A5100713041- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Nuclear Receptors and Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Epigenetics and DNA Methylation
- Tryptophan and brain disorders
- Mitochondrial Function and Pathology
- Peptidase Inhibition and Analysis
- Genetics and Neurodevelopmental Disorders
- Signaling Pathways in Disease
- Memory and Neural Mechanisms
- Nerve injury and regeneration
- Nanofabrication and Lithography Techniques
- Histone Deacetylase Inhibitors Research
- Gastric Cancer Management and Outcomes
- Electrospun Nanofibers in Biomedical Applications
- Spine and Intervertebral Disc Pathology
- Autophagy in Disease and Therapy
- Advancements in Photolithography Techniques
- Neuropeptides and Animal Physiology
- Gastrointestinal Tumor Research and Treatment
- Cholinesterase and Neurodegenerative Diseases
- Advanced Surface Polishing Techniques
- Neurogenesis and neuroplasticity mechanisms
- Anesthesia and Pain Management
Qilu Hospital of Shandong University
2025
Wuhan University
2021-2025
Renmin Hospital of Wuhan University
2021-2025
National Kaohsiung University of Science and Technology
2018-2025
Yunnan University of Traditional Chinese Medicine
2025
Liaocheng People's Hospital
2024
Chinese Academy of Medical Sciences & Peking Union Medical College
2024
Emory University
2018-2023
Huazhong University of Science and Technology
2013-2022
Tongji Hospital
2020-2022
BDNF/TrkB neurotrophic signaling regulates neuronal development, differentiation, and survival, deficient activity underlies neurodegeneration in Alzheimer's disease (AD). However, exactly how participates AD pathology remains unclear. Here, we show that deprivation of increases inflammatory cytokines activates the JAK2/STAT3 pathway, resulting upregulation transcription factor C/EBPβ. This, turn, results increased expression δ-secretase, leading to both APP Tau fragmentation by δ-secretase...
Intracellular accumulation of wild-type tau is a hallmark sporadic Alzheimer's disease (AD), but the molecular mechanisms underlying tau-induced synapse impairment and memory deficit are poorly understood. Here we found that overexpression human full-length (termed hTau) induced deficits with impairments synaptic plasticity. Both in vivo vitro data demonstrated hTau caused remarkable dephosphorylation cAMP response element binding protein (CREB) nuclear fraction. Simultaneously,...
Abstract Intracellular accumulation of tau protein is hallmark sporadic Alzheimer’s disease (AD), however, the cellular mechanism whereby causes neurodegeneration poorly understood. Here we report that overexpression human wild-type full-length (termed htau) disrupted mitochondrial dynamics by enhancing fusion and induced their perinuclear in HEK293 cells rat primary hippocampal neurons. The htau at later stage inhibited functions shown decreased ATP level, ratio ATP/ADP complex I activity....
// Yu Hu 1,* , Xia-Chun Li Zhi-hao Wang 1 Luo Xiangnan Zhang 2 Xiu-Ping Liu Qiong Feng Qun Zhenyu Yue 3 Zhong Chen Keqiang Ye 4 Jian-Zhi 1,5 and Gong-Ping Department of Pathophysiology, School Basic Medicine The Collaborative Innovation Center for Brain Science, Key Laboratory Ministry Education China Neurological Disorders, Tongji Medical College, Huazhong University Science Technology, Wuhan, Pharmacology, College Pharmaceutical Sciences, Zhejiang University, Hangzhou, Departments...
Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties synaptic plasticity. Recent studies have demonstrated the serum brain magnesium levels decreased in AD patients; however, exact role pathogenesis remains unclear. Here, we found intraperitoneal administration sulfate increased protected memory capacities streptozotocin-induced sporadic model rats. We also...
Abstract Different emotional states lead to distinct behavioural consequences even when faced with the same challenging events. Emotions affect learning and memory capacities, but underlying neurobiological mechanisms remain elusive. Here we establish models of learned helplessness (LHL) hopefulness (LHF) by exposing animals inescapable foot shocks or anticipated avoidance trainings. The LHF show spatial potentiation excitatory monosynaptic upscaling between posterior basolateral amygdale...
Abstract Gut dysbiosis contributes to Alzheimer’s disease (AD) pathogenesis, and Bacteroides strains are selectively elevated in AD gut microbiota. However, it remains unknown which species how their metabolites trigger pathologies. Here we show that fragilis 12-hydroxy-heptadecatrienoic acid (12-HHTrE) Prostaglandin E2 (PGE2) activate microglia induce pathogenesis neuronal C/EBPβ transgenic mice. Recolonization of antibiotics cocktail-pretreated Thy1-C/EBPβ mice with patient fecal samples...
Significance BDNF is important in neuronal survival and synaptic plasticity. level reduction Alzheimer’s disease (AD) well documented, but it remains unclear whether deficiency contributes to AD pathology. We show that deprivation provokes asparagine endopeptidase (AEP) activation via reducing δ-secretase T322 phosphorylation by Akt subsequently cleaves Tau at N368 residue enhances its binding with TrkB receptors, blocking the neurotrophic signals. Our data demonstrate AEP-cleaved...
The age-related cognitive decline of normal aging is exacerbated in neurodegenerative diseases including Alzheimer's disease (AD). However, it remains unclear whether regulators AD pathologies contribute to life span. Here, we show that C/EBPβ, an Aβ and inflammatory cytokine-activated transcription factor promotes via activating asparagine endopeptidase (AEP), mediates longevity a gene dose-dependent manner neuronal C/EBPβ transgenic mice. selectively triggers inhibitory GABAnergic...
Early onset familial Alzheimer's disease (FAD) with APP, PS1/2 (presenilins) mutation accounts for only a small portion of AD cases, and most are late-onset sporadic. However, majority mouse models developed to mimic the genetic cause human by overexpressing mutated forms PS1/2, and/or Tau protein, though there is no in AD, single model recapitulates all aspects pathology. Here, we report Thy1-ApoE4/C/EBPβ double transgenic that demonstrates key pathologies an age-dependent manner absence...
Abstract Abnormal tau hyperphosphorylation is an early pathological marker of Alzheimer’s disease (AD), however, the upstream factors that regulate phosphorylation are not illustrated and there no efficient strategy to arrest hyperphosphorylation. Here, we find activation endogenous EphB2 receptor by ligand stimulation (ephrinB1/Fc) or ectopic expression plus induces a remarkable dephosphorylation at multiple AD-associated sites in SK-N-SH cells human embryonic kidney stably express...
Non-healing pressure ulcers impose heavy burdens on patients and clinicians. Cord blood mononuclear cells (CB-MNCs) are a novel type of tissue repair seed cells. However, their clinical application is restricted by low retention survival rates post-transplantation. This study aims to investigate the role thermo-sensitive chitosan/hydroxyethyl cellulose/glycerophosphate (CS/HEC/GP) hydrogel encapsulated CB-MNCs in ulcer wound healing. Pressure were induced backs aged mice. After construction...
Early life experience modulates resilience to stress in later life. Previous research implicated maternal care as a key mediator of behavioral responses the adversity adolescence, but details molecular mechanisms remain elusive. Here, we show social activates transcription factor C/EBPβ mPFC neurons adolescent mice, which transcriptionally upregulates Dnm1l and promotes mitochondrial dysfunction, thereby conferring susceptibility mice. Moreover, different separation differentially regulates...
To conduct a comprehensive bibliometric analysis of LL-37, summarize its development trends and patterns, identify emerging research hotspots. Bibliometric Knowledge Graph Analysis Literature Data Related to LL-37 in the WOSCC Database Using Citespace Vosviewer. A total 2,814 articles were analyzed, revealing steady increase recent publications. The USA Sweden main contributors, with PLOS One publishing most articles. Research on cancer mast cells is as new focus. status quantitatively...