A5100389732- Alzheimer's disease research and treatments
- Cholinesterase and Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- Supramolecular Self-Assembly in Materials
- Cytokine Signaling Pathways and Interactions
- Asthma and respiratory diseases
- Cell death mechanisms and regulation
- Biofield Effects and Biophysics
- Advanced Glycation End Products research
- Genetics, Aging, and Longevity in Model Organisms
- Protein Structure and Dynamics
- Medicinal Plant Pharmacodynamics Research
- Retinoids in leukemia and cellular processes
- Natural Antidiabetic Agents Studies
- Computational Drug Discovery Methods
- Neuroscience and Neuropharmacology Research
- S100 Proteins and Annexins
- Medicinal Plants and Neuroprotection
Shandong University
2024
Shandong Provincial QianFoShan Hospital
2024
Xingtai Medical College
2021
Xingtai University
2021
Soochow University
2021
Xi'an Honghui Hospital
2020
Xi'an Jiaotong University
2020
Peking University
2019
Chengde Medical University
2016
Southeast University
2016
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by β amyloid (Aβ) deposition and neurofibril tangles. It has been reported that bioflavonoid, quercetin, could ameliorate AD phenotypes in C. elegans mice. However, the mechanism underlying ameliorative effect of quercetin not fully understood yet. Drosophila models recapitulate AD-like phenotypes, such as shortened lifespan, impaired locomotive ability well defects learning memory. So this study, we...
Alzheimer's disease (AD) is one of the neurodegenerative brain disorders inducing nearly half dementia cases, and diagnosis treatment AD are primary issues clinically. However, there a lack effective biomarkers drugs for therapeutics so far. In this study, bioinformatics analysis combined with an experimental verification strategy was used to identify quercetin targets treatment. First, differentially expressed genes in were identified by microarray data analysis. Second, quercetin,...
TTP488, an antagonist of the receptor for advanced glycation end-products, was evaluated as a potential treatment patients with mild-to-moderate Alzheimer's disease (AD). However, mechanism underlying protective action TTP488 against AD has not yet been fully explored.Healthy male rats were exposed to aberrant amyloid β (Aβ) 1-42. Lipopolysaccharide (LPS) and NOD-like family pyrin domain containing 1 (NLRP1) overexpression lentivirus injected activate NLRP1 inflammasome exacerbate AD....
Background and purpose: The Bushenyiqi decoction (BYD), a contemporary prescription of traditional Chinese medicine (TCM), has been observed to significantly ameliorate asthma symptoms in patients based on clinical observations. Although multi-component multi-target characteristics are important attributes BYD treatment, its pharmacological effect the underlying mechanism action remain unclear. Method: Network pharmacology: asthma-related genes were retrieved from GeneCards OMIM database....
Amyloid fibril surfaces can convert soluble proteins into toxic oligomers and are attractive targets for intervention of protein aggregation diseases. Thus far, molecules identified with inhibitory activity either large or flat cyclic compounds lacking in specificity. The main design difficulty is flatness amyloid the lack knowledge on binding interfaces. Here, we demonstrate, first time, a rational alpha-helical peptide inhibitors targeting amyloid-beta 40 (Aβ40) surfaces, based our silico...
Excitotoxicity refers to the ability of excessive extracellular excitatory amino acids damage neurons via receptor activation. It is a crucial pathogenetic process in neurodegenerative diseases. TP53 confirmed be involved excitotoxicity. demonstrated that induced glycolysis and apoptotic regulator (TIGAR)-regulated metabolic pathway can protect against neuronal injury. However, role TIGAR excitotoxicity specific mechanisms still unknown. In this study, an vivo model was constructed...
5XFAD transgenic (Tg) mice express 5 human familial Alzheimer’s Disease (AD) gene mutations ‐ Amyloid Precursor Protein from the Swedish, Florida and London families, along with 2 in presenilin‐1. Their early onset brain pathology, accelerated Aβ 42 amyloid deposition, age‐dependent neurodegeneration cognitive decline, make these an attractive translatable AD model. We used behavioral, biochemical electrophysiological analyses to track changes mice, compared their age‐matched wild‐type mice....
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