Publications by authors named "Yi-Feng Du"

Objectives: To quantitatively assess and compare retinal macular structures of rural-dwelling older adults in China using two different optical coherence tomography (OCT) scanners and to examine their associations with demographic, lifestyle, clinical and ocular factors.

Design, Setting And Participants: This population-based, cross-sectional study included 971 participants (age ≥60 years) derived from the Multimodal Interventions to Delay Dementia and Disability in Rural China study. We collected data on demographics, lifestyle factors, clinical conditions (eg, cardiovascular disease (CVD)) and ocular factors (eg, visual acuity and spherical equivalent).

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No data are available on the serum metabolomics and lipidomics profiles of people with asymptomatic intracranial arterial stenosis. We explored the characteristic metabolites of individuals with asymptomatic severe intracranial arterial stenosis (asICAS) using untargeted serum metabolomics and lipidomics analyses based on ultra-high-performance liquid chromatography high-resolution mass spectrometry (UPLC-HRMS). This case-control study included 25 participants with asICAS and 25 age- and sex-matched controls free of asICAS, who were all diagnosed by using magnetic resonance angiography and derived from the same population-based study.

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Hyperphosphorylated tau is one of the key characteristics of Alzheimer's disease (AD), and tau pathology correlates with cognitive impairment in AD better than amyloid-β (Aβ) pathology. Thus, a complete understanding of the relevant factors involved in tau phosphorylation is important for AD treatment. APOEɛ4, the strongest genetic risk factor for AD, was found to be involved in tau pathology in frontotemporal dementia.

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Accumulating evidence has shown that tauroursodeoxycholic acid (TUDCA) is neuroprotective in different animal models of neurological diseases. However, whether TGR5 agonist TUDCA can improve lipopolysaccharide (LPS)-induced cognitive impairment in mice is less clear. Using a model of cognitive impairment with LPS (2.

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Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by cognitive deficits and neuronal loss. Deposition of beta-amyloid peptide (Aβ) causes neurotoxicity through the formation of plaques in brains of Alzheimer's disease. Numerous studies have indicated that the neuropeptides including ghrelin, neurotensin, pituitary adenylate cyclase-activating polypeptide (PACAP), neuropeptide Y, substance P and orexin are closely related to the pathophysiology of Alzheimer's disease.

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To investigate the relationships among the degree of intracranial atherosclerotic stenosis (ICAS), plaque enhancement (PE), and ischemic stroke events (ISEs) using 3. 0 T high-resolution magnetic resonance imaging (HR-MRI). Fifty-two ICAS patients who underwent HR-MRI were retrospectively analyzed.

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The recombinant adeno-associated virus human thioredoxin-PR39 (rAAV/hTRX-PR39) has been demonstrated to have a protective effect on hypoxic cells. The present study aimed to explore the potential effect of rAAV/hTRX-PR39 on acute cerebral infarction in rats. Middle cerebral artery occlusion (MCAO) model rats were produced and divided into three groups: Normal saline group, empty virus group (rAAV, without hTRX-PR39 cDNA) and rAAV/hTRX-PR39 group.

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Neuroinflammation plays an important role in the pathophysiology of Alzheimer's disease (AD) and memory impairment. Herein, we evaluated the neuroprotective effects of 6-ethyl-23(S)-methyl-cholic acid (INT-777), a specific G-protein coupled bile acid receptor 1 (TGR5) agonist, in the LPS-treated mouse model of acute neurotoxicity. Single intracerebroventricular (i.

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Increasing evidence demonstrates that the neurotoxicity of amyloid-beta (Aβ) deposition plays a causative role in Alzheimer's disease (AD). Herein, we evaluated the neuroprotective effects of 6α-ethyl-23(S)-methylcholic acid (S-EMCA, INT-777), a specific G-protein coupled bile acid receptor 1 (TGR5) agonist, in the Aβ-treated mouse model of acute neurotoxicity. Single intracerebroventricular (i.

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Aims: To investigate restorative effects of the receptor for advanced glycation end products (RAGE)-specific inhibitor FPS-ZM1 on abnormal amyloid β (Aβ) influx across the blood brain-barrier (BBB) and cognitive deficits in db/db mice.

Methods: Aβ influx across the BBB was determined by intra-arterial infusion of I-Aβ. Receptor for advanced glycation end products (RAGE), Aβ, NF-κB p65, caspase-3, Bax, Bcl-2, PSD-95 and synaptophysin were assayed by Western blot, immunohistochemistry or RT-PCR.

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Background: Recent studies demonstrated beneficial effects of zileuton, a 5-lipoxygenase (5LO) inhibitor, on some brain diseases in animal models, but the role of zileuton in the depression remains unknown.

Methods: We investigated the effects of zileuton on depressive behaviors using tail suspension test (TST), forced swimming test (FST) and novelty-suppressed feeding test (NSFT) in mice injected with lipopolysaccharide (LPS). The 5LO level, activation of microglia, NF-κB p65, TNF-α, IL-1β, brain-derived neurotrophic factor (BDNF), and c-AMP response element-binding protein (CREB) were determined in the mouse hippocampus.

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Purpose: Stroke is a major public health concern with high rates of morbidity and mortality worldwide. Cerebral ischemia and infarction are commonly associated with stroke. Currently used medications, though effective, are also associated with adverse effects.

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Studies have confirmed that low-frequency repetitive transcranial magnetic stimulation can decrease the activity of cortical neurons, and high-frequency repetitive transcranial magnetic stimulation can increase the excitability of cortical neurons. However, there are few studies concerning the use of different frequencies of repetitive transcranial magnetic stimulation on the recovery of upper-limb motor function after cerebral infarction. We hypothesized that different frequencies of repetitive transcranial magnetic stimulation in patients with cerebral infarction would produce different effects on the recovery of upper-limb motor function.

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Orexins including two peptides, orexin-A and orexin-B, are produced in the posterior lateral hypothalamus. Much evidence has indicated that central orexinergic systems play numerous functions including energy metabolism, feeding behavior, sleep/wakefulness, and neuroendocrine and sympathetic activation. Morphological studies have shown that the hippocampal CA1 regions receive orexinergic innervation originating from the hypothalamus.

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The aim of this study was to investigate the relationship between chronic cerebral hypoperfusion and the occurrence and development of Alzheimer's disease (AD). A cerebral hypoperfusion rat model was established by two vessels occlusion (2VO). The cognitive function of the rats with chronic cerebral hypoperfusion and the expression of p-Tau protein in the hippocampus were observed dynamically.

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The aim of the present study was to successfully construct a recombinant adeno-associated virus (rAAV) vector containing the human thioredoxin (hTRX)-PR39 chimeric gene (rAAV/hTRX-PR39), and verify that the vector was able to maintain a sustained, stable and efficient expression to achieve protein production in the cell. In the present study, a chicken embryo model was utilized to analyze the therapeutical effect of rAAV/hTRX-PR39 in cerebral ischemia diseases. ECV304 cells were transfected with rAAV/hTRX-PR39 and incubated under conditions of 20, 5 and 1% O.

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Background And Objectives: Carotid artery stenting (CAS) is an important therapeutic strategy for patients with carotid artery stenosis. However, the potential influence of CAS on cognitive function in patients with carotid artery stenosis and cerebral lacunar infarction has not been determined. This study investigated changes in cognitive function associated with CAS and the factors related to these changes.

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Objective: A large body of evidence suggests that stroke and depression are accompanied by activation of inflammatory pathways. Thus, the primary purpose of this study was to assess the high-sensitivity C-reactive protein (Hs-CRP) to the presence of post stroke depression (PSD).

Methods: Two hundred and twenty-six ischemic stroke patients admitted to the hospital within the first 24 hours after stroke onset were consecutively recruited and followed up for 6 months.

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Leukoaraiosis (LA) is a leading cause of gait disturbance in the elderly and well known as a type of cerebrovascular diseases. LA is mainly caused by the focal ischemic damage in cerebral white matter. Cognitive impairment in patients with LA is difficult to treat.

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Article Synopsis
  • Diabetic encephalopathy (DE) is linked to Alzheimer's disease and has been shown to impair learning and memory in animal studies, while neurotrophic peptides can improve these conditions.
  • APP 17-mer peptide offers neural protection but is prone to degradation; however, its modified version, P165, resists degradation and can be taken orally to protect neurons.
  • The study used high glucose and Aβ25-35 to damage human neuroblastoma cells and streptozotocin to induce diabetes in mice, finding that P165 positively influences synaptic and insulin signaling proteins, suggesting its potential as an Alzheimer's treatment.
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There is compelling evidence that postural instability occurs at very early clinical stages of Parkinson's disease (PD), making it tempting to speculate that changes in postural sway may even occur at a prodromal phase. Studies estimate that approximately half of patients with idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) will eventually develop PD, so RBD may be an indicator of prodromal PD. This study was undertaken to investigate postural sway and its relation to stereopsis function in patients with RBD.

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Two major active species of β-amyloid protein (Aβ), fibrillar Aβ1-42 (FAβ) and soluble Aβ1-42 oligomers (AβO), are known to play important roles in the pathogenesis of Alzheimer's disease. However, the differences between them are largely unknown. In this study, we explored the effects of FAβ and AβO on cognitive functions and hippocampal inflammatory response through a 30-days infusion of FAβ or AβO (144pmol/d) into the left lateral ventricles of the rat brain.

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To investigate the effects of fibrillar Aβ(1-40) on the morphology and viability of cholinergic neurons and the involvement of the insulin-signaling pathway, we established primary cultures of rat basal forebrain cholinergic neurons and observed their responses to treatment with fibrillar Aβ(1-40) at different concentrations for different durations. Cell morphology was examined under microscope after immunofluorescence staining for neurofilament protein, cell vitality accessed by the Methyl thiazolyl tetrazolium assay, and expressions of a panel of insulin signaling-related proteins was detected by Western blot analysis. We show here that, at low concentrations of 0.

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Objective: To investigate the therapeutic effect of neurotrophin-3 (NT-3) modified olfactory ensheathing cell (OEC) upon experimental allergic encephalomyelitis (EAE).

Methods: OEC-NT-3 gene engineering cell, constructed by neurotrophin-3 transinfecting GEC inducted by retrovirus, was transplanted into lateral ventricle. The migration and distribution were observed and compared with control group and OEC transplantation group.

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