EVOS M5000 in Neuroscience & Neurodegeneration: Independent Studies — Wave 3 Part 1
Peer-reviewed studies discovered independently of Thermo Fisher's curated EVOS M5000 citations. Each paper was full-text verified to mention the EVOS M5000 Imaging System as a microscope. Cards link to Google Scholar, PubMed, PMC and DOI.
EVOS M5000IndependentWave 3
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Attenuation of Oxidative Stress by Cannabinoids and Cannabis Extracts in Differentiated Neuronal Cells.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
In this proof-of-concept study, the antioxidant activity of phytocannabinoids, namely cannabidiol (CBD) and Δ9- tetrahydrocannabinol (THC), were investigated using an in vitro system of differentiated human neuronal SY-SH5Y cells. The oxidative stress was induced by hydrogen peroxide, as reactive oxygen species (ROS). Alzheimer's disease (AD)-like pathological conditions were m
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FDA-approved 5-HT
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Vascular and mitochondrial dysfunction are well-established consequences of spinal cord injury (SCI). Evidence suggests mitigating these dysfunctions may be an effective approach in treating SCI. The goal of this study was to elucidate if mitochondrial biogenesis (MB) induction with a new, selective and FDA-approved 5-hydroxytryptamine receptor 1F (5-HT
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Delivering progranulin to neuronal lysosomes protects against excitotoxicity.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Loss-of-function mutations in progranulin (GRN) are a major genetic cause of frontotemporal dementia (FTD), possibly due to loss of progranulin's neurotrophic and anti-inflammatory effects. Progranulin promotes neuronal growth and protects against excitotoxicity and other forms of injury. It is unclear if these neurotrophic effects are mediated through cellular signaling or thr
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The requirement of ubiquitin C-terminal hydrolase L1 in mouse ovarian development and fertility†.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Ubiquitin C-terminal hydrolase L1 (UCHL1) is a de-ubiquitinating enzyme enriched in neuronal and gonadal tissues known to regulate the cellular stores of mono-ubiquitin and protein turnover. While its function in maintaining proper motor neuron function is well established, investigation into its role in the health and function of reproductive processes is only just beginning t
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Brain Cells Release Calreticulin That Attracts and Activates Microglia, and Inhibits Amyloid Beta Aggregation and Neurotoxicity.
Cell type: Macrophage | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Calreticulin is a chaperone, normally found in the endoplasmic reticulum, but can be released by macrophages into the extracellular medium. It is also found in cerebrospinal fluid bound to amyloid beta (Aβ). We investigated whether brain cells release calreticulin, and whether extracellular calreticulin had any effects on microglia and neurons relevant to neuroinflammation and
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Mapping cis-regulatory elements in human neurons links psychiatric disease heritability and activity-regulated transcriptional programs.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Genome-wide association studies (GWASs) have identified hundreds of loci associated with psychiatric diseases, yet there is a lack of understanding of disease pathophysiology. Common risk variants can shed light on the underlying molecular mechanisms; however, identifying causal variants remains challenging. We map cis-regulatory elements in human neurons derived from pluripote
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Ligand-free mitochondria-localized mutant AR-induced cytotoxicity in spinal bulbar muscular atrophy.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Spinal bulbar muscular atrophy (SBMA), the first identified CAG-repeat expansion disorder, is an X-linked neuromuscular disorder involving CAG-repeat-expansion mutations in the androgen receptor (AR) gene. We utilized CRISPR-Cas9 gene editing to engineer novel isogenic human induced pluripotent stem cell (hiPSC) models, consisting of isogenic AR knockout, control and disease li
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Differences in the Autophagy Response to Hypoxia in the Hippocampus and Neocortex of Rats.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Autophagy is a regulated mechanism of degradation of misfolded proteins and organelles in the cell. Neurons are highly differentiated cells with extended projections, and therefore, their functioning largely depends on the mechanisms of autophagy. For the first time in an animal model using immunohistochemistry, dot analysis, and qRT-PCR, the autophagy (macroautophagy) activity
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Expanding the phenotypic variability of MORC2 gene mutations: From Charcot-Marie-Tooth disease to late-onset pure motor neuropathy.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
MORC2 gene encodes a ubiquitously expressed nuclear protein involved in chromatin remodeling, DNA repair, and transcriptional regulation. Heterozygous mutations in MORC2 gene have been associated with a spectrum of disorders affecting the peripheral nervous system such as Charcot-Marie-Tooth (CMT2Z), spinal muscular atrophy-like with or without cerebellar involvement, and a dev
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Severe congenital myasthenic syndromes caused by agrin mutations affecting secretion by motoneurons.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Congenital myasthenic syndromes (CMS) are predominantly characterized by muscle weakness and fatigability and can be caused by a variety of mutations in genes required for neuromuscular junction formation and maintenance. Among them, AGRN encodes agrin, an essential synaptic protein secreted by motoneurons. We have identified severe CMS patients with uncharacterized p.R1671Q, p
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Lipids uniquely alter rates of insulin aggregation and lower toxicity of amyloid aggregates.
Cell type: T cell | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Amyloid formation is a hallmark of many medical diseases including diabetes type 2, Alzheimer's and Parkinson diseases. Under these pathological conditions, misfolded proteins self-assemble forming oligomers and fibrils, structurally heterogeneous aggregates that exhibit a large variety of shapes and forms. A growing body of evidence points to drastic changes in the lipid profi
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Nanoparticle-mediated selective Sfrp-1 silencing enhances bone density in osteoporotic mice.
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Osteoporosis (OP) is characterized by a loss in bone mass and mineral density. The stimulation of the canonical Wnt/β-catenin pathway has been reported to promote bone formation, this pathway is controlled by several regulators as secreted frizzled-related protein-1 (Sfrp-1), antagonist of the pathway. Thus, Sfrp-1 silencing therapies could be suitable for enhancing bone growth
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Small-molecule compound from AlphaScreen disrupts tau-glycan interface.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Tauopathies are neurodegenerative diseases characterized by intracellular abnormal tau deposits in the brain. Tau aggregates can propagate from one neuron to another in a prion-like manner, mediated by the interaction between tau and cell surface heparan sulfate proteoglycans. We developed an AlphaScreen assay, with His-tagged tau and biotinylated heparin, to represent the tau-
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Selective inhibition of excitatory synaptic transmission alters the emergent bursting dynamics of
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Neurons
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Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Myelin is a multilayered membrane that tightly wraps neuronal axons, enabling efficient, high-speed signal propagation. The axon and myelin sheath form tight contacts, mediated by specific plasma membrane proteins and lipids, and disruption of these contacts causes devastating demyelinating diseases. Using two cell-based models of demyelinating sphingolipidoses, we demonstrate
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Syk inhibitors protect against microglia-mediated neuronal loss in culture.
Cell type: Macrophage | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Microglia are brain macrophages and play beneficial and/or detrimental roles in many brain pathologies because of their inflammatory and phagocytic activity. Microglial inflammation and phagocytosis are thought to be regulated by spleen tyrosine kinase (Syk), which is activated by multiple microglial receptors, including TREM2 (Triggering Receptor Expressed on Myeloid Cells 2),
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Patients with sporadic FTLD exhibit similar increases in lysosomal proteins and storage material as patients with FTD due to GRN mutations.
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Loss of function progranulin (GRN) mutations are a major autosomal dominant cause of frontotemporal dementia (FTD). Patients with FTD due to GRN mutations (FTD-GRN) develop frontotemporal lobar degeneration with TDP-43 pathology type A (FTLD-TDP type A) and exhibit elevated levels of lysosomal proteins and storage material in frontal cortex, perhaps indicating lysosomal dysfunc
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Metformin Improves Functional Outcomes, Activates Neural Precursor Cells, and Modulates Microglia in a Sex-Dependent Manner After Spinal Cord Injury.
Cell type: Cell culture models | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Spinal cord injury (SCI) results in devastating patient outcomes with few treatment options. A promising approach to improve outcomes following SCI involves the activation of endogenous precursor populations including neural stem and progenitor cells (NSPCs) which are located in the periventricular zone (PVZ), and oligodendrocyte precursor cells (OPCs) found throughout the pare
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Multi-transcriptomics reveals brain cellular responses to peripheral infection in Alzheimer's disease model mice.
Cell type: Macrophage | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Peripheral inflammation has been linked to various neurodegenerative disorders, including Alzheimer's disease (AD). Here we perform bulk, single-cell, and spatial transcriptomics in APP/PS1 mice intranasally exposed to Staphylococcus aureus to determine how low-grade peripheral infection affects brain transcriptomics and AD-like pathology. Chronic exposure led to increased amyl
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Preclinical Study on Biodistribution of Mesenchymal Stem Cells after Local Transplantation into the Brain.
Cell type: Stem cell | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Therapeutic efficacy of mesenchymal stem cells (MSCs) is determined by biodistribution and engraftment
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Senataxin helicase, the causal gene defect in ALS4, is a significant modifier of C9orf72 ALS G4C2 and arginine-containing dipeptide repeat toxicity.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Identifying genetic modifiers of familial amyotrophic lateral sclerosis (ALS) may reveal targets for therapeutic modulation with potential application to sporadic ALS. GGGGCC (G4C2) repeat expansions in the C9orf72 gene underlie the most common form of familial ALS, and generate toxic arginine-containing dipeptide repeats (DPRs), which interfere with membraneless organelles, su
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LRPAP1 is released from activated microglia and inhibits microglial phagocytosis and amyloid beta aggregation.
Cell type: Cell culture models | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Low-density lipoprotein receptor-related protein-associated protein 1 (LRPAP1), also known as receptor associated protein (RAP), is an endoplasmic reticulum (ER) chaperone and inhibitor of LDL receptor related protein 1 (LRP1) and related receptors. These receptors have dozens of physiological ligands and cell functions, but it is not known whether cells release LRPAP1 physiolo
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Low-intensity pulsed ultrasound enhances neurite growth in serum-starved human neuroblastoma cells.
Cell type: T cell | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Low-intensity pulsed ultrasound (LIPUS) is a recognized tool for promoting nerve regeneration and repair; however, the intracellular mechanisms of LIPUS stimulation remain underexplored. The present study delves into the effects of varying LIPUS parameters, namely duty cycle, spatial average-temporal average (SATA) intensity, and ultrasound amplitude, on the therapeutic efficac
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Phospholipids and Cholesterol Determine Molecular Mechanisms of Cytotoxicity of α-Synuclein Oligomers and Fibrils.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta, hypothalamus, and thalamus is a hallmark of Parkinson's disease. Neuronal death is linked to the abrupt aggregation of α-synuclein (α-Syn), a small membrane protein that regulates cell vesicle trafficking. α-Syn aggregation rate, as well as the secondary structure and toxicity of α-Syn fibrils,
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Homocysteine potentiates amyloid
Cell type: Endothelial | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Cerebrovascular dysfunction has been implicated as a major contributor to Alzheimer's Disease (AD) pathology, with cerebral endothelial cell (cEC) stress promoting ischemia, cerebral-blood flow impairments and blood-brain barrier (BBB) permeability. Recent evidence suggests that cardiovascular (CV)/cerebrovascular risk factors, including hyperhomocysteinemia (Hhcy), exacerbate
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Hippocampal hyperphosphorylated tau-induced deficiency is rescued by L-type calcium channel blockade.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Aging and Alzheimer's disease are associated with chronic elevations in neuronal calcium influx
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Detection of pTDP-43 via routine muscle biopsy: A promising diagnostic biomarker for amyotrophic lateral sclerosis.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease, pathologically characterized by TDP-43 aggregates. Recent evidence has been indicated that phosphorylated TDP-43 (pTDP-43) is present not only in motor neurons but also in muscle tissues. However, it is unclear whether testing pTDP-43 aggregation in muscle tissue would assist in the diagnosis of ALS
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Leflunomide Treatment Does Not Protect Neural Cells following Oxygen-Glucose Deprivation (OGD) In Vitro.
Cell type: T cell | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Neonatal hypoxia-ischemia (HI) affects 2-3 per 1000 live births in developed countries and up to 26 per 1000 live births in developing countries. It is estimated that of the 750,000 infants experiencing a hypoxic-ischemic event during birth per year, more than 400,000 will be severely affected. As treatment options are limited, rapidly identifying new therapeutic avenues is cri
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Alternative splicing controls teneurin-3 compact dimer formation for neuronal recognition.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Neuronal network formation is facilitated by recognition between synaptic cell adhesion molecules at the cell surface. Alternative splicing of cell adhesion molecules provides additional specificity in forming neuronal connections. For the teneurin family of cell adhesion molecules, alternative splicing of the EGF-repeats and NHL domain controls synaptic protein-protein interac
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Prolonged depletion of profilin 1 or F-actin causes an adaptive response in microtubules.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
In addition to its well-established role in actin assembly, profilin 1 (PFN1) has been shown to bind to tubulin and alter microtubule growth. However, whether PFN1's predominant control over microtubules in cells occurs through direct regulation of tubulin or indirectly through the polymerization of actin has yet to be determined. Here, we manipulated PFN1 expression, actin fil
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Intrathecal gastrodin alleviates allodynia in a rat spinal nerve ligation model through NLRP3 inflammasome inhibition.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Gastrodin (GAS), a main bioactive component of the herbal plant, Gastrodia elata Blume, has shown to have beneficial effects on neuroinflammatory diseases such as Alzheimer's disease in animal studies and migraine in clinical studies. Inflammasome is a multimeric protein complex having a core of pattern recognition receptor and has been implicated in the development of neuroinf
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iPSC-derived hindbrain organoids to evaluate escitalopram oxalate treatment responses targeting neuropsychiatric symptoms in Alzheimer's disease.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Alzheimer's disease (AD) is the most common cause of dementia, and the gradual deterioration of brain function eventually leads to death. Almost all AD patients suffer from neuropsychiatric symptoms (NPS), the emergence of which correlates with dysfunctional serotonergic systems. Our aim is to generate hindbrain organoids containing serotonergic neurons using human induced Plur
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Tubulin-binding region alters tau-lipid interactions and changes toxicity of tau fibrils formed in the presence of phosphatidylserine lipids.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Alzheimer's disease is the fastest-growing neurodegenerative disease that affects over six million Americans. The abnormal aggregation of amyloid β peptide and Tau protein is the expected molecular cause of the loss of neurons in brains of AD patients. A growing body of evidence indicates that lipids can alter the aggregation rate of amyloid β peptide and modify the toxicity of
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FABP5-binding lipids regulate autophagy in differentiated SH-SY5Y cells.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
The motor features of Parkinson's disease result from loss of dopaminergic neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. While a large body of work focusing on protein effectors of autophagy has been reported, regulation of autophagy by lipids has garnered far less attention. Therefore, we sought to identify endogenous lipid mo
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GDF-15 Attenuates the Epithelium-Mesenchymal Transition and Alleviates TGFβ2-Induced Lens Opacity.
Cell type: Epithelial | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
We sought to evaluate the efficacy of growth differentiation factor (GDF)-15 treatment for suppressing epithelial-mesenchymal transition (EMT) and alleviating transforming growth factor β2 (TGFβ2)-induced lens opacity. To test whether GDF-15 is a molecule that prevents EMT, we pretreated the culture with GDF-15 in neural progenitor cells, retinal pigment epithelial cells, and l
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Metabolic resistance of Aβ3pE-42, a target epitope of the anti-Alzheimer therapeutic antibody, donanemab.
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
The amyloid β peptide (Aβ), starting with pyroglutamate (pE) at position 3 and ending at position 42 (Aβ3pE-42), predominantly accumulates in the brains of Alzheimer's disease. Consistently, donanemab, a therapeutic antibody raised against Aβ3pE-42, has been shown to be effective in recent clinical trials. Although the primary Aβ produced physiologically is Aβ1-40/42, an explan
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Bioreactor-produced iPSCs-derived dopaminergic neuron-containing neural microtissues innervate and normalize rotational bias in a dose-dependent manner in a Parkinson rat model.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
A breadth of preclinical studies now support the rationale of pluripotent stem cell-derived cell replacement therapies to alleviate motor symptoms in Parkinsonian patients. Replacement of the primary dysfunctional cell population in the disease, i.e. the A9 dopaminergic neurons, is the major focus of these therapies. To achieve this, most therapeutical approaches involve grafti
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Activation of the Gut-Brain Interaction by Urolithin A and Its Molecular Basis.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
<b>Background:</b> Urolithin A (Uro-A), a type of polyphenol derived from pomegranate, is known to improve memory function when ingested, in addition to its direct effect on the skin epidermal cells through the activation of longevity gene SIRT1. However, the molI ecular mechanism by which orally ingested Uro-A inhibits cognitive decline via the intestine remains unexplored. <b
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Proximity-dependent biotinylation reveals an interaction between ubiquitin-specific peptidase 46 and centrosome-related proteins.
Cell type: Cell culture models | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Protein ubiquitination extensively modulates protein functions and controls various biological processes, such as protein degradation, signal transduction, transcription, and DNA repair. Ubiquitination is a reversible post-translational modification, and deubiquitinating enzymes cleave ubiquitin from proteins. Ubiquitin-specific peptidase 46 (USP46), a deubiquitinase, is highly
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Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury-An In Vitro Model Approach.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Traumatic brain injury (TBI) is caused by an external mechanical force to the head, resulting in abnormal brain functioning and clinical manifestations. Antisecretory factor (AF16) is a potential therapeutic agent for TBI treatment due to its ability to inhibit fluid secretion and decrease inflammation, intracranial pressure, and interstitial fluid build-up, key hallmarks prese
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Palmitoyl-L-carnitine induces tau phosphorylation and mitochondrial dysfunction in neuronal cells.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Alzheimer's disease (AD) is characterized by cognitive decline and memory loss, involving mechanisms such as tau hyperphosphorylation and mitochondrial dysfunction. Increasing evidence suggests that age-related alterations in metabolite levels are crucial for the pathogenesis of AD. Here, we analyzed serum metabolites from mice of various ages (2, 4, 14, and 21 months old) usin
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Dysregulation of protein degradation and alteration of secretome in α-synuclein-exposed astrocytes: implications for dopaminergic neuronal dysfunction.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
A key factor in the propagation of α-synuclein pathology is the compromised protein quality control system. Variations in membrane association and astrocytic uptake between different α-synuclein forms suggest differences in exocytosis or membrane cleavage, potentially impacting the secretome's influence on dopaminergic neurons. We aimed to understand differences in protein degr
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Tubulin-Binding Region Modulates Cholesterol-Triggered Aggregation of Tau Proteins.
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
A hallmark of Alzheimer disease (AD) and tauopathies, severe neurodegenerative diseases, is the progressive aggregation of Tau, also known as microtubule-associated Tau protein. Full-length Tau
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Targeting early tau pathology: probiotic diet enhances cognitive function and reduces inflammation in a preclinical Alzheimer's model.
Cell type: Biological samples | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Alzheimer's disease (AD) remains incurable, yet its long prodromal phase offers a crucial window for early intervention. Pretangle tau, a precursor to neurofibrillary tangles, plays a key role in early AD pathogenesis. Intervening in pretangle tau pathology could significantly delay the progression of AD. The gut-brain axis, increasingly recognized as a contributor to AD, repre
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miRNA profiling of hiPSC-derived neurons from monozygotic twins discordant for schizophrenia.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Schizophrenia is a complex developmental disorder whose molecular mechanisms are not fully understood. The developmental course of schizophrenia can be modeled with human induced pluripotent stem cell (hiPSC) -derived brain cells that carry patient-specific genetic risk factors for the disorder. Although transcriptomic characterization of the patient-derived cells is a standard
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Characterization of the
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
In vivo cell type-specific genetic recombination based on the Cre-loxP system has contributed to the understanding of biological processes and diseases. Neuronal nuclei (NeuN)/RBFOX3 is a widely used mature neuron marker in developmental biology and neuroscience. Here, we generated
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Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Mitochondrial dysfunction is an expected cause of etiology and progression in numerous human neurological pathologies, including stroke, Alzheimer's, and Parkinson's diseases. Therefore, a neuroprotective treatment is an urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD NFs) exhibit unique biological properties. However, neuroprotective properties of these
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The role of phospholipid saturation and composition in α-synuclein aggregation and toxicity: A dual in vitro and in vivo approach.
Cell type: Cell culture models | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Parkinson's disease is characterized by a progressive accumulation of α-synuclein (α-syn) aggregates in Lewy bodies, extracellular deposits found in the midbrain, hypothalamus, and thalamus. The rate of α-syn aggregation, as well as the secondary structure of α-syn oligomers and fibrils, can be uniquely altered by lipids. However, the role of saturation of fatty acids (FAs) in
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Integrated analysis of molecular atlases unveils modules driving developmental cell subtype specification in the human cortex.
Cell type: Cell culture models | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Human brain development requires generating diverse cell types, a process explored by single-cell transcriptomics. Through parallel meta-analyses of the human cortex in development (seven datasets) and adulthood (16 datasets), we generated over 500 gene co-expression networks that can describe mechanisms of cortical development, centering on peak stages of neurogenesis. These m
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Exercise-Induced Hippocampal Neurogenesis Is Attenuated by Inhibition of Monocarboxylate Transporter 2.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Several studies have suggested that lactate mediates exercise-induced hippocampal neurogenesis. To investigate this, we used a monocarboxylate transporter (MCT) inhibitor, alpha-cyano-4-hydroxycinnamic acid (4CIN), to attenuate the signaling effect of endogenous lactate in the hippocampus. Ten-week-old ICR mice were intraperitoneally injected with 100 mg/kg 4CIN before beginnin
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Distinct proliferative and neuronal programmes of chromatin binding and gene activation by ASCL1 are cell cycle stage-specific.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
ASCL1 is a potent proneural factor with paradoxical functions during development, promoting both progenitor pool expansion and neuronal differentiation. How a single factor executes and switches between these potentially opposing functions remains to be understood. Using human neuroblastoma cells as a model system, we show that ASCL1 exhibits cell cycle phase-dependent chromati
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The potent neuroepithelium-promoting activity of Otx2 during gastrulation, as demonstrated by its exogenous epiblast-wide expression in chicken embryos.
Cell type: Stem cell | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Although Otx2 has been a topic of research for over 3 decades, the role of Otx2 expressed in the brain-forming anterior epiblast during gastrulation has not been clarified. We focused on epiblast regions where Otx2 expression is absent or downregulated, namely, the posterior epiblast and tissue belts along the bending of the neural plate. The developmental events that occurred
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Estrogenic regulation of perineuronal nets in the mouse insular cortex and hippocampus.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Estrogen has profound effects on the brain, affecting neuronal plasticity and behavior. Perineuronal nets (PNNs) are perforated extracellular matrix structures that mostly surround parvalbumin (PV)-expressing inhibitory interneurons and regulate neuronal activity, synaptic plasticity and behavior. PNNs have sex-specific effects on behavior, suggesting that hormones like estroge
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Delivering Progranulin to Astrocytic Lysosomes Promotes Growth of Co-Cultured Neurons.
Cell type: Neuron | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
Progranulin (GRN) mutations, most of which cause progranulin haploinsufficiency, are a major genetic cause of frontotemporal dementia (FTD). Restoring progranulin to people with GRN mutations is a promising therapeutic strategy and understanding progranulin's mechanism of action may enable the design of optimal progranulin-based therapies. Progranulin is constitutively secreted
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APPswe mutation causes functional deficits in endothelial cells generated by transient ETV2 overexpression in human iPSCs.
Cell type: Endothelial | Technique: Fluorescence imaging | Disease/area: Neuroscience & Neurodegeneration
BACKGROUND: Brain endothelial cells (ECs) lining blood vessels are essential for the normal function of the brain. They form the first layer of the blood-brain barrier (BBB) and regulate nutrient exchange, immune responses, and angiogenesis. Numerous studies have reported the disruption of the BBB in neurodegenerative diseases, including Alzheimer’s disease (AD). However, the i
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