Inhibition of autophagy attenuates cognitive decline and mitochondrial dysfunction in an Alzheimer's disease mouse model with chronic cerebral hypoperfusion.

This study aimed to investigate the impact of chronic cerebral hypoperfusion (CCH) on cognitive function, amyloid-β (Aβ) deposition, cellular autophagy, and mitochondrial dynamics in an Alzheimer's disease (AD) mouse model, and to evaluate the intervention effects of autophagy modulation on these outcomes. Utilizing the APP/PS1 mouse model combined with CCH, we assessed cognitive function, Aβ deposition, and the expression levels of relevant proteins through behavioral tests and immunohistochemical analysis. Our findings revealed pronounced cognitive deficits and increased Aβ deposition in the AD + CCH group mice, along with upregulation of mitochondrial fission proteins (Drp1, Fis1) and downregulation of mitochondrial fusion proteins (Opa1, Mfn1), indicating a shift towards mitochondrial fission and promoting cell apoptosis.

Prognostic value of plasma Aβ1-40 for Alzheimer's disease.

Objective: To investigate the clinical significance of plasma p-amyloid 1-40 (Aβ1-40) in patients with Alzheimer's disease (AD).

Methods: In this retrospective study, the clinical data of 305 patients, with or without Alzheimer's disease (AD), who were treated at the Affiliated Hospital of Youjiang Medical University for Nationalities and the People's Hospital of Baise between January 2018 and December 2021 were analyzed. Patients were divided into two groups: an AD group (n=147) and a non-AD group (without AD, n=158 cases).

p75NTR enhances cognitive dysfunction in a mouse Alzheimer's disease model by inhibiting microRNA-210-3p-mediated PCYT2 through activation of NF-κB.

Alzheimer's disease (AD) is a main cause of dementia and exhibits abnormality in cognitive behaviors. Here, we probed into the role of p75 neurotrophin receptor (p75NTR) in cognitive dysfunction in AD. Primarily, C57BL/6 mouse and neuroblastoma cells were treated by amyloid-beta1-42 (Aβ), respectively, to establish the in vivo and in vitro models of AD.

Transcriptome Comparison of Brain and Kidney Endothelial Cells in Homeostasis.

Endothelial cells are heterogeneous, stemming from multiple organs, but there is still little known about the connection between the brain and kidney endothelial cells, especially in homeostasis. In this study, scRNA-seq results were obtained to compare genetic profiles and biological features of tissue-specific endothelial cells. On this basis, seven endothelial cell subpopulations were identified, two of which were upregulated genes in pathways related to stroke and/or depression, as characterized by neuroinflammation.

Corrigendum: Microglia Mediate the Occurrence and Development of Alzheimer's Disease Through Ligand-Receptor Axis Communication.

[This corrects the article DOI: 10.3389/fnagi.2021.

RNA-seq of buffalo fibroblasts over-expressed pluripotent-related genes to investigate characteristics of its preliminarily reprogrammed stage.

Induced pluripotent stem cells (iPSCs) can enhance the efficiency of buffalo genetic improvements because of their differentiation potential and proliferation ability, which are similar to those of embryonic stem cells. However, very few studies have focussed on buffalo iPSCs, and a stable induction system has not been established for buffalo somatic cell reprogramming. In this study, we constructed a PiggyBac transposon vector co-expressing buffalo OCT4, C-MYC, KLF4 and SOX2 genes (PB_OMKS) separated by the nucleotide sequence of three 2A peptides and established the buffalo foetal skin fibroblast (BFSF) cell line BFSF_OMKS.

Microglia Mediate the Occurrence and Development of Alzheimer's Disease Through Ligand-Receptor Axis Communication.

Alzheimer's disease (AD) is a common neurodegenerative disease. Its onset is insidious and its progression is slow, making diagnosis difficult. In addition, its underlying molecular and cellular mechanisms remain unclear.

Up-regulation of SETD3 may contribute to post-stroke depression in rat through negatively regulating VEGF expression.

Post-stroke depression (PSD) is one of the most familiar complications of stroke, which refers to stroke patients who have varying degrees of depression (lasts for >2 weeks). SET domain-containing 3 (SETD3) is a conserved histone H3 methyltransferase, and the role of SETD3 in some diseases is increasingly being explored. However, the effects of SETD3 in PSD remain unclear.

Identification of an miRNA Regulatory Network and Candidate Markers for Ischemic Stroke Related to Diabetes.

Purpose: Type 2 diabetes mellitus (T2DM) increases the risk of ischemic stroke and poor prognosis. This study aimed to identify molecular mechanisms that are dysregulated in T2DM-associated ischemic stroke and candidate genes that might serve as biomarkers.

Methods: The top 25% variance genes in the GSE21321 and GSE22255 datasets were analyzed for coexpression.

Screening for Core Genes Related to Pathogenesis of Alzheimer's Disease.

Alzheimer's disease (AD), a nervous system disease, lacks effective therapies at present. RNA expression is the basic way to regulate life activities, and identifying related characteristics in AD patients may aid the exploration of AD pathogenesis and treatment. This study developed a classifier that could accurately classify AD patients and healthy people, and then obtained 3 core genes that may be related to the pathogenesis of AD.

Potential Genes and Mechanisms Linking Intracerebral Hemorrhage and Depression: A Bioinformatics-Based Study.

Purpose: The purpose of this study was to investigate the potential pathogenic mechanisms of post-intracerebral hemorrhage depression.

Methods: Profiles of gene expression in brain tissue of patients with intracerebral hemorrhage (ICH) or depression were downloaded from the Gene Expression Omnibus (GEO) database. We analyzed differentially expressed genes (DEGs) for the two diseases separately.

Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury.

Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN.

Using mRNA deep sequencing to analyze differentially expressed genes during Panax notoginseng saponin treatment of ischemic stroke.

Treatment with Panax notoginseng saponin (PNS) can prevent neurological damage in middle cerebral artery occlusion model rats to promote recovery after a stroke. However, the exact molecular mechanisms are unknown and require further study. In the present study, mRNA sequencing was employed to investigate differential gene expression between model and sham groups, and between model and PNS‑treated groups.

Intranasal insulin administration may be highly effective in improving cognitive function in mice with cognitive dysfunction by reversing brain insulin resistance.

It is well known in clinical practice that Alzheimer's disease (AD) is closely associated with brain insulin resistance, and the cerebral insulin pathway has been proven to play a critical role in the pathogenesis of AD. However, finding the most efficient way to improve brain insulin resistance remains challenging. Peripheral administration of insulin does not have the desired therapeutic effect and may induce adverse reactions, such as hyperinsulinemia, but intranasal administration may be an efficient way.

Evaluation of miR-34b/c polymorphisms to the risk of ischemic stroke.

Objectives: Polymorphisms in microRNA genes are related to the risk of ischemic stroke, but the association between miR-34b/c polymorphisms and the risk of ischemic stroke has not been reported.

Methods: MiR-34b/c rs2187473 and rs4938723 polymorphisms were genotyped by Snapshot assay among 495 controls and 492 ischemic stroke patients. Expression levels of miR-34b and miR-34c were quantified by real-time PCR.

Involvement of p75NTR in the effects of Aβ on L-type Ca channel in cultured neuronal networks.

Ca overload in neurons has been implicated in Alzheimer's Disease (AD). Upregulation of Ca through L-type Ca channels was known to be involved in the neurodegeneration induced by amyloid-β (Aβ) peptides in AD. However, little is known about the mechanism by which upregulation of L-type Ca channel currents is linked to Aβ-induced neuronal toxicity.

20S proteasome and glyoxalase 1 activities decrease in erythrocytes derived from Alzheimer's disease patients.

As a result of accumulating methylglyoxal and advanced glycation end products in the brains of patients with Alzheimer's disease, it is considered a protein precipitation disease. The ubiquitin proteasome system is one of the most important mechanisms for cells to degrade proteins, and thus is very important for maintaining normal physiological function of the nervous system. This study recruited 48 individuals with Alzheimer's disease (20 males and 28 females aged 75 ± 6 years) and 50 healthy volunteers (21 males and 29 females aged 72 ± 7 years) from the Affiliated Hospital of Youjiang Medical University for Nationalities (Baise, China) between 2014 and 2017.

Analysis of transcription factor- and ncRNA-mediated potential pathogenic gene modules in Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disease that ranks as the fourth most common cause of death in developed countries. In our study, genes differentially expressed between AD and healthy individuals were identified and used to construct protein-protein interaction (PPI) networks. The AD-related PPI network was used to identify functional modules, and enrichment analysis showed that they were significantly involved in "Alzheimer's disease", "apoptosis", and related pathways.

Neuroprotective effect of salidroside against central nervous system inflammation-induced cognitive deficits: A pivotal role of sirtuin 1-dependent Nrf-2/HO-1/NF-κB pathway.

Central nervous system (CNS) inflammation occurs in cognitive dysfunctions, but the underlying mechanisms remain unclear. Here, we investigated the role of sirtuin 1 (SIRT1) and salidroside in CNS inflammation-induced cognitive deficits model. In vivo, CNS inflammation was initiated by a single intracerebroventricular injection of lipopolysaccharide (LPS).

Panax notoginseng Saponins Attenuate Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury in Human SH-SY5Y Cells by Regulating the Expression of Inflammatory Factors through miR-155.

Panax notoginseng saponins (PNS) have been widely used in China to treat stroke. Accumulating evidence has found that microRNA (miR)-155 plays critical roles in the pathology of ischemic stroke. Here we investigated whether PNS plays a protective effect against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced focal inflammation and injury in SH-SY5Y cells by regulating miR-155 expression.

Sirt1 protects neural stem cells from apoptosis by decreasing acetylation of histone 3K9.

Objective: To explore the role and mechanism of Sirt1 in protecting neural stem cells (NSCs) from apoptosis.

Materials And Methods: Transfection was used to overexpress Sirt1 in rat NSCs. The effect of Sirt1 overexpression on camptothecin-induced apoptosis of NSCs was evaluated.

A prenatal interruption of DISC1 function in the brain exhibits a lasting impact on adult behaviors, brain metabolism, and interneuron development.

Mental illnesses like schizophrenia (SCZ) and major depression disorder (MDD) are devastating brain disorders. The SCZ risk gene, disrupted in schizophrenia 1 (), has been associated with neuropsychiatric conditions. However, little is known regarding the long-lasting impacts on brain metabolism and behavioral outcomes from genetic insults on fetal NPCs during early life.

MicroRNA expression profiles in chronic epilepsy rats and neuroprotection from seizures by targeting miR-344a.

MicroRNA (miRNA) is believed to play a crucial role in the cause and treatment of epilepsy by controlling gene expression. However, it is still unclear how miRNA profiles change after multiple prolonged seizures and aggravation of brain injury in chronic epilepsy (CE). To investigate the role of miRNA in epilepsy, we utilized the CE rat models with pentylenetetrazol (PTZ) and miRNA profiles in the hippocampus.