A5000968181- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Inflammasome and immune disorders
- Memory and Neural Mechanisms
- Neuroendocrine regulation and behavior
- Receptor Mechanisms and Signaling
- Neurological Disease Mechanisms and Treatments
- Immune cells in cancer
- Inflammation biomarkers and pathways
- Bullying, Victimization, and Aggression
- Effects and risks of endocrine disrupting chemicals
- Cholinesterase and Neurodegenerative Diseases
- Nitric Oxide and Endothelin Effects
- MicroRNA in disease regulation
- Biological and pharmacological studies of plants
- Pharmaceutical and Antibiotic Environmental Impacts
- Youth Development and Social Support
- Plant and animal studies
- Barrier Structure and Function Studies
- Histone Deacetylase Inhibitors Research
- RNA regulation and disease
- Genomics and Phylogenetic Studies
- Ear and Head Tumors
- Apelin-related biomedical research
Nanjing Drum Tower Hospital
2019-2024
University of South China
2024
Nanjing Brain Hospital
2023
Nanjing University
2020-2023
Jiangsu Provincial Hospital of Traditional Chinese Medicine
2023
Pharmaceutical Biotechnology (Czechia)
2023
State Key Laboratory of Pharmaceutical Biotechnology
2023
Nanjing Medical University
2021
Nanjing University of Chinese Medicine
2021
Jiangsu Province Blood Center
2020-2021
Action against bullying in schools has been quite extensive over the last decade. The article reports a survey of 2308 pupils aged 10-14 years, from 19 across England. Frequencies being bullied and others suggest some decline earlier findings, which may reflect positive results achieved by concerned about issue. Victims report variety coping strategies, varying with age. Bullies often feeling that victim deserved it, response especially marked older boys. A `culture silence' still persists...
Abstract Choline acetyltransferase neurons in the vertical diagonal band of Broca (vChATs) degenerate early stage Alzheimer’s disease (AD). Here, we report that vChATs directly innervate newly generated immature (NGIs) dorsal hippocampus (dNGIs) adult mice and regulate both dNGIs survival spatial pattern separation. In a mouse model exhibits amyloid-β plaques similar to AD patients, cholinergic synaptic transmission, dNGI separation are impaired. Activation with theta burst stimulation (TBS)...
Abstract Ischemic stroke leads to white matter damage and neurological deficits. However, the characteristics of injury repair after are unclear. Additionally, precise molecular communications between microglia during rehabilitation phase remain elusive. In this current study, MRI DTI scan immunofluorescence staining were performed trace in mouse transient middle cerebral artery occlusion (tMCAO) model. We found that most serious was on Day 7 ischemic stroke, then it recovered gradually from...
Chronic cerebral ischemia induces white matter injury (WMI) contributing to cognitive decline. Both astrocytes and microglia play vital roles in the demyelination remyelination processes, but underlying mechanism remains unclear. This study aimed explore influence of chemokine CXCL5 on WMI decline chronic mechanism.Bilateral carotid artery stenosis (BCAS) model was constructed mimic 7-10 weeks old male mice. Astrocytic Cxcl5 conditional knockout (cKO) mice were with overexpressing generated...
Abstract Background Patients with Alzheimer’s disease (AD) are often co-morbid unprovoked seizures, making clinical diagnosis and management difficult. Although it has an important role in both AD epilepsy, abnormal γ-aminobutyric acid (GABA)ergic transmission is recognized only as a compensative change for glutamatergic damage. Neuregulin 1 (NRG1)-ErbB4 signaling can promote GABA release suppress epileptogenesis, but its effects on cognition still controversial. Methods Four-month-old...
Synaptic spine loss is one of the major preceding consequences stroke damages, but its underlying molecular mechanisms remain unknown. Here, we report that a direct interaction DAPK1 with Tau causes and subsequently neuronal death in mouse model stroke. We found phosphorylates protein at Ser262 (pS262) cortical neurons mice. Either genetic deletion kinase domain (KD) mice (DAPK1-KD−/−) or blocking DAPK1-Tau by systematic application membrane permeable peptide protects damages improves...
Alzheimer's disease (AD) is the most common neurodegenerative disorder leading to dementia in elderly, and mechanisms of AD are not fully defined. MicroRNAs (miRNAs) have been shown contribute memory deficits AD. In this study, we identified that miR-204-3p was downregulated hippocampus plasma 6-month-old APPswe/PS1dE9 (APP/PS1) mice. overexpression attenuated synaptic APP/PS1 The amyloid levels oxidative stress were decreased mice after overexpression. Nicotinamide adenine dinucleotide...
Abstract Aims Ischemic stroke is a life‐threatening disease with limited therapeutic strategies. Blood‐brain barrier (BBB) disruption critical pathological process that contributes to poor outcomes in ischemic stroke. We previously showed the microglial inhibition of inflammasome sensor absent melanoma 2 (AIM2) suppressed inflammatory response and protected against However, whether AIM2 involved BBB during cerebral ischemia unknown. Methods Middle artery occlusion (MCAO) oxygen‐glucose...
Abstract White matter injury (WMI), which reflects myelin loss, contributes to cognitive decline or dementia caused by cerebral vascular diseases. However, because pharmacological agents specifically for WMI are lacking, novel therapeutic strategies need be explored. It is recently found that adaptive myelination required homeostatic control of brain functions. In this study, myelination‐related applied explore the treatment ischemic WMI‐related dysfunction. Here, bilateral carotid artery...
The inflammatory response plays a pivotal role in blood-brain barrier (BBB) destruction following ischemic brain injury. Enhanced leukocyte adhesion to vascular endothelial cells is an essential event the process. TMEM16A, newly discovered protein regulating calcium-activated chloride channels, widely expressed eukaryotes. Recent studies have suggested that upregulated expression of TMEM16A associated with occurrence and development many diseases. However, BBB integrity after stroke has not...
The over-production of β-amyloid (Aβ) has been strongly correlated to neuronal dysfunction and altered synaptic plasticity in Alzheimer's disease (AD). Accordingly, it proposed that disrupted transmission network instability underlie memory failure is evident the early phases AD. Homeostatic (HSP) serves restrain activity within a physiological range. Therefore disruption this mechanism may lead destabilization neural circuit function. Here, we report during HSP by deprivation, application...
Excitatory pyramidal neurons in the entorhinal cortical layer II region (ECII PN ) form functional excitatory synapses with CA1 parvalbumin inhibitory (CA1 PV and undergo selective degeneration early stages of Alzheimer's disease (AD). Here, we show that death-associated protein kinase 1 (DAPK1) is selectively activated ECII AD mice. Inhibition DAPK1 by deleting a catalytic domain or death rescues -CA1 synaptic loss improves spatial learning memory This study demonstrates activation...
Pattern separation (PS) dysfunction is a type of cognitive impairment that presents early during the aging process, and this deficit has been attributed to structural functional alterations in dentate gyrus (DG) hippocampus. Absent melanoma 2 (AIM2) an essential component inflammasome. However, whether AIM2 plays role aging-associated remains unclear. Here, we found PS function was impaired mice accompanied by marked synaptic loss increased expression DG. Subsequently, used overexpression...
Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), and emerging evidence has shown that microRNAs (miRs) are alternative biomarkers therapeutic targets for synaptic dysfunctions AD. In this study, we found level miR-431 was downregulated plasma patients with amnestic mild cognitive addition, it decreased hippocampus APPswe/PS1dE9 (APP/PS1) mice. Lentivirus-mediated overexpression CA1 ameliorated memory deficits APP/PS1 mice, while did not...
Dysfunction of synaptic plasticity leads to memory impairment in Alzheimer's disease (AD). Muscone (Mus) has shown neuroprotective effects cerebral ischemic models. However, little is known Mus on AD.To investigate the functions and 6-month-old APP/PS1 double-transgenic mice explore potential mechanisms.Mus was intraperitoneally injected into or wild-type mice, cognitive function assessed by Novel object recognition Morris water maze tests. The levels amyloid-β (Aβ) were evaluated...
Abstract Aims Synaptic dysfunction is a hallmark pathology of Alzheimer's disease (AD) and strongly associated with cognitive impairment. Abnormal phagocytosis by the microglia one main causes synapse loss in AD. Previous studies have shown that absence melanoma 2 (AIM2) inflammasome activity increased hippocampus APP/PS1 mice, but role AIM2 AD remains unclear. Methods Injection Aβ 1‐42 into bilateral hippocampal CA1 was used to mimic an mouse model (AD mice). C57BL/6 mice injected...