ) to animals has been extensively used to model the processes of demyelination and remyelination, with many papers adopting a narrative linked to demyelinating conditions like multiple sclerosis (MS), the aetiology of which is unknown. However, no current animal model faithfully replicates the myriad of symptoms seen in the clinical condition of MS. CPZ ingestion causes mitochondrial and endoplasmic reticulum stress and subsequent apoptosis of oligodendrocytes leads to central nervous system demyelination and glial cell activation. Although there are a wide variety of behavioural tests available for characterizing the functional deficits in animal models of disease, including that of CPZ-induced deficits, they have focused on a narrow subset of outcomes such as motor performance, cognition, and anxiety. The literature has not been systematically reviewed in relation to these or other symptoms associated with clinical MS. This paper reviews these tests and makes recommendations as to which are the most important in order to better understand the role of this model in examining aspects of demyelinating diseases like MS. [ABSTRACT FROM AUTHOR]

Gender equality or the lack thereof is a constantly recurring theme. Here, we sought to provide an overview of the status with respect to the participation and leadership of female doctors in clinical neuroscience analyzing different disciplines (neurosurgery, neurology and psychiatry). A total of 1910 articles published in six representative journals (07–12/2020) were reviewed. Of these, 1327 were original research papers, 145 invited publications and 303 letters/comments. Out of a total of 15,080 authors, 4365 (29%) were women. The percentage of female authors was found to differ significantly between the different specialties (19% in neurosurgery, 39% in neurology and 45% in psychiatry). Women were last authors in 9.5% of the papers in neurosurgery, 29% in neurology and 39% in psychiatry Based on these findings, it can be concluded that gender disparity in academic neuroscience is quite conspicuous. Our review seeks to address the reasons behind this phenomenon in the context of new publications as well as various cultural and historical underpinnings. • The percentage of female authors was found to differ significantly between the different specialties. • Articles without any female participation made up 29% in neurosurgery and 10% in neurologic and psychiatric journals. • All analyzed specialties still show gender disparity to a certain extent. • Scientific quality increases with diverse teams. Thus, increase of diversity is also a scientific issue. [ABSTRACT FROM AUTHOR]

Lesch-Nyhan Disease (LND) is an X-linked recessive genetic disorder arising from hypoxanthine phosphoribosyltransferase 1 gene mutations, leading to a complete deficiency. LND presents a complex neurological profile characterized by generalized dystonia, motor dysfunctions and self-injurious behavior, which management is challenging. We conducted a systematic review of studies assessing the efficacy of pharmacological and non-pharmacological interventions in management of neurological symptoms in LND (PROSPERO registration number:CRD42023446513). Among 34 reviewed full-text papers; 22 studies were rated as having a high risk of bias. Considerable heterogeneity was found in studies regarding the timing of treatment implementation, adjunctive treatments and outcome assessment. Single-patient studies and clinical trials often showed contradictory results, while therapeutic failures were underreported. S-Adenosylmethionine and Deep Brain Stimulation were the most studied treatment methods and require further research to address inconsistencies. The evidence from levodopa studies underlines that optimal timing of treatment implementation should be thoroughly investigated. Standardized study design and reducing publication bias are crucial to overcome current limitations of assessing intervention efficacy in LND. • No current evidence-based clinical recommendations are available for LND. • Neurobehavioral symptoms are the focal point of most LND clinical trials. • LND patients often receive multi-drug regimens with unproven efficacy. • Single-patient studies and clinical trials frequently yield contradictory results. • Standardization of outcome assessment is strongly required. [ABSTRACT FROM AUTHOR]

I believe consciousness is a property of advanced nervous systems, and as such a product of evolution. Thus, to understand consciousness we need to describe the trajectory leading to its evolution and the selective advantages conferred. A deeper understanding of the neurology would be a significant contribution, but other advanced functions, such as hearing and vision, are explained with a comparable lack of detailed knowledge of the brain processes responsible. In this paper, I try to add details and credence to a previously suggested, evolution-based model of consciousness. According to this model, the feature started to evolve in early amniotes (reptiles, birds, and mammals) some 320 million years ago. The reason was the introduction of feelings as a strategy for making behavioral decisions. • A model for the evolutionary trajectory and advantages of consciousness. • The evolution of consciousness started in amniotes some 320 Mya. • The rationale was the introduction of feelings as a strategy for behavioral decisions. • Nonamniote animals are unlikely to harbor consciousness. • Advanced consciousness is not a feature with a high fitness value. [ABSTRACT FROM AUTHOR]

This paper proposes a new framework for investigating neural signals sufficient for a conscious sensation of movement and their role in motor control. We focus on signals sufficient for proprioceptive awareness, particularly from muscle spindle activation and from primary motor cortex (M1). Our review of muscle vibration studies reveals that afferent signals alone can induce conscious sensations of movement. Similarly, studies employing peripheral nerve blocks suggest that efferent signals from M1 are sufficient for sensations of movement. On this basis, we show that competing theories of motor control assign different roles to sensation of movement. According to motor command theories, sensation of movement corresponds to an estimation of the current state based on afferent signals, efferent signals, and predictions. In contrast, within active inference architectures, sensations correspond to proprioceptive predictions driven by efferent signals from M1. The focus on sensation of movement provides a way to critically compare and evaluate the two theories. Our analysis offers new insights into the functional roles of movement sensations in motor control and consciousness. [Display omitted] • New framework for studying the conscious sensation of movement. • Proprioceptive afferent signals are sufficient for conscious sensation of movement. • Efferent signals are sufficient for conscious sensation of movement. • Motor command theories explain results better than an active inference theory. [ABSTRACT FROM AUTHOR]

Accounts of shared representations posit that the experience of pain and pain empathy rely on similar neural mechanisms. Experimental research employing novel analytical and methodological approaches has made significant advances in both the identification and targeted manipulation of such shared experiences and their neural underpinnings. This revealed that painful experiences can be shared on different representational levels, from pain-specific to domain-general features, such as negative affect and its regulation. In view of direct links between such representations and social behaviors such as prosocial behavior, conditions characterized by aberrant pain processing may come along with heavy impairments in the social domain, depending on the affected representational level. This has wide potential implications in light of the high prevalence of pain-related clinical conditions, their management, and the overuse of pain medication. In this review and opinion paper, we aim to chart the path toward a better understanding of the link between shared affect and prosocial behavior. • Pain empathy is a multi-faceted experience that drives prosocial behavior. • It shares somatosensory, affective and cognitive representations with firsthand pain. • Pain-related conditions may therefore lead to difficulties in (pro)social behavior. • The extent of these difficulties depends on the affected representational levels. • We review the state-of-the-art and suggest future research avenues. [ABSTRACT FROM AUTHOR]

Out-of-body experiences (OBEs) are characterized by the subjective experience of being located outside the physical body. Little is known about the neurophysiology of spontaneous OBEs, which are often reported by healthy individuals as occurring during states of reduced vigilance, particularly in proximity to or during sleep (sleep-related OBEs). In this paper, we review the current state of research on sleep-related OBEs and hypothesize that maintaining consciousness during transitions from wakefulness to REM sleep (sleep-onset REM periods) may facilitate sleep-related OBEs. Based on this hypothesis, we propose a new conceptual model that potentially describes the relationship between OBEs and sleep states. The model sheds light on the phenomenological differences between sleep-related OBEs and similar states of consciousness, such as lucid dreaming (the realization of being in a dream state) and sleep paralysis (feeling paralyzed while falling asleep or waking up), and explores the potential polysomnographic features underlying sleep-related OBEs. Additionally, we apply the predictive coding framework and suggest a connecting link between sleep-related OBEs and OBEs reported during wakefulness. • There is a need for polysomnography, EEG and fMRI studies on OBEs emerging from sleep and dreaming states. • Sleep-related OBEs are linked to REM intrusions, dissociated REM states, and sleep-onset REM periods. • Sleep-related OBEs exhibit unique phenomenological features distinct from sleep paralysis and lucid dreaming. • Sleep-related OBEs, sleep paralysis, and lucid dreaming may emerge sequentially from wake-sleep transitions. • OBEs and sleep paralysis may represent a single type of phenomenon experienced with varying degrees of intensity. [ABSTRACT FROM AUTHOR]

Changes in sleep and dreams are often observed during pregnancy. Dreaming may represent privileged access to the inner world of individuals, providing relevant information about their well-being. For this reason, a growing but heterogeneous literature has investigated dream experiences of pregnant women. The present paper aimed to systematically review the available evidence on the relationship between pregnancy and oneric activity, focusing on dream and nightmare frequency, dream contents, and emotional features. Moreover, dream changes between pre-partum and post-partum periods and the impact of previous pregnancy-related adverse events on dreaming have been summarized. Overall, 17 studies have been examined. The reviewed evidence suggests that women tend to have an abundant production of dreams and nightmares during pregnancy, and some results support the view that a high rate of dream recall is associated with poor sleep quality. Most studies have shown a high presence of pregnancy-related dream content, likely reflecting waking experiences and concerns. Additionally, dreaming may promote psychological preparation and activation of functional coping strategies to face life changes after childbirth. • Dreams may represent privileged access to the inner world of pregnant women. • Dreaming could promote emotional regulation in pregnant women. • Literature on dreaming in pregnancy is still characterized by many methodological flaws. • The assessment of dreams may be useful for health professionals to evaluate mood-related aspects of pregnancy. [ABSTRACT FROM AUTHOR]

• Chemotherapy initiates cognitive decline in some cancer patients. • Rodent research overcomes methodological constraints in clinical practice. • Most cytotoxic chemotherapy regimens disrupt short term memory. • Mechanisms include inflammation, oxidative stress and disrupted neurogenesis. • Chemobrain executive control procedures must be homogenised in the literature. Whilst chemotherapy is a widely used anti-cancer treatment, a subset of patients experience cognitive decline. However, cancer type, treatment regimen, fatigue and anxiety can influence cognitive status. Rodent research has overcome these confounds to systematically evaluate cognitive domains and underlying neural mechanisms disrupted by chemotherapy treatment. Therefore, a systematic review was conducted in June 2017 to examine the relationship between chemotherapy and cognitive decline in animal models. A comprehensive literature search was performed in PubMed, PsycInfo, Web of Science, Scopus and Medline databases. A quality assessment yielded a total of 83 papers to be considered for the review. A critical assessment of research papers indicated that cisplatin, CMF and MTX + 5-FU chemotherapy regimens produced strong deficits in short term memory, long term memory and executive control. An assessment of specific cognitive domains illustrated that short term memory was strongly impaired by chemotherapy treatment, often associated with impaired neurogenesis, inflammation and mitochondrial dysfunction in the hippocampus. Pharmacological treatments were the most common intervention to reduce the prevalence of chemobrain. [ABSTRACT FROM AUTHOR]

My main goal in this paper is to propose a reformulation of foundational models in behavioral research, including Tinbergen's (1963) well-known four levels of analysis (namely, ontogenetic, mechanistic, functional, and evolutionary questions) and Mayr's (1961) dichotomy between proximate and ultimate causations. After critically evaluating these influential but problematic models, I present a three-level neo-Tinbergenian approach to behavior that considers the triadic integration of behavioral causes, structure, and consequences along a single temporal continuum. I then argue that object-directed play is a good candidate behavior to apply this new paradigm by presenting significant examples of the combined analysis of at least two of these three levels. Finally, I show how stone handling, a form of culturally-transmitted object play in macaques, is perfectly amenable to this unified three-level explanatory framework. My proposed approach fits recent theoretical and empirical advances in behavioral biology, has a heuristic value, and may provide numerous benefits to a range of behavioral scientists. • This paper offers a three-level neo-Tinbergenian approach to object play. • It aims to integrate the causes, structure, and consequences of this behavior. • Stone handling in macaques is amenable to this unified explanatory framework. [ABSTRACT FROM AUTHOR]

The Rorschach inkblot test allows access to psychological processes that usually do not emerge in self-report measures and it has been widely used in clinical psychological and psychiatric settings. Recordings of brain activity during the administration of the Rorschach inkblots test could provide information on neural correlates of the underlying perceptual-cognitive processing and potentially identify neuroimaging markers of psychopathology risk. The present paper offers a systematization of the available literature on the Rorschach inkblot test and neuroimaging research. The 13 selected studies had been conducted with healthy participants and using fMRI, EEG, and fNIRS to investigate the neural underpinnings of Rorschach inkblot test responses. The neural processes underlying the visual, social, and emotional processes described by the included papers are systematically summarized. Research on the neural correlates of the Rorschach inkblot test is promising and would further benefit from studies on clinical populations, broader samples, and younger age groups. • The Rorschach inkblot test is widely used in clinical psychological settings. • Brain activity during the test may shed light on the psychopathological conditions. • We describe the available literature on the Rorschach and neuroimaging research. • We summarize the neural activity underlying visual, social, and emotional processes. • Results show the need for studies on broader clinical samples and younger subjects. [ABSTRACT FROM AUTHOR]

Over 25 years ago, a seminal paper demonstrated that the ubiquitin-proteasome system (UPS) was involved in activity-dependent synaptic plasticity. Interest in this topic began to expand around 2008 following another seminal paper showing that UPS-mediated protein degradation controlled the "destabilization" of memories following retrieval, though we remained with only a basic understanding of how the UPS regulated activity- and learning-dependent synaptic plasticity. However, over the last 10 years there has been an explosion of papers on this topic that has significantly changed our understanding of how ubiquitin-proteasome signaling regulates synaptic plasticity and memory formation. Importantly, we now know that the UPS controls much more than protein degradation, is involved in plasticity underlying drugs of abuse and that there are significant sex differences in how ubiquitin-proteasome signaling is used for memory storage processes. Here, we aim to provide a critical 10-year update on the role of ubiquitin-proteasome signaling in synaptic plasticity and memory formation, including updated cellular models of how ubiquitin-proteasome activity could be regulating learning-dependent synaptic plasticity in the brain. • Degradation dependent and independent protein polyubiquitination is critical for memory formation. • Individual proteasome subunits can function both within and outside of the proteasome complex to regulate memory formation. • Sex is a critical variable when assessing the functional significance of ubiquitin-proteasome activity in memory formation and storage. • Changes in ubiquitin-proteasome activity underly neuroadapations associated with drugs of abuse. [ABSTRACT FROM AUTHOR]

The heterogeneity of the literature on empathy highlights its multidimensional and dynamic nature and affects unclear descriptions of empathy in the context of psychopathology. The Zipper Model of Empathy integrates current theories of empathy and proposes that empathy maturity is dependent on whether contextual and personal factors push affective and cognitive processes together or apart. This concept paper therefore proposes a comprehensive battery of physiological and behavioral measures to empirically assess empathy processing according to this model with an application for psychopathic personality. We propose using the following measures to assess each component of this model: (1) facial electromyography; (2) the Emotion Recognition Task; (3) the Empathy Accuracy task and physiological measures (e.g., heart rate); (4) a selection of Theory of Mind tasks and an adapted Dot Perspective Task, and; (5) an adjusted Charity Task. Ultimately, we hope this paper serves as a starting point for discussion and debate on defining and assessing empathy processing, to encourage research to falsify and update this model to improve our understanding of empathy. • The Zipper Model of Empathy details how cognitive and affective processes of empathy interact bi-directionally to achieve mature empathy (empathic behavior). • An empirical neuroclinical assessment of the Zipper model is proposed, consisting of a battery of validated clinical tasks. • Predicted outcomes of these measures with certain psychopathologies in mind, notably with psychopathic personality, but also autism spectrum disorder, and alexithymia. • Initiate discussion, debate, and falsification of empathy constructs by empirically testing and validating neuroclinical assessments. [ABSTRACT FROM AUTHOR]

It is little appreciated not only how closely linked are the disciplines of neurology, psychiatry, and anthropology but even more so the degree to which they share a "common ancestry". This paper briefly reviews the definition and historical origins of each area of study to then begin to illustrate how their "genealogies" overlap. This illustration is by way of a sampling of the many key figures who contributed to the rise of not just neurology, psychiatry or anthropology but of all three disciplines. That is, a selective review is undertaken of paragons whose careers bridged medicine, neuropsychiatry, and anthropology. A sampling from among the dozens who have made major contributions to spanning these disciplines illuminates the significant extent of their co-mingled intellectual ancestry. This series is akin to a data table of necessarily concise biographical vignettes – past scholars with some or full medical training who also advanced both anthropology and neuropsychiatry as these disciplines grew into intellectual maturity. Each is, in a sense, a data point that bolsters the overarching thesis that the intellectual history of these disciplines have shared ancestry. Thus, even this preliminary and topical survey of a few past "exemplars" underscores the importance of this unique intellectual siblingship. Moreover, there is now a profusion of living scholars who add fulsomely to what might be deemed this 'trilateral marriage' of anthropology, psychiatry, and neurology. A compilation of more contemporary contributors is well worthy of a future review that expands from this first consideration. This initial work is meant to engender more robust scholarship that better elucidates and, thereby, enriches and enlivens further work while also uncovering new avenues of deeper insight, notably as to the "conceptual and heuristic progression" of evolutionary neurosciences with respect to the normative and pathologic. • Here is offered an elaboration of an unpublished Inaugural Address as President of the American Neuropsychiatric Association. • It is meant as a crisp review of the common intellectual heritage shared by psychiatry, neurology and anthropology as formal disciplines. • This by way of historical vignettes of key medical persons who contributed to the emergence of psychiatry, neurology and anthropology. • It is just the beginning of a much larger project since each 'exemplar' might warrant a chapter or even a book. • An amiable 'aperitif and antipasto' of a later 'pranzo' all to stir yet not over-sate the intellectual appetite with more upon which to chew in the future. [ABSTRACT FROM AUTHOR]

KIYOKAWA, Y. and HENNESSY, M.B. Comparative studies of social buffering: A consideration of approaches, terminology, and pitfalls…NEUROSCI BIOBEHAV REV XXX–XXX, .- Over the past decades, there has been an increasing number of investigations of the impact of social variables on neural, endocrine, and immune outcomes. Among these are studies of “social buffering”—or the phenomenon by which affiliative social partners mitigate the response to stressors. Yet, as social buffering studies have become more commonplace, the variety of approaches taken, definitions employed, and divergent results obtained in different species can lead to confusion and miscommunication. The aim of the present paper, therefore, is to address terminology and approaches and to highlight potential pitfalls to the study of social buffering across nonhuman species. We review and categorize variables currently being employed in social buffering studies and provide an overview of responses measured, mediating sensory modalities and underlying mechanisms. It is our hope that the paper will be useful to those contemplating examination of social buffering in the context of their own research. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic, with its far-reaching influence on daily life, constituted a highly stressful experience for many people worldwide, jeopardizing individuals' mental health, particularly in vulnerable populations such as pregnant women. While a growing body of evidence links prenatal maternal stress to biological and developmental alterations in offspring, the specific impact of prenatal exposure to maternal pandemic-related stress (PRS) on infant development remains unclear. A comprehensive literature search was performed in October 2023 according to the PRISMA guidelines, which yielded a total of 28 records. The selected papers investigated a vast range of developmental and biological outcomes in the offspring with large methodological variations. The reviewed studies showed mixed results. Either direct associations between maternal PRS during pregnancy and infant temperament and socio-emotional development, or indirect links, mediated by maternal mental health, emerged in most studies. Furthermore, maternal PRS was associated with epigenetic and brain alterations in the offspring, although studies were limited in number. Collectively, the reviewed findings contribute to a deeper understanding of the role of early adverse exposures on infant development. • The COVID-19 pandemic constituted a critical period during which prenatal stressors may have been amplified. • Prenatal pandemic stress was linked to infant temperament/socio-emotional development. • Maternal mental health was often a critical mediator of the association. • Prenatal pandemic stress was related to epigenetic and brain alterations in offspring. [ABSTRACT FROM AUTHOR]

There is a reliable association between autism and Feeding and Eating Disorders. Concerningly, where these two conditions co-occur, clinical outcomes of Feeding and Eating Disorders are significantly worse, and treatment less effective, than when the Feeding and Eating Disorders occur in neurotypical individuals. Problematically, the reason for the association between autism and Feeding and Eating Disorders is poorly understood, which constrains advances in clinical care. This paper outlines several possible mechanisms that may underlie the observed association and suggests ways in which they may be empirically tested. Mechanisms are split into those producing an artefactual association, and those reflecting a genuine link between conditions. Artefactual associations may be due to conceptual overlap in both diagnostic criteria and measurement, Feeding and Eating Disorders causing transient autistic traits, or the association being non-specific in nature. A genuine association between autism and Feeding and Eating Disorders may be due to common causal factors, autism directly or indirectly causing Feeding and Eating Disorders, and Feeding and Eating Disorders being a female manifestation of autism. • There is an association between autism and Feeding and Eating Disorders. • The nature and cause of this overlap is currently poorly understood. • Potential mechanisms underlying the association are reviewed. • Methods to test each mechanism are suggested. [ABSTRACT FROM AUTHOR]

Attention-Deficit/Hyperactivity Disorder (ADHD) is associated with executive function deficits that are improved with medications. However, meta-analyses of stimulant effects on cognition have mostly tested single-dose effects, and there is no meta-analysis of non-stimulant effects. This systematic review and meta-analysis tested the clinically more relevant longer-term effects of Methylphenidate (20 studies; minimum 1 week) and Atomoxetine (8 studies; minimum 3 weeks) on reaction time, attention, inhibition, and working memory, searching papers on PubMed, Embase, Ovid MEDLINE, and PsycINFO. The meta-analysis of 18 studies in 1667 subjects showed that methylphenidate was superior to placebo in all cognitive domains with small to medium effect sizes (Hedges g of 0.34–0.59). The meta-analysis of atomoxetine included 7 studies in 829 subjects and showed no effects in working memory, but superior effects in the other domains with medium to large effect sizes (Hedge's g of 0.36–0.64). Meta-regression analysis showed no drug differences on cognitive effects. The meta-analyses show for the first time that chronic Methylphenidate and Atomoxetine have comparable effects of improving executive functions in people with ADHD. • First meta-analysis of chronic medication effects on cognition in ADHD. • Cognitive domains included attention, inhibition, reaction time and working memory. • Chronic methylphenidate improved performance on all cognitive domains. • Chronic Atomoxetine improved performance on all domains except working memory. • Methylphenidate and Atomoxetine had comparable effects on improving cognition in ADHD. [ABSTRACT FROM AUTHOR]

The lateral septum (LS) is involved in controlling anxiety, aggression, feeding, and other motivated behaviors. Lesion studies have also implicated the LS in various forms of caring behaviors. Recently, novel experimental tools have provided a more detailed insight into the function of the LS, including the specific role of distinct cell types and their neuronal connections in behavioral regulations, in which the LS participates. This article discusses the regulation of different types of maternal behavioral alterations using the distributions of established maternal hormones such as prolactin, estrogens, and the neuropeptide oxytocin. It also considers the distribution of neurons activated in mothers in response to pups and other maternal activities, as well as gene expressional alterations in the maternal LS. Finally, this paper proposes further research directions to keep up with the rapidly developing knowledge on maternal behavioral control in other maternal brain regions. [Display omitted] • Septal lesions result in the cessation of maternal behaviors. • The ventral and intermediate subdivisions of the lateral septum are activated in mothers. • In the absence of somatosensory contact with the pups, the septal activation is reduced. • The lateral septum contains receptors for oxytocin, prolactin and estrogens. • The lateral septum has neuronal connections with a variety of maternal brain centers. [ABSTRACT FROM AUTHOR]

Schizophrenia is a complex neuropsychiatric disorder with significant morbidity. Treatment options that address the spectrum of symptoms are limited, highlighting the need for innovative therapeutic approaches. Gamma Entrainment Using Sensory Stimulation (GENUS) is an emerging treatment for neuropsychiatric disorders that uses sensory stimulation to entrain impaired oscillatory network activity and restore brain function. Aberrant oscillatory activity often underlies the symptoms experienced by patients with schizophrenia. We propose that GENUS has therapeutic potential for schizophrenia. This paper reviews the current status of schizophrenia treatment and explores the use of sensory stimulation as an adjunctive treatment, specifically through gamma entrainment. Impaired gamma frequency entrainment is observed in patients, particularly in response to auditory and visual stimuli. Thus, sensory stimulation, such as music listening, may have therapeutic potential for individuals with schizophrenia. GENUS holds novel therapeutic potential to improve the lives of individuals with schizophrenia, but further research is required to determine the efficacy of GENUS, optimize its delivery and therapeutic window, and develop strategies for its implementation in specific patient populations. • GENUS is a novel non-pharmacological therapeutic intervention. • This review examines if GENUS can be applied to schizophrenia. • Specific future research directions in clinical and preclinical models are proposed. [ABSTRACT FROM AUTHOR]

The nature of play in animals has been long debated, but progress is being made in characterizing play and its variants, documenting its distribution across vertebrate and invertebrate taxa, describing its mechanisms and development, and proposing testable theories about its origins, evolution, and adaptive functions. To achieve a deeper understanding of the functions and evolution of play, integrative and conceptual advances are needed in neuroscience, computer modeling, phylogenetics, experimental techniques, behavior development, and inter- and intra-specific variation. The special issue contains papers documenting many of these advances. Here, we describe seven timely areas where further research is needed to understand this still enigmatic class of phenomena more fully. Growing empirical and theoretical evidence reveals that play has been crucial in the evolution of behavior and psychology but has been underestimated, if not ignored, in both empirical and theoretical areas of evolutionary biology and neuroscience. Play research has important ramifications for understanding the evolution of cognition, emotion, and culture, and research on animals can be both informative and transformative. • Play is important for understanding biological and cultural evolution but has largely been ignored by biological researchers. • We identify critical issues that can advance our understanding of the evolutionary processes and physiological bases of play • We describe seven timely areas where further research is needed to fully understand this enigmatic class of phenomena. • Integrating neuroscience, computer modeling, and phylogenetics will help achieve a deeper evolutionary understanding of play • The special issue documents many of these advances. [ABSTRACT FROM AUTHOR]

• Meal-related memory inhibits eating in humans. • Amnesia is associated with overeating and impaired interoception in humans. • Research in rodents and humans implicates the hippocampus in these effects. • Obesity disrupts memory and hippocampal functioning in rodents and humans. • These effects of obesity may create a vicious cycle that perpetuates obesity. This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired processing of hunger and satiety cues, disrupted memory of recent meals, and overconsumption. In healthy participants, meal-related memory limits subsequent ingestive behavior and obesity is associated with impaired memory and disturbances in the hippocampus. Evidence from rodents suggests that dorsal hippocampal neural activity contributes to the ability of meal-related memory to control future intake, that endocrine and neuropeptide systems act in the ventral hippocampus to provide cues regarding energy status and regulate learned aspects of eating, and that consumption of hypercaloric diets and obesity disrupt these processes. Collectively, this evidence indicates that diet-induced obesity may be caused and/or maintained, at least in part, by a vicious cycle wherein excess intake disrupts hippocampal functioning, which further increases intake. This perspective may advance our understanding of how the brain controls eating, the neural mechanisms that contribute to eating-related disorders, and identify how to treat diet-induced obesity. [ABSTRACT FROM AUTHOR]

• Evolutionary functions of play. • Neuroanatomical underpinning of play. • Role of the Parafascicular nucleus in play. • Functional circuits of play. • Gating, set-shifting and prepulse inhibition and its role in Play. Play has been recognized as a complex and diverse set of behaviors that has been difficult to define. Play can range from rough and tumble play among rats to a human child playing a computer game. Play has been understood to exist in multiple forms such as social, object, and locomotor (Burghardt, 2005). In this article we review the literatures on the neural basis of social play, on heart rate variability, on behavioral switching and set-shifting, on prepulse inhibition of the acoustic startle reflex, and on learning at the level of the basal ganglia. Each of these neuronal pathways, aside from heart rate variability, is rooted in the parafascicular nucleus of the thalamus, an important neural substrate for social play. We argue that social play optimally balances a number of opposing neural pathways by engaging systems involved in safety versus danger (heart rate variability), automatized reactions versus learned reactions to new stimuli (behavioral switching and set-shifting), and gating relevant versus less relevant stimuli (prepulse inhibition of the acoustic startle reflex). The idea that play, in addition to its role in interpersonal adaptation to social life, may have a central role in optimizing flexibility and creativity in individual response to novelty has been explored by previous authors (Huizinga, 1955 ; Spinka et al., 2001; Pellegrini et al., 2007; Pellis and Pellis, 2017). In this paper we explore the possible underlying neural basis for this function of play, having to do with balancing various neural networks, and in doing so propose an expanded understanding of the nature and function of social play. [ABSTRACT FROM AUTHOR]

• OCD logically would be expected to be impacted by the Covid-19 pandemic situation, including due to commonality of contamination/washing symptoms. • Longitudinal data in clinical settings suggested marked symptom worsening in 20–65 % of OCD patients; but that not all patients experience a worsening, and some experience improvement. • Cross-sectional data from general population studies implicated trait compulsivity and pandemic-related stress in OCD symptoms during the pandemic. • Studies should examine neuropsychiatric sequelae of Covid-19; and they should incorporate validated measures to quantify emergence/worsening of OCD symptoms. There has been much speculation about untoward effects of the Covid-19 pandemic on psychological symptoms. OCD may be expected to be especially impacted. Our aim was to distil the current evidence base on relationships between the pandemic and obsessive-compulsive symptoms, in patients, and general population samples. We conducted a rapid scoping review, in the form of a systematic literature search, coupled with narrative review. 32 relevant papers were identified. (1) A sizable proportion of people with OCD (but not all) experienced/reported symptom worsening during the pandemic, especially during initial restrictions (approximately 20–65 % of cases in longitudinal studies); (2) contamination/washing symptoms appeared particularly susceptible; and (3) OCD symptoms in general population samples were associated with trait compulsivity and pandemic-related-stress. The literature was heterogeneous with various methodological issues being commonplace. The review identified important unaddressed issues: how should exposure based therapy be adapted during pandemics? How can we minimise harm from exacerbation of OCD in vulnerable individuals arising from public health messaging? Why do some but not all OCD patients experience worsening? And does Covid-19 infection affect (or lead to) OCD symptoms? [ABSTRACT FROM AUTHOR]

• Sensory and emotional memories can be integrated in two ways. First, when the two memories share common content, the retrieval of one memory may call to mind the other, thereby allowing the sensory stimuli encoded as part of memory 1 to elicit responses that are appropriate to the emotional content of memory 2 ("memory chaining" at choice points). Second, as new emotional memories are encoded, past sensory memories can be activated and integrated with the emotional memory content ("online" integration), essentially resulting in formation of a false memory (or false memory content). • Here, we review studies of sensory preconditioning that have examined how sensory and emotional memories are integrated in the brain. We find that the two forms of integration are not mutually exclusive. That is, rather than the sensory and emotional memories that form in a preconditioning protocol being integrated in just one way or another, both forms of integration operate concurrently, with different protocols/parameters or training/test conditions increasing the likelihood of observing one form or another. • Chaining was observed in studies where the sensory stimuli presented in stage 1 of preconditioning were perceptually distinct, the emotional memory formed in stage 2 was very strong, and the context used for memory testing was highly familiar. • Online integration was observed in studies where the sensory stimuli presented in stage 1 of preconditioning were perceptually overlapping, the emotional memory formed in stage 2 was not over-trained, and the context used for memory testing was less familiar. Sensory preconditioning protocols can be used to assess how the brain integrates memories that share common features. In these protocols, animals are first exposed to pairings of two relatively innocuous stimuli, S2 and S1 (stage 1), and then to pairings of one of these stimuli, S1, with an event of motivational significance (stage 2). Following this training, test presentations of S2 elicit responses appropriate to the motivationally significant event, and these responses are taken to indicate formation of distinct S2-S1 and S1-event memories that are integrated in some way to generate that responding. This paper reviews studies of sensory preconditioning in rats, mice, rabbits and people to determine whether S2-S1 and S1-event memories are integrated through a chaining process at the time of their retrieval (i.e., test presentations of S2 trigger retrieval of S1, and thereby, responses appropriate to the event); or "online" at the time of memory formation (i.e., in stage 2, S1 activates a representation of S2 such that both stimuli associate with the motivationally significant event). It finds that the type of integration is determined by the manner in which stimuli are presented in preconditioning as well as their familiarity. When the stimuli in preconditioning are presented repeatedly and/or serially (i.e., one after the other), the S2-S1 and S1-event memories are chained at the time of retrieval/testing. In contrast, when the stimuli in preconditioning are relatively novel and/or presented simultaneously , the S2-S1 and S1-event memories are integrated online. These statements are related to prior claims regarding the circumstances that promote different types of memory integration and, more generally, mechanisms of information processing in the mammalian brain. [ABSTRACT FROM AUTHOR]

• Vagal dysfunction is present in fibromyalgia. • Fibromyalgia is a stress-related disorder. • Psychosocial factors can play an important role in fibromyalgia. • Stress systems alter neurotransmitters in fibromyalgia. Fibromyalgia (FM) syndrome is a common illness characterized by chronic widespread pain, sleep problems, fatigue, and cognitive difficulties. Dysfunctional neurotransmitter systems that influence the body's endogenous stress response systems are thought to underlie many of the major FM-related symptoms. A model of FM pathogenesis suggests biological and psychosocial variables interact to influence the genetic predisposition, but the precise mechanisms remain unclear. The Polyvagal Theory provides a theoretical framework from which to investigate potential biological mechanisms. The vagus nerve (VN) has anti-inflammatory properties via its afferent and efferent fibers. A low vagal tone (as assessed by low heart rate variability), has been observed in painful and inflammatory diseases, including FM, while the ventral branch of the VN is linked to emotional expression and social engagement. These anti-inflammatory and psychological (limbic system) properties of the VN may possess therapeutic potential in treating FM. This review paper summarizes the scientific literature regarding the potential role of the VN in transducing and/or therapeutically managing FM signs and symptoms. [ABSTRACT FROM AUTHOR]

• Decision-making impairment in suicidal behavior showed reinforcement learning deficit. • The impairment was described under risk but not under ambiguity conditions. • It was independent of clinical status and seemed to be a cognitive stable trait. Impaired decision-making (DM) is well-known in suicidal behavior (SB). We aimed to review the evidence on DM and its mediating factors in SB and perform a meta-analysis on DM assessed using the Iowa Gambling Task (IGT). We conducted a search on databases of papers published on DM and SB up to 2020: 46 studies were included in the systematic review, and 18 in the meta-analysis. For meta-analysis, we compared DM performance between suicide attempters (SAs) and patients (PCs) or healthy controls (HCs). The systematic review showed that SAs have greater difficulties in all DM domains. The meta-analysis found worse IGT performance among SAs in comparison with PCs and HCs. A meta-regression did not find differences for age, gender, psychiatric disorder, and clinical status. Our findings indicate that SAs exhibited deficits in DM under conditions of risk though not ambiguity. Worse DM was independent of age, gender, psychiatric disorder, and suggested that DM impairment could be considered a cognitive trait of suicidal vulnerability, a risk factor and an attribute of SAs. [ABSTRACT FROM AUTHOR]

• New generative model for selective attention during cocktail party listening. • Computational 'lesions' in the model dissociate different errors during word report. • We model different temporal hypotheses for preparatory attention. • Temporal changes in precision are necessary to explain ERPs but not reaction times. • CNV-like responses can be explained by subjective precision rather than action. In this paper, we introduce a new generative model for an active inference account of preparatory and selective attention, in the context of a classic 'cocktail party' paradigm. In this setup, pairs of words are presented simultaneously to the left and right ears and an instructive spatial cue directs attention to the left or right. We use this generative model to test competing hypotheses about the way that human listeners direct preparatory and selective attention. We show that assigning low precision to words at attended—relative to unattended—locations can explain why a listener reports words from a competing sentence. Under this model, temporal changes in sensory precision were not needed to account for faster reaction times with longer cue-target intervals, but were necessary to explain ramping effects on event-related potentials (ERPs)—resembling the contingent negative variation (CNV)—during the preparatory interval. These simulations reveal that different processes are likely to underlie the improvement in reaction times and the ramping of ERPs that are associated with spatial cueing. [ABSTRACT FROM AUTHOR]

• Systematic review of the impact of mindfulness meditation on the wandering mind. • Reviewed studies consider both first-person and behavioural/physiological measures of mind wandering. • Mindfulness-based trainings reduce mind wandering episodes. • Expert meditators self-report less task-unrelated thoughts than non-meditators. • Expert meditators show decreased Default Mode Network activity. Through the practice of Mindfulness Meditation (MM), meditators become familiar with the observation of ongoing spontaneous thoughts, while maintaining an attitude of openness and equanimity. The aim of this systematic review is to present a synthesis of available findings of the short and long-term effects of MM on mind wandering (MW). We included studies that considered both first-person and behavioral/physiological measures of MW. The search resulted in 2035 papers, 24 of which were eligible. Reviewed studies revealed a high heterogeneity in designs, outcome measures and interventions. Most of the pre-post intervention studies showed that a protracted practice of MM (at least 2 weeks) reduced MW, limiting its negative effects on different cognitive tasks. Cross-sectional studies highlighted differences between expert meditators and naïve individuals: meditators self-reported less MW and showed decreased Default Mode Network activity, during meditation and resting-state. Further studies are needed to replicate available findings and to more deeply explore how MW is influenced by meditation, also considering its qualitative characteristics that remain largely unexplored. [ABSTRACT FROM AUTHOR]

• Introducing a united framework to bridge the gap between network neuroscience and psychopathological networks. • Showcasing three methodological avenues to introduce networks of brain and behavioral data. • Creating a common language that allows to exploit synergies. In recent years, there has been an increase in applications of network science in many different fields. In clinical neuroscience and psychopathology, the developments and applications of network science have occurred mostly simultaneously, but without much collaboration between the two fields. The promise of integrating these network applications lies in a united framework to tackle one of the fundamental questions of our time: how to understand the link between brain and behavior. In the current overview, we bridge this gap by introducing conventions in both fields, highlighting similarities, and creating a common language that enables the exploitation of synergies. We provide research examples in autism research, as it accurately represents research lines in both network neuroscience and psychological networks. We integrate brain and behavior not only semantically, but also practically, by showcasing three methodological avenues that allow to combine networks of brain and behavioral data. As such, the current paper offers a stepping stone to further develop multi-modal networks and to integrate brain and behavior. [ABSTRACT FROM AUTHOR]

Background Bipolar disorder phenomenologically is a biphasic disorder of energy availability; increased in mania and decreased in depression. In consort, there is accumulating evidence indicating increased mitochondrial respiration and ATP production in bipolar mania which contrasts with decreased mitochondrial function in patients in the euthymic or depressive phase of the illness. Consequently, the central thesis of this paper is that bipolar disorder is due to a phasic dysregulation of mitochondrial biogenergetics. The elements responsible for this dysregulation may thus represent critical treatment targets for mood disorders, and are the subject of this paper. Discussion There are many potential mediators of mitochondrial function which collectively are implicated in bipolar disorder. Levels of oxidative stress, pro-inflammatory cytokines and intracellular calcium ions are all higher in bipolar mania than in the euthymic and depressive phases of the illness. Increased levels of calcium ions can partly account for increased oxidative phosphorylation via well documented pathways such as the modulation of the F 1 –F O elements of ATP synthase. Likewise, increased levels of oxidative stress and pro-inflammatory cytokines lead to the upregulation of AMPK, SIRT-1, SIRT-3 and NAD + which directly stimulate oxidative phosphorylation. Uric acid and melatonin are also differentially elevated in bipolar mania and both molecules stimulate the production of ATP. The pro-apoptotic, neurotoxic and mitotoxic effects of elevated glutamate, dopamine and GSK-3 in bipolar mania may be counterbalanced by higher basal levels and activity of p53, Bcl-2, PI3K and Akt in an environment of elevated uric acid and decreased BDNF. Summary Details of these pathways are discussed as an explanatory model for the existence of increased ATP generation in mania. We also offer a model explaining the biphasic nature of mitochondrial respiration in bipolar disorder and the transition between mania and depression based on increasing levels of TNFα, ROS, NO, AMPK and SIRT-1 together with the antagonistic relationship between p53 and NF-κB. [ABSTRACT FROM AUTHOR]

As the physiological impact of chronic stress is difficult to study in humans, naturalistic stressors are invaluable sources of information in this area. This review systematically evaluates the research literature examining biomarkers of chronic stress, including neurocognition, in informal dementia caregivers. We identified 151 papers for inclusion in the final review, including papers examining differences between caregivers and controls as well as interventions aimed at counteracting the biological burden of chronic caregiving stress. Results indicate that cortisol was increased in caregivers in a majority of studies examining this biomarker. There was mixed evidence for differences in epinephrine, norepinephrine and other cardiovascular markers. There was a high level of heterogeneity in immune system measures. Caregivers performed more poorly on attention and executive functioning tests. There was mixed evidence for memory performance. Interventions to reduce stress improved cognition but had mixed effects on cortisol. Risk of bias was generally low to moderate. Given the rising need for family caregivers worldwide, the implications of these findings can no longer be neglected. [ABSTRACT FROM AUTHOR]

Child maltreatment (CM) encompasses sexual abuse, physical abuse, emotional abuse, neglect, and exposure to domestic and family violence. Epigenetic research investigating CM has focused on differential DNA methylation (DNAm) in genes associated with the stress response, but there has been limited evaluation of the specific effects of subtypes of CM. This systematic review of literature investigating DNAm associated with CM in non-clinical populations aimed to summarise the approaches currently used in research, how the type of maltreatment and age of exposure were encoded via methylation, and which genes have consistently been associated with CM. A total of fifty-four papers were eligible for review, including forty-one candidate gene studies, eight epigenome-wide association studies, and five studies with a mixed design. The ways in which the various forms of CM were conceptualised and measured varied between papers. Future studies would benefit from assessments that employ conceptually robust definitions of CM, and that capture important contextual information such as age of exposure and subtype of CM. • We review original research on childhood maltreatment and DNA methylation. • The 54 studies were mainly cross-sectional and candidate-gene focussed. • Methodological errors and weak conceptualisations of maltreatment were common. • Measurement tools of included studies did not capture all necessary information. • Few studies investigate the associated effects of maltreatment subtypes. [ABSTRACT FROM AUTHOR]

Reward-related cues are an important part of our daily life as they often influence and guide our actions. This paper reviews one of the experimental paradigms used to study the effects of cues, the Pavlovian to Instrumental Transfer paradigm. In this paradigm, cues associated with rewards through Pavlovian conditioning alter motivation and choice of instrumental actions. The first transfer experiments date back to the 1940s, but only in the last decade has it been fully recognised that there are two types of transfer, specific and general. This paper presents a systematic review of both the neural substrates and the behavioral factors affecting both types of transfer. It also examines the recent application of the paradigm to study the effect of cues on human participants, both in normal and pathological conditions, and the interactions of transfer with drugs of abuse. Finally, the paper analyses the theoretical aspects of transfer to build an overall picture of the phenomenon, from early theories to recent hierarchical accounts. [ABSTRACT FROM AUTHOR]

This paper systematically reviews the literature pertaining to the use of resting-state functional magnetic resonance imaging (rsfMRI) in anorexia nervosa (AN), classifying studies on the basis of different analysis approaches. We followed PRISMA guidelines. Fifteen papers were included, investigating a total of 294 participants with current or past AN and 285 controls. The studies used seed-based, whole-brain independent component analysis (ICA), network-of-interest ICA based and graph analysis approaches. The studies showed relatively consistent overlap in results, yet little overlap in their analytical approach and/or a-priori assumptions. Functional connectivity alterations were mainly found in the corticolimbic circuitry, involved in cognitive control and visual and homeostatic integration. Some overlapping findings were found in brain areas putatively important in AN, such as the insula. These results suggest altered functional connectivity in networks/areas linked to the main symptom domains of AN, such as impaired cognitive control and body image disturbances. These preliminary evidences suggest that more targeted treatments need to be developed that focus on these two symptom domains. Further studies with multi-approach analyses and longitudinal designs are needed to better understand the complexity of AN. [ABSTRACT FROM AUTHOR]