Topic: schizophrenia

Thalamic networks, at the core of thalamocortical and thalamosubcortical communications, underlie processes of perception, attention, memory, emotions, and the sleep-wake cycle, and are disrupted in mental disorders, including schizophrenia and autism. However, the underlying mechanisms of pathology are unknown. I will present novel evidence on key organizational principles, structural, and molecular features of thalamocortical networks, as well as critical thalamic pathway interactions that are likely affected in disorders. This data can facilitate modeling typical and abnormal brain function

Predictive processing is a computational framework that aims to explain how the brain processes sensory information by making predictions about the environment and minimizing prediction errors. It can also be used to explain some of the key symptoms of psychotic disorders such as schizophrenia. In my talk, I will provide an overview of our progress in this endeavor.

The human voice is possibly the most important sound category in the social landscape. Compared to other non-verbal emotion signals, the voice is particularly effective in communicating emotions: it can carry information over large distances and independent of sight. However, the study of vocal emotion expression and perception is surprisingly far less developed than the study of emotion in faces. Thereby, its neural and functional correlates remain elusive. As the voice represents a dynamically changing auditory stimulus, temporally sensitive techniques such as the EEG are particularly info

The use of molecular imaging, particularly PET and SPECT, has significantly transformed the treatment of schizophrenia with antipsychotic drugs since the late 1980s. It has offered insights into the links between drug target engagement, clinical effects, and side effects. A therapeutic window for receptor occupancy is established for antipsychotics, yet there is a divergence of opinions regarding the importance of blood levels, with many downplaying their significance. As a result, the role of therapeutic drug monitoring (TDM) as a personalized therapy tool is often underrated. Since molecular

Schizophrenia is a neuropsychiatric disorder characterized by positive symptoms (such as hallucinations and delusions), negative symptoms (such as avolition and withdrawal) and cognitive dysfunction1. Schizophrenia is highly heritable, and genetic studies are playing a pivotal role in identifying potential biomarkers and causal disease mechanisms with the hope of informing new treatments. Genome-wide association studies (GWAS) identified nearly 270 loci with a high statistical association with schizophrenia risk; however each locus confers only a small increase in risk therefore it is difficul

Schizophrenia is considered to be a complex illness with multiple pathways contributing to its clinical phenotype and is argued to be a disorder of disrupted brain network organization. Structural covariance in schizophrenia indicates a system-level brain maturation disruption overlapping with patterns of disturbed functional connectivity. Structural covariance networks are typically computed at the group-level, which prevents individualized inferences. To advance precision medicine of schizophrenia, a reliable mapping of brain system-level heterogeneity at the subject-level is critical. Here,

Genome-wide association studies (GWAS) have identified multiple disease-associated genetic variations across different psychiatric disorders raising the question of how these genetic variants relate to the corresponding pharmacological treatments. In this talk, I will outline our work investigating whether functional information from a range of open bioinformatics datasets such as protein interaction network (PPI), brain eQTL, and gene expression pattern across the brain can uncover the relationship between GWAS-identified genetic variation and the genes targeted by current drugs for psychiatr

Three intimately related dimensions of the mammalian genome—linear DNA sequence, gene transcription, and 3D genome architecture—are crucial for the development of nervous systems. Changes in the linear genome (e.g., de novo mutations), transcriptome, and 3D genome structure lead to debilitating neurodevelopmental disorders, such as autism and schizophrenia. However, current technologies and data are severely limited: (1) 3D genome structures of single brain cells have not been solved; (2) little is known about the dynamics of single-cell transcriptome and 3D genome after birth; (3) true de nov

Playing action video games involves both explicit (conscious) and implicit (non-conscious) expectations of timed events, such as the appearance of foes. While studies revealed that explicit attention skills are improved in action video game players (VGPs), their implicit skills remained untested. To this end, we investigated explicit and implicit temporal processing in VGPs and non-VGPs (control participants). In our variable foreperiod task, participants were immersed in a virtual reality and instructed to respond to a visual target appearing at variable delays after a cue. I will present beh

People with chronic schizophrenia die on average 10-15 years sooner than the general population, mostly due to physical comorbidity. While sociodemographic, chronic lifestyle and iatrogenic factors are important contributors to this comorbidity, a growing body of research is beginning to suggest that early signs of cardiometabolic dysfunction may be present from the onset of psychosis in some young adults, and may even be detectable before the onset of psychosis. Given that primary prevention is the best means to prevent the onset of more chronic and severe cardiometabolic phenotypes such as C

Common factors are omnipresent in everyday life, e.g., it is widely held that there is a common factor g for intelligence. In vision, however, there seems to be a multitude of specific factors rather than a strong and unique common factor. In my thesis, I first examined the multidimensionality of the structure underlying visual illusions. To this aim, the susceptibility to various visual illusions was measured. In addition, subjects were tested with variants of the same illusion, which differed in spatial features, luminance, orientation, or contextual conditions. Only weak correlations were o

Time and again we are faced with the question at what point in the treatment of schizophrenia a depot formulation should be used. The data on the so-called LAIs (Long-Acting Injectables) has steadily increased in recent years. Today, we have very good evidence for the early use of depot therapies. However, the willingness and consent of the patient for this form of pharmacotherapy remains central to the successful use of LAIs. In his lecture, Prof. Correll will talk about the current evidence for the use of LAIs summarizing the latest studies.

In this lecture, Dr Stevens will discuss recent work that implicates brain immune cells, called microglia, in sculpting of synaptic connections during development and their relevance to autism, schizophrenia and other brain disorders. Her recent work revealed a key role for microglia and a group of immune related molecules called complement in normal developmental synaptic pruning, a normal process required to establish precise brain wiring. Emerging evidence suggests aberrant regulation of this pruning pathway may contribute to synaptic and cognitive dysfunction in a host of brain disorders,

The establishment of effective therapies for neurodegenerative and neuropsychiatric diseases is still challenging and one of the reasons is that especially for age-associated neurodegenerative diseases pathology accumulates long before there are any clinical signs of disease. Thus, patients are often only diagnosed at an already advanced state of molecular pathology, when causative therapies fail. Thus, there is an urgent need for molecular biomarkers that could detect individuals at risk for developing a CNS disease and stratify patients. I will address epigenetic processes such as histone-mo

Background: Recent discovery of hundreds of common gene variants associated with schizophrenia has enabled polygenic risk scores (PRS) to be measured in the population. It is hypothesized that normal variation in genetic risk of schizophrenia should be associated with MRI changes in brain morphometry and tissue composition. Methods: We used the largest extant genome-wide association dataset (N = 69,369 cases and N = 236,642 healthy controls) to measure PRS for schizophrenia in a large sample of adults from the UK Biobank (Nmax = 29,878) who had multiple micro- and macro-structural MRI metrics

Although substance use disorders (SUDs) occur commonly in patients with schizophrenia and significantly worsen their clinical course, the neurobiological basis of SUDs in schizophrenia is not well understood. Therefore, there is a critical need to understand the mechanisms underlying SUDs in schizophrenia in order to identify potential targets for therapeutic intervention. Since drug use usually begins in adolescence, it is also important to understand the long-term effects of adolescent drug exposure on schizophrenia- and reward- related behaviors and circuitry. This talk will combine pharmac

Despite the consistency of symptoms at the cognitive level, we now know that brain disorders like Autism and Schizophrenia can each arise from mutations in >100 different genes. Presumably there is a convergence of “symptoms” at the level of neural circuits in diagnosed individuals. In this talk I will argue that redundancy in neural circuit parameters implies that we should take a circuit-function rather that circuit-component approach to understanding these disorders. Then I will present our recent empirical work testing a circuit-function theory for Autism: the idea that neural circuits sho

Among the brain structures affected in Schizophrenia is the hippocampus. In addition to structural changes [1], dysfunctions of the synaptic plasticity have also been observed supporting cognitive impairment [2]. To study these phenomena in depth, we aim to develop and match two models of the pathology, computational and experimental. Our work is based on an existing computational hippocampus model [3] and a 3-hits mouse model [4]. For that purpose, we analyze electrophysiological signals recorded with Multi-Electrode Array (MEA) on hippocampal slices to extract synaptic transmission character

Schizophrenia is a complex mental illness, with a higher risk of onset among young men. Schizophrenia is nowadays considered to result from a defective connectivity, having a neurodevelopmental origin, between several integrative regions. Morphological anomalies consistent with early brain development disturbances have been described at the level of the patients'left prefrontal cortex (PFC). Furthermore, psychotomimetic such as the noncompetitive NMDA/glutamate receptor antagonist ketamine, can induce psychotic symptoms in healthy subjects and exacerbate them in schizophrenia patients. Taking

Recent research highlights inflammation's pivotal role in the etiology of psychotic disorders, emphasizing the potential of inflammatory markers as diagnostic and prognostic tools. This study aimed to elucidate the differential profiles of neutrophil-to-lymphocyte ratio(NLR), monocyte-to-lymphocyte ratio(MLR), platelet-to-lymphocyte ratio(PLR), and systemic immune-inflammatory index(SII) in schizophrenia versus acute psychosis. Conducting a retrospective analysis, we included 126 patients from Prof. Dr. Alexandru Obregia Hospital in Bucharest, divided into two cohorts: 67 patients diagnosed wi

SP4 gene is one of the two risk genes implicated in schizophrenia in recent large unpublished case-controlled genomic and exomic sequencing studies. Data on Spatio-temporal SP4 expression in the brain and it's biological functions are sparse in published literature. Bulk RNA sequencing and single-cell high-resolution mid-gestation Spatio-temporal RNA sequencing studies on SP4 from certain brain regions were collated and analysed from published and unpublished databases. The results of bulk RNA sequencing show that SP4 is mainly expressed in the fetal brain. Single-cell RNA sequencing of the mi