Neurobiology of social behavior and psychiatric diseases

In 2015, the United Nations set 17 Sustainable Development Goals (SDGs), which include ensuring healthy lives and well-being for all at all ages. One of the health focus areas is to maintain mental health. Differences in social behaviour are the result of a complex interplay of genetic and environmental factors and range from mild behavioural disorders to life-threatening suicide attempts. While research over the past decade has focused on genetic factors, more recently there has been increasing attention to the role of environmental influences: we now know that the development of psychiatric disorders can be linked to modern lifestyles, abnormal birth events or traumatic childhood experiences. The potential impact of these environmental factors has been amplified by the COVID epidemic, and the importance of mental health maintenance is further highlighted by the emergence of 'mental pandemics' and post-COVID syndrome with psychiatric symptoms as a consequence of pandemic and isolation.  
A common feature of mental illnesses is that, although they are known to be caused by abnormal brain function, their neuronal network background is not yet sufficiently understood and therefore their outpatient treatment is not yet solved. During early life, the nervous system undergoes a dynamic process of change and is particularly sensitive to external environmental factors, which are a risk factor for psychiatric disorders with subsequent disturbances in social behaviour. Understanding these is essential for the development of effective therapies in adulthood as well as early interventions.
In this research programme, we will use relevant animal models and clinical studies, state-of-the-art behavioural and network neurobiology to explore the neurobiological basis of social behaviour and its disorders, with a view to identifying new drug targets. The economic exploitation of our results makes our fruitful decade-long collaboration with original pharmaceutical R&D partners in the field of psychiatric diseases (Richter Gedeon Rt., Janssen) a realistic alternative.

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Autism spectrum disorder

ASD is a complex neurodevelopmental condition caused by interactions of environmental and genetic factors. Recently, maternal viral infections during pregnancy and their immunological consequences have received particular interest in research as risk factors for neurodevelopmental disorders. 

MPTP induced Pakinson model

Parkinson’s disease (PD) is a chronic, progressive neurodegenerative condition; characterized with the degeneration of the nigrostriatal dopaminergic pathway and neuroinflammation. 

Mania model

Purinergic dysfunction are involved in the pathological process of mania and depression, but the essential association is not fully understood. The activation of the purinergic P2X7 receptor (P2X7R) plays a central role in inflammation, microglia activation and IL-1β release and activates NLRP3 inflammasome. We investigated whether the d-amphetamine (AMPH) has an inflammatory profile, and the P2X7R has an effect via IL-1β in this model.

Major depression

Depression - diagnosed as a condition lasting at least 2 weeks, with lethargy and/or loss of pleasure as the leading symptoms - is the most common psychiatric disorder in the world.


Schizophrenia is a complex neurodevelopmental disorder that affects approximately 0.5%–1% of the global population and is 1 of the top 10 global causes of disability.  Like most mental disorders, schizophrenia appears to be caused by a combination of genetic, environmental, and social risk factors linked to each other by epigenetic mechanisms regulating gene expression levels and molecular pathways. . Although the pathophysiology of schizophrenia is still not completely understood, there is a growing awareness that dysregulation of immune system components is fundamentally linked to the disorder.  

Investigation of cortical abnormalities in schizophrenia patients

In collaboration with the Szent Borbála Hospital in Tatabánya, we investigate brain samples of patients diagnosed with schizophrenia post mortem, which we compare with control subjects without neurological disease. The samples are fixed shortly after death and are therefore suitable for the detection of subtle structural abnormalities.