The 40-Hz White Light Emitting Diode to Alleviate Psychiatric Symptoms Induced by Streptozotocin In Vivo.

Introduction: A 40-Hz white light emitting diode (WLED) has emerged as an alternative nonpharmacological and noninvasive approach to Alzheimer disease (AD). Here, we investigated the therapeutic effects of 40-Hz WLED on psychiatric symptoms (PS) and the contribution of mitochondrial factors in the early stages of sporadic AD (sAD) in rats.

Methods: In male Wistar rats, the AD model was induced via intracerebroventricular (ICV) injection of streptozotocin (STZ).

Predicting Survival in Glioblastoma Using Gene Expression Databases: A Neural Network Analysis.

Glioblastoma (GBM) is the most aggressive and lethal brain tumor. Artificial neural networks (ANNs) have the potential to make accurate predictions and improve decision making. The aim of this study was to create an ANN model to predict 15-month survival in GBM patients according to gene expression databases.

Comprehensive analysis of lncRNA-associated ceRNA network reveals novel potential prognostic regulatory axes in glioblastoma multiforme.

Deciphering the lncRNA-associated competitive endogenous RNA (ceRNA) network is essential in decoding glioblastoma multiforme (GBM) pathogenesis by regulating miRNA availability and controlling mRNA stability. This study aimed to explore novel biomarkers for GBM by constructing a lncRNA-miRNA-mRNA network. A ceRNA network in GBM was constructed using lncRNA, mRNA and miRNA expression profiles from the TCGA and GEO datasets.

Deciphering molecular bridges: Unveiling the interplay between metabolic syndrome and Alzheimer's disease through a systems biology approach and drug repurposing.

The association between Alzheimer's disease and metabolic disorders as significant risk factors is widely acknowledged. However, the intricate molecular mechanism intertwining these conditions remains elusive. To address this knowledge gap, we conducted a thorough investigation using a bioinformatics method to illuminate the molecular connections and pathways that provide novel perspectives on these disorders' pathological and clinical features.

mRNA markers for survival prediction in glioblastoma multiforme patients: a systematic review with bioinformatic analyses.

Background: Glioblastoma multiforme (GBM) is a type of fast-growing brain glioma associated with a very poor prognosis. This study aims to identify key genes whose expression is associated with the overall survival (OS) in patients with GBM.

Methods: A systematic review was performed using PubMed, Scopus, Cochrane, and Web of Science up to Journey 2024.

Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.

Alzheimer's disease (AD) is a devastating neurodegenerative disease characterized by memory impairment and a progressive decline in cognitive function. Mitochondrial dysfunction has been identified as an important contributor to the development of AD, leading to oxidative stress and energy deficits within the brain. While current treatments for AD aim to alleviate symptoms, there is an urgent need to target the underlying mechanisms.

Comprehensive somatic mutational analysis in glioblastoma: Implications for precision medicine approaches.

Glioblastoma multiforme (GBM), a malignant neoplasm originating from glial cells, remains challenging to treat despite the current standard treatment approach that involves maximal safe surgical resection, radiotherapy, and adjuvant temozolomide chemotherapy. This underscores the critical need to identify new molecular targets for improved therapeutic interventions. The current study aimed to explore the somatic mutations and potential therapeutic targets in GBM using somatic mutational information from four distinct GBM datasets including CGGA, TCGA, CPTAC and MAYO-PDX.

MicroRNA-140-5p inhibitor attenuates memory impairment induced by amyloid-ß oligomer in vivo possibly through Pin1 regulation.

Aims: The peptidyl-prolyl cis/trans isomerase, Pin1, has a protective role in age-related neurodegeneration by targeting different phosphorylation sites of tau and the key proteins required to produce Amyloid-β, which are the well-known molecular signatures of Alzheimer's disease (AD) neuropathology. The direct interaction of miR-140-5p with Pin1 mRNA and its inhibitory role in protein translation has been identified. The main purpose of this study was to investigate the role of miRNA-140-5p inhibition in promoting Pin1 expression and the therapeutic potential of the AntimiR-140-5p in the Aß oligomer (AßO)-induced AD rat model.

The p75 neurotrophin receptor inhibitor, LM11A-31, ameliorates acute stroke injury and modulates astrocytic proNGF.

The precursor form of nerve growth factor (proNGF) is essential to maintain NGF survival signaling. ProNGF is also among endogenous ligands for p75 neurotrophin receptor (p75ntr). Mounting evidence implies that p75ntr signaling contributes to neural damage in ischemic stroke.

MicroRNA modulation is a potential molecular mechanism for neuroprotective effects of intranasal insulin administration in amyloid βeta oligomer induced Alzheimer's like rat model.

Substantial evidence indicates that imbalance in the expression of miR-132-3p, miR-181b-5p, miR-125b-5p, miR-26a-5p, miR-124-3p, miR-146a-5p, miR-29a-3p, and miR-30a-5p in the AD brain are associated with amyloid-beta (Aβ) aggregation, tau pathology, neuroinflammation, and synaptic dysfunction, the major pathological hallmarks of Alzheimer's disease)AD(. Several studies have reported that intranasal insulin administration ameliorates memory in AD patients and animal models. However, the underlying molecular mechanisms are not yet completely elucidated.

Implication of thyroid hormone receptors in methamphetamine neurocognitive effects.

Methamphetamine (MA) induces neurocognitive effects via several mechanisms. In the present study, we investigated the alteration of thyroid hormone receptor's expression in the context of MA-induced memory impairment and explored the protective effects of exogenous thyroid hormones (THs). Male wistar rats, received increasing regimen of MA (1-10 mg/kg, intraperitoneal, twice a day for 10 days), were treated with T3 (40 μg/rat/day; intranasal, 2.

Comparison of Rat Primary Midbrain Neurons Cultured in DMEM/F12 and Neurobasal Mediums.

Introduction: Midbrain dopaminergic neurons are involved in various brain functions, including motor behavior, reinforcement, motivation, learning, and cognition. Primary dopaminergic neurons and also several lines of these cells are extensively used in cell culture studies. Primary dopaminergic neurons prepared from rodents have been cultured in both DMEM/F12 and neurobasal mediums in several studies.

Does Alzheimer's disease stem in the gastrointestinal system?

Over the last decades, our knowledge of the key pathogenic mechanisms of Alzheimer's disease (AD) has dramatically improved. Regarding the limitation of current therapeutic strategies for the treatment of multifactorial diseases, such as AD, to be translated into the clinic, there is a growing trend in research to identify risk factors associated with the onset and progression of AD. Here, we review the current literature with a focus on the relationship between gastrointestinal (GI)/liver diseases during the lifespan and the incidence of AD, and discuss the possible mechanisms underlying the link between the diseases.

The role of microRNA-34 family in Alzheimer's disease: A potential molecular link between neurodegeneration and metabolic disorders.

Growing evidence indicates that overexpression of the microRNA-34 (miR-34) family in the brain may play a crucial role in Alzheimer's disease (AD) pathogenesis by targeting and downregulating genes associated with neuronal survival, synapse formation and plasticity, Aβ clearance, mitochondrial function, antioxidant defense system, and energy metabolism. Additionally, elevated levels of the miR-34 family in the liver and pancreas promote the development of metabolic syndromes (MetS), such as diabetes and obesity. Importantly, MetS represent a well-documented risk factor for sporadic AD.

Insulin Promotes Schwann-Like Cell Differentiation of Rat Epidermal Neural Crest Stem Cells.

Schwann cells (SCs) are considered potentially attractive candidates for transplantation therapies in neurodegenerative diseases. However, problems arising from the isolation and expansion of the SCs restrict their clinical applications. Establishing an alternative Schwann-like cell type is a prerequisite.

How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.

Ischemic stroke is the second leading cause of mortality and disability globally. Neuronal damage following ischemic stroke is rapid and irreversible, and eventually results in neuronal death. In addition to activation of cell death signaling, neuroinflammation is also considered as another pathogenesis that can occur within hours after cerebral ischemia.

Imipramine alleviates memory impairment and hippocampal apoptosis in STZ-induced sporadic Alzheimer's rat model: Possible contribution of MAPKs and insulin signaling.

Alzheimer's disease (AD) is the most common age-related neurodegenerative disease, associated with several pathophysiological complaints. Impaired insulin signaling in the brain, is one of the important characteristic features of AD which is accompanied by cognitive deficits. According to the multifactorial and complicated pathology of AD, no modifying therapy has been approved yet.

OPRM1 and CYP3A4 association with methadone dose in Iranian patients undergoing methadone maintenance therapy.

Background: Investigations proposed that genetic polymorphisms within proteins in methadone pharmacokinetic and pharmacodynamics are critical factors in determination of methadone dose in methadone maintenance therapy (MMT).

Objective: This study aimed to assess the associations between two polymorphisms, (rs2740574) and (rs1799971), with dose of methadone in Iranian patients undergoing MMT.

Methods: A total of 124 Iranian male subjects aged 18-65 years old who were confirmed to be addicted by the addiction diagnostic tests and underwent MMT were assessed.

Lipopolysaccharide Pre-conditioning Attenuates Pro-inflammatory Responses and Promotes Cytoprotective Effect in Differentiated PC12 Cell Lines Pre-activation of Toll-Like Receptor-4 Signaling Pathway Leading to the Inhibition of Caspase-3/Nuclear Factor-κappa B Pathway.

Lipopolysacharide (LPS) pre-conditioning (PC), has been shown to exert protective effects against cytotoxic effects. Therefore, we hypothesized, the tolerance produced by LPS PC will be resulted by the alterations and modifications in gene and protein expression. With reference to the results of MTT assays, AO/PI staining, and Annexin V-FITC analyses of LPS concentration (0.

Intranasal insulin improves mitochondrial function and attenuates motor deficits in a rat 6-OHDA model of Parkinson's disease.

Aims: Experimental and clinical evidences demonstrate that common dysregulated pathways are involved in Parkinson's disease (PD) and type 2 diabetes. Recently, insulin treatment through intranasal (IN) approach has gained attention in PD, although the underlying mechanism of its potential therapeutic effects is still unclear. In this study, we investigated the effects of insulin treatment in a rat model of PD with emphasis on mitochondrial function indices in striatum.

LPS Preconditioning Attenuates Apoptosis Mechanism by Inhibiting NF-κB and Caspase-3 Activity: TLR4 Pre-activation in the Signaling Pathway of LPS-Induced Neuroprotection.

Neuroinflammation, an inflammatory response within the nervous system, has been shown to be implicated in the progression of various neurodegenerative diseases. Recent in vivo studies showed that lipopolysaccharide (LPS) preconditioning provides neuroprotection by activating Toll-like receptor 4 (TLR4), one of the members for pattern recognition receptor (PRR) family that play critical role in host response to tissue injury, infection, and inflammation. Pre-exposure to low dose of LPS could confer a protective state against cellular apoptosis following subsequent stimulation with LPS at higher concentration, suggesting a role for TLR4 pre-activation in the signaling pathway of LPS-induced neuroprotection.

Preconditioning by ultra-low dose of tramadol reduces the severity of tramadol-induced seizure: Contribution of glutamate receptors.

Tramadol, a weak agonist of mu-opioid receptors, causes seizure via several mechanisms. Preconditioning has been purposed to reduce the epileptic seizures in animal models of epilepsy. The preconditioning effect of tramadol on seizure is not studied yet.