Trends and latest results in Hungarian brain research at the NAP3.0 conference
When it was launched in 2013, the National Brain Research Programme (NAP) was one of the biggest undertakings of our Academy. On 6 and 7 May this year, participants of the third edition of the NAP presented their results at the Puchner Castle Hotel in Bikal.
The NAP 3.0 consortium, led by academician Zoltán Nusser, brings together 38 research groups from 10 institutions across the country, only two of which were not represented.
The first four presentations were open to the press, and short interviews with the presenters were also organised to inform taxpayers interested in the programme about their work.
Dr. Ádám Dénes, head of the Neuroimmunology Group at HUN-REN KOKI, spoke about the bilateral links between the immune and nervous systems in his presentation entitled "Inflammation and neurodegenerative diseases: why it is important to explore the links".
- What do chronic diseases such as diabetes, atherosclerosis, hypertension or obesity have to do with neuroscience?
- These diseases also cause a chronic inflammatory state in the body, causing damaging changes in the vascular pathways of many organs, including the blood vessels of the central nervous system. Circulating inflammatory proteins also reach the brain and cause fundamental changes in the function of the brain's primary immune cells, the microglia cells. In addition to its immune functions, microglia also play an essential role in maintaining the health of nerve cells and blood vessels.
- He also highlighted the role of microglia in the brain effects of COVID19!
- The state of microglia is fundamentally altered by COVID-19 infection, and the synapses essential for blood vessel and nerve cell communication in inflamed brain areas are also damaged. These changes can be assessed by clinical imaging measurements and the results correlate with acute or post-COVID neurological symptoms.
- How would you summarise your work?
Our research shows that understanding and properly regulating inflammatory processes in the nervous system can help to develop new diagnostic and therapeutic approaches for a wide range of neurological diseases.
"Identifying mechanisms and new therapeutic options for chronic stress-induced pain"
Pain is one of the most common sensations that no one can avoid in their lifetime, but chronic pain is an enormous health and social burden. Dr Zsuzsanna Helyes (PTE) presented research on chronic stress-induced pain.
- Why should this be a priority?
- Approximately ten percent of the population suffers from primary chronic pain. This pain is defined by the International Pain Society 2021 as lasting for at least 3 months, but can last for years or even decades, however, the exact cause is not known. No nerve damage, no inflammation. Such as widespread pain in the musculoskeletal system, fibromyalgia, which is also associated with sleep disturbance, lethargy, constant feeling of fatigue. It includes chronic regional pain syndrome (CRPS), where a small injury triggers a large and long-lasting immune response, inflammation and pain in a well-defined area of the limbs, and chronic low back pain, usually caused by psychosocial stress.
- How can such patients be treated?
- Classical painkillers are not effective enough in these conditions and/or their many side effects make long-term use unlikely, so new and safe medicines are needed. The development of breakthrough new medicines requires clinical trial designs, complex analytical and bioinformatics methods and experimental systems to understand the pathophysiology and identify new targets.
The short title of the presentation by Dr. Balázs Hangya (HUN-REN KOKI) immediately attracted interest. "The conductor of memory"
- The basis of learning in the brain is the connection between neurons, the synapse. According to Hebb's rule, the synapse is strengthened when two cells involved are active at the same time. When memories are stored, the simultaneously active cells thus form an activated network within which connections are strengthened. According to the principle of autoassociative memory, when memories are recalled, partial memories activate part of the network, and then the whole network is activated through the previously strengthened connections. This process is called pattern completion.
- What exactly was studied?
- Our experiments were designed to answer how the brain regulates the storage and retrieval of memories. Although we experience it as happening all at once, it actually alternates between 8 and 10 times per second, according to a so-called theta rhythm. The CA1 subarea of the hippocampus communicates with the entorhinal cortex during memory storage and interacts with the hippocampal CA3 area during memory recall.
During memory storage, area CA1 communicates with the entorhinal cortex area, indicated by faster "moderately fast" gamma rhythms appearing in the theta peaks, while during memory recall it interacts more with hippocampal area CA3, which in turn is accompanied by slow gamma rhythms appearing in the theta valleys.
- But how do the entorhinal cortex and CA3 know when to "talk" to CA1?
- This is controlled by the medial septum, which is also important in generating the theta rhythm, and whose cells show activity correlated with the gamma rhythms of the hippocampus at different frequencies, hence their name as the conductors of memory.
"What will tourism do to you? Blue algae toxins and their possible (neuro)physiological effects "
Dr. Zsolt Pirger (HUN-REN BLKI) talked about the neurological investigation of blue algae toxins (cyanotoxins) accumulating after algal blooms.
- Which neurological lesions can be caused by these cyanotoxins?
- One of these cyanotoxins, BMAA, has been linked to several neurodegenerative diseases (ALS, Alzheimer's disease, Parkinson's disease). After entering the intestinal tract, the BMAAA is retrogradely transported to the central nervous system, where it can induce protein plaques, mitochondrial dysfunction and neurodegeneration through structural changes in proteins.
- What experiments have been done to demonstrate the damaging effects of toxins?
- Our experimental model system was the simpler, more detailed, neurotrophic large marsh snail (Lymnaea). The neurobehavioural effects of cyanotoxins have been studied at the individual, cellular and molecular levels using neurophysiological and microelectrophysiological methods, and our results are applicable to higher organisms.
- Do you have any that are already available?
- It already has so much practical use that, in the case of a localised algal bloom, recommendations to help decision-makers take the necessary action.