A5008360061- Alzheimer's disease research and treatments
- Supramolecular Self-Assembly in Materials
- Cholinesterase and Neurodegenerative Diseases
- Computational Drug Discovery Methods
- Neuroscience and Neuropharmacology Research
- Aquatic Ecosystems and Phytoplankton Dynamics
- Trace Elements in Health
- Chemical Synthesis and Analysis
- Marine Invertebrate Physiology and Ecology
- Drug Transport and Resistance Mechanisms
- Protein Structure and Dynamics
- Protein Hydrolysis and Bioactive Peptides
- Stress Responses and Cortisol
- Plant-based Medicinal Research
- Biochemical effects in animals
- Prion Diseases and Protein Misfolding
- Infrared Thermography in Medicine
- Proteins in Food Systems
- Neurological Disorders and Treatments
- S100 Proteins and Annexins
- Click Chemistry and Applications
- Biotin and Related Studies
- Genetics, Aging, and Longevity in Model Organisms
- Biocrusts and Microbial Ecology
- Spaceflight effects on biology
University of Szeged
2012-2023
Genomics (United Kingdom)
2011
Bay Zoltán Foundation for Applied Research
2010-2011
Hungarian Academy of Sciences
2005-2007
Brain Aβ1-42 accumulation is considered an upstream event in pathogenesis of Alzheimer's disease. However, accumulating evidence indicates that other neurochemical changes potentiate the toxicity this constitutively generated peptide. Here we report interaction with extracellular Zn2+ essential for vivo rapid uptake and into dentate granule cells normal rat hippocampus. The both was blocked by CaEDTA, chelator, Cd2+, a metal displaces binding. In perforant pathway LTP unaffected perfusion...
Amyloid fibrils are self-associating filamentous structures, the deposition of which is considered to be one most important factors in pathogenesis Alzheimer's disease and various other disorders. Here we used single molecule manipulation methods explore mechanics structural dynamics amyloid fibrils. In mechanically manipulated fibrils, formed from either β (Aβ) peptides 1-40 or 25-35, β-sheets behave as elastic structures that can "unzipped" fibril with constant forces. The unzipping forces...
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β peptides (Aβ) as perivascular deposits and senile plaques in brain. The intake polyunsaturated fatty acid docosahexaenoic (DHA) has been associated with decrea
Abstract It has been proved that the principal component of senile plaques is aggregates β‐amyloid peptide (Aβ) in cases one most common forms age‐related neurodegenerative disorders, Alzheimer's disease (AD). Although synthetic methods for synthesis Aβ peptides have developed since their first syntheses, Aβ[1‐42] still problematic to prepare. The highly hydrophobic composition results aggregation between resin‐bound chains or intrachain which leads a decrease rates deprotection and...
Oligomeric amyloid-β is currently of interest in mediated toxicity and the pathogenesis Alzheimer’s disease. Mapping interaction partners could help to discover novel pathways disease pathogenesis. To partners, we applied a protein array with more than 8100 unique recombinantly expressed human proteins. We identified 324 proteins as potential interactors oligomeric amyloid-β. The Gene Ontology functional analysis these showed that bound multiple diverse functions both from extra...
The underlying cause of Alzheimer's disease (AD) is thought to be the beta-amyloid aggregates formed mainly by Abeta1-42 peptide. Protective pentapeptides [e.g., Leu-Pro-Phe-Phe-Asp (LPFFD)] have been shown prevent neuronal toxicity arresting and reversing fibril formation. Here we report that an endogenous tetrapeptide, endomorphin-2 (End-2, amino acid sequence: YPFF), defends against induced neuromodulatory effects at cellular level. Although End-2 does not interfere with kinetics Abeta...
Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disorders even so exact pathomechanism still unclear. Recently, it widely accepted that amyloid-beta peptide (Aβ) toxicity positively linked to Aβ oligomers, which may be responsible for initiation AD. For this reason, AD research requires well defined aggregation state and structure Aβ. Precursor 'iso-Aβ1-42' makes possible use Aβ1-42 with well- in vitro vivo experiments. The aim study was identify protein expression...
Twelve compounds (1⁻12) were isolated from the methanol extract of brick cap mushroom (Hypholoma lateritium (Schaeff.) P. Kumm.). The structures elucidated using extensive spectroscopic analyses, including NMR and MS measurements. Lanosta-7,9(11)-diene-12β,21α-epoxy-2α,3β,24β,25-tetraol (1) 8-hydroxy-13-oxo-9E,11E-octa-decadienoic acid (2) identified as new natural products, together with ten known compounds, which 3β-hydroxyergosta-7,22-diene (4), demethylincisterol A2 (5), cerevisterol...
The aggregated form of amyloid-beta (Abeta) (1-42) has been shown to increase N-methyl-D-aspartic acid (NMDA) evoked neuronal activity in vivo. Here we further characterized this phenomenon by investigating the role integrin activation and downstream Src kinase using vivo electrophysiology vitro intracellular Ca (2+) measurements. Pretreatment differentiated SH-SY5Y cells with fibrillar Abeta markedly enhanced calcium increases caused NMDA receptor (NMDA-R) stimulation. Function blocking...
Background: Adiponectin and leptin are implicated in the initiation pathomechanism of Alzheimer's disease (AD). The serum concentrations these adipokines has been extensively studied AD, however little is known about their receptors this disease. Objective: We developed a novel approach to examine whether adiponectin (AdipoR1 -R2) and/or (LepR) can contribute AD pathomechanism. To achieve this, we investigated effect both genetic environmental factors associated with on expression receptors....
Neurodegenerative diseases are linked to a systemic enzyme resistance of toxic aggregated molecules and their pathological consequences. This paper presents unique phenomenon that Philodina acuticornis, bdelloid rotifer, is able catabolize different types neurotoxic peptide protein aggregates (such as beta-amyloids /Aβ/, alpha-synuclein, prion) without suffering any damage. P. acuticornis capable using these an exclusive energy source (i.e., 'food', identified in the digestive system body)...
Alzheimer's disease is one of the most common chronic neurodegenerative disorders. Despite several in vivo and clinical studies, cause poorly understood. Currently, amyloid β (Aβ) peptide its tendency to assemble into soluble oligomers are known as a main pathogenic event leading interruption synapses brain degeneration. Targeting neurotoxic Aβ can help recognize at an early stage or it be potential therapeutic approach. Unnatural β-peptidic foldamers successfully used against many different...
The in vivo investigation of kynurenic acid (KYNA) and its analogs is one the recent exciting topics pharmacology. In current study we assessed biological effects these molecules on bdelloid rotifers (Philodina acuticornis Adineta vaga) by monitoring changes their survival phenotypical characteristics. addition to longitudinal (slowly changing) markers (survival, number alive body size index), some dynamic (quickly responding) ones (cellular reduction capacity mastax contraction frequency)...