Annual Meeting of the Hungarian Neuroscience Society MITT 2025

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disorder, representing the most common form of dementia. In Hungary, there are an estimated 200,000 individuals living with dementia, with Alzheimer's disease accounting for 3.8% of total deaths between 2011 and 2015. The accumulation of β-amyloid protein in the extracellular spaces and twisted strands of tau protein in the intracellular compartments of neurons is a defining characteristic of AD. Over the past two decades, both experimental and clinical data have indicated that protein aggregation in AD results in chronic neuronal hyperexcitability, which may significantly enhance neurodegeneration and inflammation. Chronic inflammation and uncontrolled microglia activation are believed to contribute to and exacerbate neuronal injury in AD. As there is currently no effective therapy against AD, the identification of novel molecular targets is of fundamental importance.

• Botond Penke (professor emeritus, Department of Medical Chemistry, Albert Szent-Györgyi Medical School, University of Szeged) — Novel targets and drug candidates for preventing the progression of Alzheimer's disease
• Anita Kamondi (professor, Department of Neurology, Semmelweis University, Budapest) — Hyperexcitability as a modifiable risk factor of Alzheimer's disease
• Ádám Dénes (professor, "Momentum" Neuroimmunology Research Group, Institute of Experimental Medicine, Budapest) — Modulation of neurovascular responses by microglia
• Melinda E. Tóth (research associate, HUN-REN Biological Research Centre, Szeged) — Heat shock proteins and Alzheimer's disease
• Ákos Menyhárt (assistant professor, Department of Cell Biology and Molecular Medicine, University of Szeged) — Alzheimer–stroke continuum: the role of spreading depolarization

Brain damage after stroke, injuries or due to neurodegeneration leads to serious health problems, and several attempts have been made to reconstruct the nervous system. A wide range of molecules play an essential role in the process. Understanding the specificities requires preclinical models, among which those based on human induced pluripotent stem cells are very popular. The symposium introduces promising approaches for studying and reconstructing brain damage; these studies may provide insights into the pathomechanism and may lead to improved therapeutic strategies for neural repair and recovery.

• Alán Alpár (Semmelweis University, Budapest) — Secretagogin, a calcium-sensor protein shapes neuronal migration and regeneration
• Sofia Grade (IMBA, Vienna) — Cell transplantation for the reconstruction of neuronal circuits after brain damage
• Kornélia Szebényi (HUN-REN TTK, Budapest) — Brain disease models in human cortical organoids
• Alwyn Dady (UPEC, Paris) — Chicken embryo as a tool for studying regeneration of human iPSC grafts

The symposium focuses on the most recent findings obtained in any field of invertebrate neuroscience, from functional anatomy to molecular aspects of behaviour and learning. Priority is given to evolutionary aspects from the perspective of vertebrate neuroscience, with special emphasis on cutting-edge technologies in invertebrate neuroscience and on the potential of invertebrate models to address a wide range of neurobiological questions.

• István Fodor and Zsolt Pirger (HUN-REN BLKI) — Tracing the evolution of the neuroendocrine system behind animal reproduction: functional and evolutionary insights from mollusks
• George Kemenes et al. (Sussex Neuroscience, University of Sussex) — A circuit mechanism linking past and future learning through shifts in perception
• Veronica Rivi et al. (University of Modena and Reggio Emilia) — A translational and multidisciplinary approach to studying the Garcia effect, a higher form of learning with deep evolutionary roots
• Luis Alfonso Yañez Guerra et al. (University of Southampton) — Large-scale deorphanisation of GPCRs in placozoans reveals the ancestral origin of neurotransmitter signalling systems
• László Molnár et al. (HUN-REN BLKI) — Neural dependence and genes of the CNS regeneration

The symposium focuses on the potential therapeutic benefit of both endogenous and novel exogenous sigma-1 receptor (S1R) ligands for the treatment of CNS disorders. S1Rs are intracellular receptors located on segments of the endoplasmic reticulum membrane physically associated with mitochondria, abundantly expressed in neurons, oligodendrocytes and ependymocytes. They regulate lipid rafts, neuroreceptors and ion channels, influence signal transduction and neuronal plasticity, accumulate in nuclear inclusions in neurodegenerative diseases and are a major factor in cellular calcium homeostasis. Experimental results show that both endogenous (DMT) and newly synthesized S1R ligands such as (S)-L1 are protective in preclinical models of global and focal cerebral ischemia: S1R agonism supports neuronal and astrocyte survival, modulates microglial activity and protects the blood-brain barrier, emerging as a potential adjuvant pharmacological therapy in cerebral ischemia.

• Szabolcs Dvorácskó (HUN-REN Biological Research Centre, Szeged; NIH/NIAAA, Rockville) — Potential use of sigma-1 receptor ligands and cannabinoid allosteric modulators in brain disorders
• István Pesti (HCEMM-USZ Cerebral Blood Flow and Metabolism Research Group, University of Szeged) — Does N,N-dimethyltryptamine modulate microglial activity?
• Sándor Nardai (Heart and Vascular Center, Semmelweis University) — Protective effect of DMT on blood-brain barrier dysfunction in preclinical stroke models
• Szilvia Kecskés (HCEMM-USZ Cerebral Blood Flow and Metabolism Research Group, University of Szeged) — Effects of natural and synthetic sigma-1 receptor agonists in experimental cerebral ischemia