A5082940933- Alzheimer's disease research and treatments
- Chemical Synthesis and Analysis
- Neuropeptides and Animal Physiology
- Cholinesterase and Neurodegenerative Diseases
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Computational Drug Discovery Methods
- Supramolecular Self-Assembly in Materials
- Protein Structure and Dynamics
- Analytical Chemistry and Chromatography
- Neuroendocrine regulation and behavior
- Neuroinflammation and Neurodegeneration Mechanisms
- DNA and Nucleic Acid Chemistry
- Carbohydrate Chemistry and Synthesis
- Stress Responses and Cortisol
- Biochemical effects in animals
- RNA and protein synthesis mechanisms
- Tryptophan and brain disorders
- Antimicrobial Peptides and Activities
- Pharmacological Receptor Mechanisms and Effects
- Monoclonal and Polyclonal Antibodies Research
- Memory and Neural Mechanisms
- Drug Transport and Resistance Mechanisms
- Endoplasmic Reticulum Stress and Disease
- Peptidase Inhibition and Analysis
University of Szeged
2014-2023
Hungarian Academy of Sciences
2006-2016
Bay Zoltán Foundation for Applied Research
2009-2012
National University of San Luis
2009
University of Groningen
2009
Eötvös Loránd University
2006
Semmelweis University
1981-2006
Laboratoire Francis Perrin
2005
University of Toronto
2003-2005
Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2005
Alzheimer's disease is associated with an increased risk of unprovoked seizures. However, the underlying mechanisms seizure induction remain elusive. Here, we performed video-EEG recordings in mice carrying mutant human APPswe and PS1dE9 genes (APdE9 mice) their wild-type littermates to determine prevalence In two recording episodes at onset amyloid beta (Abeta) pathogenesis (3 4.5 months age), least one was detected 65% APdE9 mice, which 46% had multiple seizures 38% a generalized seizure....
Microglial activation is a key feature in Alzheimer's disease and considered to contribute progressive neuronal injury by release of neurotoxic products. The innate immune receptor Toll-like-receptor 4 (TLR4), localized on the surface microglia, first-line host defense against invading microorganisms. Here, we show that spontaneous loss-of-function mutation Tlr4 gene strongly inhibits microglial monocytic aggregated Alzheimer amyloid peptide resulting significantly lower inflammatory...
Microglia activated by extracellularly deposited amyloid β peptide (Aβ) act as a two-edged sword in Alzheimer's disease pathogenesis: on the one hand, they damage neurons releasing neurotoxic proinflammatory mediators (M1 activation); other protect triggering anti-inflammatory/neurotrophic M2 activation and clearing Aβ via phagocytosis. TLRs are associated with Aβ-induced microglial inflammatory internalization, but mechanisms remain unclear. In this study, we used real-time surface plasmon...
Antisera to the amino acid gamma-aminobutyric (GABA) have been developed with aim of immunohistochemical visualization neurons that use it as a neurotransmitter. GABA bound bovine serum albumin was immunogen. The reactivities sera and variety structurally related compounds were tested by coupling these nitrocellulose paper activated polylysine glutaraldehyde incubating unlabeled antibody enzyme method, thus simulating immunohistochemistry tissue sections. antisera did not react L-glutamate,...
The amyloid β peptide 42 (Aβ42) plays a key role in neurotoxicity Alzheimer's disease. Mononuclear phagocytes, i.e. microglia, have the potential to clear Aβ by phagocytosis. Recently, lipopolysaccharide (LPS) receptor CD14 was shown mediate phagocytosis of bacterial components and furthermore contribute neuroinflammation Here, we investigated whether this innate immunity can interact with Aβ42 peptide. Using flow cytometry, confocal microscopy two-photon fluorescence lifetime imaging (FLIM)...
To rapidly respond to invading microorganisms, humans call on their innate immune system. This occurs by microbe-detecting receptors, such as CD14, that activate cells eliminate the pathogens. Here, we link lipopolysaccharide receptor CD14 with Alzheimer's disease, a severe neurodegenerative disease resulting in dementia. We demonstrate this key immunity interacts fibrils of Alzheimer amyloid peptide. Neutralization antibodies against and genetic deficiency for significantly reduced peptide...
An antiserum to gamma-aminobutyric acid (GABA) was tested for the localization of GABAergic neurons in central nervous system using unlabeled antibody enzyme method under pre- and postembedding conditions. GABA immunostaining compared with glutamate decarboxylase (GAD) immunoreactivity cerebellar cortex normal colchicine-injected neocortex hippocampus cat. The types, distribution, proportion nerve terminals stained either sera showed good agreement all areas. Colchicine treatment had little...
Abstract Whereas a cardinal role for β‐amyloid protein (Aβ) has been postulated as major trigger of neuronal injury in Alzheimer's disease, the pathogenic mechanism by which Aβ deranges nerve cells remains largely elusive. Here we report correlative vitro and vivo evidence that an excitotoxic cascade mediates neurotoxicity rat magnocellular nucleus basalis (MBN). In application to astrocytes elicits rapid depolarization astroglial membranes with concomitant inhibition glutamate uptake....
Alzheimer disease is characterized by accumulation of the β-amyloid peptide (Aβ) generated β- and γ-secretase processing amyloid precursor protein (APP). The intake polyunsaturated fatty acid docosahexaenoic (DHA) has been associated with decreased deposition a reduced risk in several epidemiological trials; however, exact underlying molecular mechanism remains to be elucidated. Here, we systematically investigate effect DHA on amyloidogenic nonamyloidogenic APP potential cross-links...
The disordered tubulin polymerization promoting protein (TPPP/p25) was found to be co-enriched in neuronal and glial inclusions with α-synuclein Parkinson disease multiple system atrophy, respectively; however, co-occurrence of β-amyloid (Aβ) human brain has been recently reported, suggesting the existence mixed type pathologies that could result obstacles correct diagnosis treatment. Here we identified TPPP/p25 as an interacting partner soluble Aβ oligomers major risk factors for Alzheimer...
The assembly mechanisms of amyloid fibrils, tissue deposits in a variety degenerative diseases, is poorly understood. With simply modified application the atomic force microscope, we monitored growth, on mica surface, individual fibrils beta25-35 peptide with near-subunit spatial and subsecond temporal resolution. Fibril was polarized discontinuous. Bursts rapid (up to 300-nm(-1)) growth phases that extended fibril by approximately 7 nm or its integer multiples were interrupted pauses....
Hsp27 belongs to the small heat shock protein family, which are ATP-independent chaperones. The most important function of is based on its ability bind non-native proteins and inhibit aggregation incorrectly folded maintaining them in a refolding-competent state. Additionally, it has anti-apoptotic antioxidant activities. To study effect memory synaptic functions, amyloid-β (Aβ) accumulation, neurodegeneration, we generated transgenic mice overexpressing human crossed with APPswe/PS1dE9...