An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.

Background: Baicalin has been shown to promote spatial learning and neural regeneration, which might increase the differentiation of neural stem cells in Alzheimer's disease (AD) rat models. We aimed to study the role of baicalin on neuronal pentraxin-1 (NPTX-1), neuronal pentraxin-2 (NPTX-2), and C-reactive protein (CRP) in AD model rats.

Methods: The 30 male Sprague Dawley rats were divided into three groups: the control group, the AD model group, and the AD + baicalin group.

KDM1A-mediated upregulation of METTL3 ameliorates Alzheimer's disease via enhancing autophagic clearance of p-Tau through m6A-dependent regulation of STUB1.

Background: Alzheimer's disease (AD) is a severe neurodegenerative disorder that progressively destroys cognitive skills. Exploring the mechanism underlying autophagic clearance of phosphorylated tau (p-Tau) contributes to developing novel therapeutic strategies for AD.

Methods: SH-SY5Y and HT22 cells were treated with Aβ to establish an in vitro model of AD.

Investigation on Potential Biomarkers and Immune-Related Mechanisms of Ischemic Stroke.

Background: This study aimed to reveal the detailed immune-related mechanisms underlying ischemic stroke (IS) and identify new immune-associated biomarkers for clinical management.

Methods: Differentially expressed genes (DEGs) between IS samples and normal controls were identified using the GSE16561 dataset. The feature genes of the immune cells were investigated using the GSE72642 dataset.

LncRNA nuclear-enriched abundant transcript 1 aggravates cerebral ischemia/reperfusion injury through activating early growth response-1/RNA binding motif protein 25 axis.

Ischemic stroke is a major global health issue. Ischemia and subsequent reperfusion results in stroke-related brain injury. Previous studies have demonstrated that nuclear-enriched abundant transcript 1 (NEATa and early growth response 1 (EGR1) are involved in ischemia reperfusion (IR) injury).

lncRNA MIR600HG Knockdown Alleviates Cognitive Impairment in Alzheimer's Disease Through NEDD4L Mediated PINK1 Degradation.

Background: Growing evidence has demonstrated that long non-coding RNAs (lncRNAs) play a critical role in Alzheimer's disease (AD), which is characterized by sustained mitochondrial dysfunction, inevitable memory loss, and cognitive decline. However, the potential function of lncRNAs MIR600 Host Gene (MIR600HG) in AD remains unanswered.

Objective: Our study aimed to investigate the role of MIR600HG and its related molecular mechanism in AD.

Exosomes Derived from MicroRNA-146a-5p-Enriched Bone Marrow Mesenchymal Stem Cells Alleviate Intracerebral Hemorrhage by Inhibiting Neuronal Apoptosis and Microglial M1 Polarization.

Introduction: Intracerebral hemorrhage (ICH) is a devastating type of stroke with high mortality, and the effective therapies for ICH remain to be explored. Exosomes (Exos) have been found to play important roles in cell communication by transferring molecules, including microRNAs (miRNAs/miRs). MiRNAs are critical regulators of genes involved in many various biological processes and have been demonstrated to aggravate or alleviate brain damages induced by ICH.

Effect of MicroRNA-126a-3p on Bone Marrow Mesenchymal Stem Cells Repairing Blood-brain Barrier and Nerve Injury after Intracerebral Hemorrhage.

Objective: Intracerebral hemorrhage (ICH) is a disease that threatens human health due to its high morbidity and mortality. On behalf of finding the better methods in the treatment of ICH, researchers pay more attention to a new technology which is finding effective genes to modify stem cells.

Methods: In this study, we isolated, cultured and identified bone marrow mesenchymal stem cells (MSCs) in vitro.

Olfactory Impairment and Hippocampal Volume in a Chinese MCI Clinical Sample.

Purpose: The aim of this study was to evaluate the relationship between olfactory function and hippocampal volume in patients with mild cognitive impairment (MCI).

Methods: We enrolled a total of 31 MCI patients and 9 normal control subjects. All participants underwent 3.

Molecular differences in Alzheimer's disease between male and female patients determined by integrative network analysis.

Alzheimer's disease (AD) is a complex neurodegenerative disease and the most common cause of dementia among the elderly. There has been increasing recognition of sex differences in AD prevalence, clinical manifestation, disease course and prognosis. However, there have been few studies on the molecular mechanism underlying these differences.

Baicalin and ginsenoside Rb1 promote the proliferation and differentiation of neural stem cells in Alzheimer's disease model rats.

Background: This study aimed to explore the effects of ginsenoside Rb1 and baicalin on the proliferation and differentiation of neural stem cells (NSC) in Alzheimer's disease model rats.

Method: The healthy Sprague Dawley male rats were randomly divided into 4 groups: control group, model group, ginsenoside Rb1 group and baicalin group. Besides, the animal model of dementia was induced by the injection of Aβ1-40.

Higher expression of monocyte chemoattractant protein 1 and its receptor in brain tissue of intractable epilepsy patients.

We aimed to explore the pathogenesis of monocyte chemoattractant protein-1 (MCP1) and CC chemokine receptor 2 (CCR2) in brain tissue of patients with intractable epilepsy (IE). Hippocampi or temporal lobe tissues were obtained from 40 patients with IE and five patients without IE who had undergone surgical decompression and debridement. The levels of MCP1 and CCR2 were evaluated using immunohistochemistry.

Identification of pivotal markers in vascular dementia based on proteomics data.

Objective: The aim of this study was to analyze protein expression profiles of vascular dementia (VaD) subjects for investigating the underlying therapeutic markers.

Methods: Protein expression profile data were acquired from a quantitative clinical proteomic study, including 10 nondemented elderly controls and 10 age-matched VaD subjects. Differentially expressed proteins (DEPs) were identified between VaD subjects and controls, followed by function prediction using DAVID (Database for Annotation, Visualization, and Integrated Discovery).

Vitamin D receptor gene polymorphisms and the risk of Parkinson's disease.

The effect of vitamin D receptor (VDR) gene polymorphisms on Parkinson's disease (PD) has recently gained interest. However, evidence on this relationship is controversial. We searched PubMed, EMBASE and the Cochrane Library database targeted all studies that evaluated VDR gene polymorphisms and PD up to April 2,014.

Mild hypothermia reduces expression of Fas/FasL and MMP-3 after cerebral ischemia-reperfusion in rats.

Objectives: To investigate the effects of local mild hypothermia on the expression of Fas, FasL and MMP-3 after cerebral ischemia-reperfusion in rats.

Materials And Methods: Male Wistar rats were divided into sham-operated group (Sham), normothermia group (NT), and hypothermia group (HT). MCAO/R model was established by Longa's method, and reperfusion was allowed after 2 hr occlusion.

The value of the ucN13-P15 interpeak latency predicted acute posterior circulation ischemia and the chronic outcome.

Objective: To determine the sensitivity and specificity of the ucN13-P15 (CV2-Fz) and IcN13-P15 (CV7-Fz) interpeak latencies when used to predict acute posterior circulation ischemia.

Methods: A total of 426 consecutive patients who were hospitalized within 3 days of the onset of stroke were prospectively enrolled in the study. Of these patients, 110 had infarct lesions in the posterior circulation territory.

Vitamin D status and the risk of multiple sclerosis: a systematic review and meta-analysis.

To estimate the associations between vitamin D status and multiple sclerosis (MS). We searched electronic databases of the human literature in PubMed, EMBASE and the Cochrane Library up to February, 2014 using the following keywords: 'vitamin D' or '25(OH)D' and 'status' or 'deficiency' or 'insufficiency' and 'multiple sclerosis'. A systematic review and meta-analysis were conducted on observational studies that reported the association between blood vitamin D levels and MS.

Effect of focal mild hypothermia on expression of MMP-9, TIMP-1, Tau-1 and β-APP in rats with cerebral ischaemia/reperfusion injury.

Primary Objective: Following stroke, hypothermia is reported to reduce both cellular and extracellular damage. This study aimed to examine the effects of focal mild hypothermia on proteins associated with both extracellular (matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of MMP-9 (TIMP-1)) and cellular damage (Tau-1 and β-amyloid precursor protein (β-APP)) to characterize the protective effects of hypothermia.

Methods And Procedures: Male Wistar rats received ischaemic damage using a transient, focal ischaemia/reperfusion model.

IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease.

Associations between interleukin 6 (IL-6) polymorphisms and Alzheimer's disease (AD) remain controversial and ambiguous. The aim of this meta-analysis is to explore more precise estimations for the relationship between IL-6-174 G/C and -572 C/G polymorphisms and risk for AD. Electronic searches for all publications in databases PubMed and EMBASE were conducted on the associations between IL-6 polymorphisms and risk for AD until January 2012.

Increased levels of IL-23 and osteopontin in serum and cerebrospinal fluid of multiple sclerosis patients.

Osteopontin (OPN) and interleukin-23 (IL-23) are pro-inflammatory cytokines proposed to play central roles to the development of multiple sclerosis (MS). The aim of this study was to evaluate levels of OPN, IL-23 and other inflammatory cytokines and investigate their relationships in serum and cerebrospinal fluid (CSF) in patients with MS. Fifty one MS patients and 48 patients with non-inflammatory neurological diseases (NIND) were recruited from clinic.

High expression of ubiquitin conjugates and NF-κB in unstable human intracranial atherosclerotic plaques.

Arteries from the first segment of the middle cerebral and adjacent normal blood vessel specimens were collected from 19 patients who had died from cerebral infarction. According to morphologic examination the atherosclerotic plaque present was classified as stable or unstable. The expression of ubiquitin conjugates and nuclear factor kappa B (NF-κB) was assessed and found significantly higher in plaques than normal tissue and higher in unstable plaques than in stable plaques.

Acute disseminated encephalomyelitis associated with Influenza A H1N1 infection.

Previous studies had not suggested acute disseminated encephalomyelitis (ADEM) during Influenza A H1N1 infection. We report the case of patient who had predominant neurological complication following Influenza A H1N1 infection. The patient, who showed clinical and MRI evidence of ADEM, had significant recovery, which in part, may be related to early treatment.

Perihematomal pathological changes in neurons and astrocytes following acute cerebral hemorrhage.

We aim to investigate the pathological temporospatial characteristics of brain cell injury in the perihematomal areas. Brain autopsy samples from 44 consecutive cases of intracerebral hemorrhage were processed and analyzed following immunohistochemical staining for neurofilament (NF) and glial fibrillary acidic protein (GFAP). NF and GFAP positive cells were scored and graded according to the distance from the hematoma and the time from the onset of hematoma formation.

Protective effect of edaravone against PrP106-126-induced PC12 cell death.

The prion protein peptide PrP106-126 induces cell apoptosis through mechanisms involving production of intracellular reactive oxygen species. The present study investigated the effects of edaravone, a potent free radical scavenger in clinical use, on cell cytotoxicity induced by PrP106-126. Results showed that PrP106-126 decreased PC12 cell viability in a dose- and time-dependent manner.

Expression of nestin and glial-derived neurotrophic factor in human endogenous neural stem cells following ischemia.

Objectives: We investigated the relationship between glial cell line-derived neurotrophic factor (GDNF), nestin, and the activation of endogenous neural stem cells (NSCs) following cerebral infarction in humans.

Methods: Post-mortem brain specimens from patients who died following cerebral infarction were examined.

Results: Compared with the controls, the number of nestin-positive cells was increased at 4·5-10 hours in the subgranular zone of the hippocampus dentate gyrus and at 24-72 hours in the subventricular zone, reaching maximum levels at 120-144 hours.

Ischemia induces endoplasmic reticulum stress and cell apoptosis in human brain.

In animal models, endoplasmic reticulum (ER) stress and apoptosis take place around cerebral infarction areas during ischemia, which presumably protect tissues from necroses-induced injury as well as promote cells toward death. We examined whether these pathological changes, especially temporal occurrence, were present in patients who suffered from cerebral ischemia. The studies by immunohistochemistry show that ER chaperone glucose-regulated protein (GRP78) and caspase-9 elevate around infarction areas.