A5057469411- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Retinal Development and Disorders
- Dementia and Cognitive Impairment Research
- Intracranial Aneurysms: Treatment and Complications
- Stress Responses and Cortisol
- Tryptophan and brain disorders
- Regulation of Appetite and Obesity
- Mitochondrial Function and Pathology
- Genetic Neurodegenerative Diseases
- Neurological disorders and treatments
- Parkinson's Disease Mechanisms and Treatments
- Neurological Disease Mechanisms and Treatments
- Anesthesia and Neurotoxicity Research
- Neural dynamics and brain function
- Intracerebral and Subarachnoid Hemorrhage Research
- S100 Proteins and Annexins
- Mesenchymal stem cell research
- Receptor Mechanisms and Signaling
- Neuroendocrine regulation and behavior
- Photoreceptor and optogenetics research
- Traumatic Brain Injury and Neurovascular Disturbances
Central South University
2016-2025
Shandong University
2024-2025
First Affiliated Hospital of Bengbu Medical College
2024
Xiangya Hospital Central South University
2017-2022
Yantai University
2022
China University of Mining and Technology
2019
First Affiliated Hospital of Zhengzhou University
2017
Southern Illinois University School of Medicine
2007-2016
Southern Illinois University Carbondale
2007-2016
University of California, Irvine
1996-2002
Mutations in SCN1A, the gene encoding α subunit of Nav1.1 channel, can cause epilepsies with wide ranges clinical phenotypes, which are associated contrasting effects channel loss-of-function or gain-of-function. In this project, CRISPR/Cas9- and TALEN-mediated genome-editing techniques were applied to induced pluripotent stem cell (iPSC)-based-disease model explore mechanism epilepsy caused by SCN1A mutation. By fluorescently labeling GABAergic subtype iPSC-derived neurons using...
Abstract Alzheimer disease (AD) is the leading cause of dementia that affects millions old people. Despite significant advances in understanding AD pathobiology, no modifying treatment available. MicroRNA‐124 (miR‐124) most abundant miRNA normal brain with great potency to ameliorate AD‐like pathology, while it deficient brain. Herein, authors develop a DNA nanoflowers (DFs)‐based delivery system realize exogenous supplementation miR‐124 for therapy. The DFs well‐controlled size and...
Abstract The presence of neuritic plaques is a pathological hallmark Alzheimer’s disease (AD). However, the origin extracellular β‐amyloid peptide (Aβ) deposits and process plaque development remain poorly understood. present study attempted to explore pathogenesis by localizing β‐secretase‐1 (BACE1) elevation relative Aβ accumulation synaptic/neuritic alterations in forebrain, using transgenic mice harboring familial AD (FAD) mutations (5XFAD 2XFAD) as models. In animals with fully...
Chronic neuroinflammation is thought to play an etiological role in Alzheimer's disease (AD) which characterized pathologically by amyloid and tau formation, as well neuritic dystrophy synaptic degeneration. The causal relationship between these pathological events a topic of ongoing research discussion. Recent data from transgenic AD models point tight spatio-temporal link pathology, with the obligatory enzyme for β-amyloid (Aβ) production, namely β-secretase-1 (BACE1), being overexpressed...
Abstract In vitro studies have established the prevalent theory that mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson’s disease (PD). However, difficulty detecting endogenous protein rodent brains and cell lines has prevented rigorous investigation of vivo role PINK1. Here we report form is selectively expressed human monkey brains. CRISPR/Cas9-mediated deficiency causes similar fetal adult monkeys as well cultured neurons without affecting...
The deposition of β-amyloid (Aβ) in the brain is a pathologic hallmark Alzheimer's disease (AD), appearing years before onset symptoms, and its detection incorporated into clinical diagnosis. Here, we have discovered developed class diaryl-azine derivatives for detecting Aβ plaques AD using PET imaging. After set comprehensive preclinical assessments, screened out promising Aβ-PET tracer, [18F]92, with high binding affinity to aggregates, significant ability sections, optimal pharmacokinetic...
Abstract INTRODUCTION Aging is one of the risk factors for early onset Alzheimer's disease (AD). We previously discovered that age‐dependent increase in Ubiquitin Conjugating Enzyme E2 N (UBE2N) plays a role accumulation misfolded proteins through K63 ubiquitination, which has been linked to AD pathogenesis. However, impact UBE2N on amyloid pathology and clearance remained unknown. RESULTS observed elevated during beta (Aβ) generation brains 5×FAD, APP/PS1 mice, patients with AD, comparison...
Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular disease that usually has poor prognosis. Heat shock proteins (HSPs) have been implicated in the mechanisms of SAH-associated damage, including increased inflammation and reduced neurogenesis. The aim this study was to investigate effects HSP90 inhibition on neurogenesis mouse model experimental SAH induced by endovascular surgery. Western blotting showed levels be decreased, while neurogenesis, evaluated...
Extensive studies have been conducted on unmanned vehicle recently due to its bright prospect. However, few of them studied the technology driverless bus. In this paper, a path planning and navigation control system is designed for 12-m length electric The global adopted by Dijkstra algorithm based analysis tool ArcGIS. For local planning, triple-layer finite-state machine proposed plan driving maneuver, it reduces computational complexity improves effectiveness. Then, optimal trajectory...
Parkinson's disease (PD) is characterized by age-dependent neurodegeneration and the accumulation of toxic phosphorylated α-synuclein (pS129-α-syn). The mechanisms underlying these crucial pathological changes remain unclear. Mutations in parkin RBR E3 ubiquitin protein ligase (PARK2), gene encoding that PTEN-induced putative kinase 1 (PINK1) to participate mitophagy, cause early onset PD. However, current parkin-KO mouse pig models do not exhibit neurodegeneration. In study, we utilized...
Abstract Active caspase‐3 immunoreactivity was detected in the rat forebrain proliferative regions at birth and remained high these areas for about 2 weeks, during which period labeled cells were present centroperipherally across olfactory bulb. By end of third postnatal week, only a small number immunolabeled structures. immunolabeling localized mostly to cell nuclei co‐localized partially with TuJ1 NeuN immunoreactivity, but not glial fibrially acidic protein, OX‐42, γ‐aminobutyric acid,...
Alzheimer's disease (AD) is the most common dementia-causing disorder in elderly; it may be related to multiple risk factors, and characterized pathologically by cerebral hypometabolism, paravascular β-amyloid peptide (Aβ) plaques, neuritic dystrophy, intra-neuronal aggregation of phosphorylated tau. To explore potential pathogenic links among some these lesions, we examined β-secretase-1 (BACE1) alterations relative Aβ deposition, pathology vascular organization aged monkey AD human cortex....