A5100727512- Alzheimer's disease research and treatments
- Neuropeptides and Animal Physiology
- Peptidase Inhibition and Analysis
- Nuclear Receptors and Signaling
- Gut microbiota and health
- Inflammatory mediators and NSAID effects
- Biochemical effects in animals
- Redox biology and oxidative stress
- Nerve injury and regeneration
- Medicinal plant effects and applications
- Telomeres, Telomerase, and Senescence
- Fish Ecology and Management Studies
- Dementia and Cognitive Impairment Research
- Genomics, phytochemicals, and oxidative stress
- Semiconductor Lasers and Optical Devices
- Glycosylation and Glycoproteins Research
- Reproductive biology and impacts on aquatic species
- RNA Interference and Gene Delivery
- Acute Myeloid Leukemia Research
- Manufacturing Process and Optimization
- Fish Biology and Ecology Studies
- Glutathione Transferases and Polymorphisms
- Migraine and Headache Studies
- Tryptophan and brain disorders
- Advanced Glycation End Products research
Emory University
2018-2023
Tongji University
2023
Tongji Hospital
2023
Zhejiang Institute of Special Equipment Inspection
2019
Zhejiang University
2004-2019
Hangzhou Xixi hospital
2019
Nanjing Medical University
2007
Jiangsu Province Hospital
2007
Daping Hospital
2006
Army Medical University
2006
Objective This study is to investigate the role of gut dysbiosis in triggering inflammation brain and its contribution Alzheimer’s disease (AD) pathogenesis. Design We analysed microbiota composition 3×Tg mice an age-dependent manner. generated germ-free recolonisation with fecal samples from both patients AD age-matched healthy donors. Results Microbial 16S rRNA sequencing revealed Bacteroides enrichment. found a prominent reduction cerebral amyloid-β plaques neurofibrillary tangles...
The gut-brain axis is bidirectional, and gut microbiota influence brain disorders including Alzheimer's disease (AD). CCAAT/enhancer binding protein β/asparagine endopeptidase (C/EBPβ/AEP) signaling spatiotemporally mediates AD pathologies in the via cleaving both β-amyloid precursor Tau. We show that dysbiosis occurs 5xFAD mice, associated with escalation of C/EBPβ/AEP pathway age. Unlike aged wild-type 3xTg mice accelerate pathology young accompanied by active brain. Antibiotic treatment...
Significance In this study, we used a prodrug strategy to improve the druggability of 7,8-DHF, which mimics physiological actions BDNF in variety animal models but with modest oral bioavailability, by improving its PK profiles. 5XFAD mouse model, demonstrate that optimal R13 increases half-life, and brain exposure 7,8-DHF. Most importantly, robustly displays promising therapeutic efficacy strongly activating TrkB repressing AEP, plays crucial role pathogenesis Alzheimer’s disease (AD),...
Abstract To date, there is no validated fluid biomarker for tau pathology in Alzheimer’s disease, with contradictory results from studies evaluating the correlation between phosphorylated CSF PET imaging. Tau protein subjected to proteolytic processing into fragments before being secreted CSF. A recent study suggested that cleavage after amino acid 368 by asparagine endopeptidase (AEP) upregulated disease. We used immunoprecipitation followed mass spectrometric analyses evaluate presence of...
BDNF/TrkB neurotropic pathway, essential for neural synaptic plasticity and survival, is deficient in neurodegenerative diseases including Alzheimer's disease (AD). Our previous works support that BDNF diminishes AD pathologies by inhibiting delta-secretase, a crucial age-dependent protease simultaneously cleaves both APP Tau promotes pathologies, via Akt phosphorylation. Small molecular TrkB receptor agonist 7,8-dihydroxyflavone (7,8-DHF) binds activates the its downstream signaling,...
Significance The molecular mechanisms accounting for the environmental risk factor stimulation of Alzheimer’s disease (AD) pathogenesis including traumatic brain injury, diabetes, and chronic cerebral hypoperfusion remain unclear. BDNF/TrkB signaling pathway plays a critical role in neuronal synaptic plasticity survival. Since is reduced during aging AD human brains, we hypothesize that crosstalk between these factors deficiency may mediate pathologies. Our previous studies establish...
Abstract Solid tumors start as a local disease, but some are capable of metastasizing to the lymph nodes and distant organs. The hypoxic microenvironment, which is critical during cancer development, plays key role in regulating progression metastasis. However, molecular mechanisms mediating disseminated cell metastasis remain incompletely understood. Here, we show that C/EBPβ/AEP signaling upregulated breast cancers mediates oxidative stress lung metastasis, inactivation asparagine...
7,8-DHF was transported across Caco-2 cell monolayers by passive transport with carrier-mediated influx and efflux transporters.
Web services define a new paradigm in collaborative applications development enterprises. They span systems and organizations. The use of CAD calls for more productive work on the Internet. An efficient framework will bring great deal convenience to meet this demand. Considering inherent advantages services, paper presented working based described architecture detail. Furthermore, several key technologies used are discussed, including division method, which guarantees highly feasible...
<div>Abstract<p>Solid tumors start as a local disease, but some are capable of metastasizing to the lymph nodes and distant organs. The hypoxic microenvironment, which is critical during cancer development, plays key role in regulating progression metastasis. However, molecular mechanisms mediating disseminated cell metastasis remain incompletely understood. Here, we show that C/EBPβ/AEP signaling upregulated breast cancers mediates oxidative stress lung metastasis, inactivation...
<p>Supplementary figs</p>
<div>Abstract<p>Solid tumors start as a local disease, but some are capable of metastasizing to the lymph nodes and distant organs. The hypoxic microenvironment, which is critical during cancer development, plays key role in regulating progression metastasis. However, molecular mechanisms mediating disseminated cell metastasis remain incompletely understood. Here, we show that C/EBPβ/AEP signaling upregulated breast cancers mediates oxidative stress lung metastasis, inactivation...
<p>Supplementary figs</p>
<div>Abstract<p>NF-κB may be a potential therapeutic target for acute myelogenous leukemia (AML) because NF-κB activation is found in primitive human AML blast cells. In this report, we initially discovered that the potent antineoplastic effect of niclosamide, Food and Drug Administration–approved antihelminthic agent, was through inhibition pathway Niclosamide inhibited transcription DNA binding NF-κB. It blocked tumor necrosis factor–induced IκBα phosphorylation, translocation...