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| CHINMULTIHIT – Identifikácia malých molekúl z tradičných čínskych bylín na multicieľovú terapiu neurodegenerat ívnych ochorení a objasnenie mechanizmu účinku | |
| Discovery and Mechanism of Small Molecules from Traditional Chinese Herbs for Multitarget directed Therapy of Neurodegenerative Diseases | |
| Program: | Bilateral – other |
| Project leader: | doc. RNDr. Gažová Zuzana, DrSc. |
| Annotation: | Protein misfolding neurodegenerative diseases (NDDs), such as Alzheimer\’s and Parkinson\’s diseases, result inextensive cellular and neuronal loss within the central nervous system. Despite the distinct manifestations of thesedisorders, they share several common pathogenic mechanisms. Current pharmacological interventions areineffective. Moreover, the complexity of NDDs necessitates innovative therapeutic approaches. In this project, thenovel "multi-target-directed ligands" (MTDLs) strategy will be employed as it focuses on development of novelcompounds modulating multiple factors simultaneously. We will focus on Chinese herbs – Angelica sinensis,Ligusticum chuanxiong, and Cinnamomum cassia. The project aims to explore the anti-aggregation potential ofthese herbal extracts and their derivatives targeting both Aβ peptide and α -synuclein, showcasing neuroprotectiveand anti-inflammatory properties to pave the way for the development of novel t herapeutic strategies for NDDs.The project combines the expertise and experience of both research teams in the field of protein misfolding andNDDs pathology, allowing us to acquire complex data with the aid of complementary approaches, leading to thesuggestion of possible alternatives of therapy against these devastating diseases. Moreover, this collaborativeresearch partnership will present an excellent opportunity for both teams\’ young members to learn new techniquesin the well-equipped laboratories at East China University and IEP SAS and gain new experience by working in aninternational scientific environment. |
| Duration: | 1.7.2024 – 30.6.2026 |
| LEAPAB – Inhibícia agregácie A-beta peptidov proteínmi vyskytujúcimi sa počas neskorej embryogenézy: nový prístup liečby Alzheimerovej choroby | |
| Inhibition of A-beta Peptides Aggregation by Late Embryogenesis Abundant Proteins: A New Approach for Alzheimer’s Disease Treatment | |
| Program: | Bilateral – other |
| Project leader: | RNDr. Bednáriková Zuzana, PhD. |
| Annotation: | Alzheimer’s disease (AD) is the most common neurodegenerative disorder, sharing unclear pathophysiology and massive social costs. Today, more than 55 million people have been diagnosed with AD, which is forecast to increase more than twice by 2050. AD is tightly associated with the formation of deposits containing amyloid β (Aβ) peptide organized into insoluble amyloid fibrils. Despite numerous contemporary studies focused on reducing Aβ aggregation, a cure for AD has not yet been found. Our project intends to implement the elements of molecular mechanisms underlying the remarkable phenomenon of plant desiccation tolerance and develop a new Aβ anti-aggregation strategy. Late Embryogenesis Abundant proteins (LEAPs) are markedly induced upon desiccation and can stabilize the native structure of proteins and membranes by a mechanism that is not fully understood. The primary project aim is to investigate the structural properties of Ramonda serbica LEAPs and their interactions with Aβ peptides and aggregation. Firstly, we will recombinantly produce LEAPs with the highest potential to inhibit Aβ aggregation. Further, we will analyze LEAPs’ secondary structure under different conditions, focusing on their order-to-disorder transitions. The final aim is to identify Aβ/LEAPs interactions and assess the Aβ anti-aggregation potential of LEAPs in vitro, which will impact the development of new strategies for AD treatment. The collaborating teams involved in this project (Slovak – IEP SAS and Serbian – IMGGE) were selected based on their expertise in protein production, protein structure analysis and amyloid aggregation. The expertise transfer between partner laboratories will be ensured by mutual training of PhD and postdoc researchers involved in the project. |
| Duration: | 1.4.2024 – 31.12.2025 |
National
| R1-Kareem Abdul – Štipendiá pre excelentných PhD. študentov a študentky (R1) – UEF SAV | |
| Misfolding proteins in amyloid diseases and their prevention/therapy | |
| Program: | Plán obnovy EÚ |
| Project leader: | MTech. Kareem Hanan Abdul |
| Duration: | 1.9.2023 – 31.8.2027 |
| Objasnenie počiatočných štádií amyloidnej agregácie proteínov – od mechanizmu k terapii | |
| Unraveling the early events of protein amyloid aggregation – from mechanism to therapy | |
| Program: | VEGA |
| Project leader: | doc. RNDr. Gažová Zuzana, DrSc. |
| Annotation: | Structural changes of poly/peptides leading to the formation of amyloid aggregates are associated with incurablediseases, like Alzheimer\’s disease or diabetes. While the general mechanisms of fibril formation and theircharacterization are well reported, the early events during poly/peptide fibrillation are still unclear. The project isfocused on understanding the early events mechanisms leading to the formation of pre-fibrillar (partially un/foldedintermediates, nuclei, oligomers) and fibrillar amyloid aggregates of selected globular and intrinsically disorderedproteins. Our focus will be the study of the kinetics of pre-fibrillar structures formation, their morphology, andcytotoxicity, under various experimental conditions, and in the presence of selected interacting partners (smallmolecules, nanoparticles). The obtained results will contribute to understanding the early events of amyloidaggregation and identifying the inhibitors with therapeutic potential for amyloid diseases. |
| Duration: | 1.1.2021 – 31.12.2024 |