Excited to announce the release of this important article on midbrain organoids and alpha-synuclein aggregation, a significant advancement in modeling Parkinson's disease in vitro 🧠 This paper titled "Exploring Alpha-synuclein Pathology: Insights from a Midbrain Organoid Model of Familial Parkinson's Disease" shows the results of many years of work on the field of alpha-synuclein aggregation and astrocyte senescence 🔬 Find it now at Molecular and Cellular Neuroscience ➡ https://lnkd.in/gfp-NTzs #ParkinsonsResearch #Neuroscience #organoids #senescence
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Our new article “Alpha-synuclein pathology is associated with astrocyte senescence in a midbrain organoid model of familial Parkinson's disease” is now available at Molecular and Cellular Neuroscience. Being able to show alpha-Synuclein aggregation in patient specific midbrain organoids is a major step for in vitro modeling of the pathological processes involved in PD. https://lnkd.in/eXtWXR97 #parkinsons #synuclein #organoids #astrocytes #senescence
Alpha-synuclein pathology is associated with astrocyte senescence in a midbrain organoid model of familial Parkinson's disease
sciencedirect.com
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In their latest publication published in EMBO Reports (PMID 38413732), Yook et al. suggest PSD-95 as an early-stage biomarker and a novel therapeutic target for Alzheimer’s disease. Using our monoclonal Homer1b/c antibody as postsynaptic marker, they were able to reveal the underlying mechanism of elevated seizure activity during early-stage Abeta pathology. https://lnkd.in/euiVbgzH #neuroscience #antibodies #Homer1bc
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If you are attending Society for Neuroscience #SFN2024, drop by our booth or posters to see how iPSC derived models can de-risk your drug discovery program. Our SFN activities Booth 368 - come meet the Ncardia team; Peter Udall John Lamb Debbie D. Jeroen De Groot Posters - Evaluation of human induced pluripotent stem cell (hiPSC)-derived tri-culture as in vitro model for Alzheimer’s Disease Board B60; In-Person Presentation Time: Sun., Oct. 6 2024 1-2pm. Cellular and Molecular Mechanisms of Tauopathies, Synucleinopathies, and Other Degenerative Diseases Board C7; In-Person Presentation Time: Tue., Oct. 8, 2024 10 - 11 a.m. Leveraging a hiPSC derived 3D tri-culture model to accelerate neuronal maturation and induce microglial dysfunction in a model of tauopathy Board B134; In-Person Presentation Time: Tue., Oct. 8, 2024 10 - 11 a.m. Development of iPSC-based Parkinson’s disease model for drug discovery Board B139; In-Person Presentation Time: Tue., Oct. 8, 2024 4 - 5 p.m #SFN2024 #Neuroscience #Discovery
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Sait Ashina The complexity of Trigeminal Neuralgia (TN) lies in its multifaceted molecular mechanisms, involving genetic mutations in ion channels and polymorphisms affecting neurotransmitter regulation. Research highlights the role of mutations in sodium and calcium channels, such as SCN9A, SCN3, SCN8A, and TRPM8, TRPM7, which are critical in the development of TN. Structural changes from nerve compression induce downstream effects like imbalances in Nav channels, contributing to increased nerve sensitivity and abnormal impulse generation. Hyperexcitability of trigeminal neurons, changes in potassium channel-mediated resting potential, neuronal apoptosis, and myelin-associated glycoprotein downregulation in Schwann cells further complicate TN pathology. Additionally, ectopic impulses and ephaptic crosstalk leading to central sensitization, along with elevated levels of substance P, CGRP, and inflammatory cytokines such as TNF and IL-6, underscore the intricate network of factors contributing to TN. Continued research is essential for advancing diagnosis and treatment strategies for this debilitating condition. #TrigeminalNeuralgia #Neurology #Neurosurgery #Dentistry #FacialPain #MedicalResearch #PainManagement #Pain #Genetics #IonChannels #Cytokines #Neuroinflammation #Molecular #Inflammation #CGRP #Neuroscience
Understanding the precise molecular mechanisms underlying Trigeminal Neuralgia (TN) is still a challenge. Evidence from current research indicates several mutations in genes encoding ion channels, particularly sodium and calcium channels, as well as polymorphisms affecting serotonin transporters and monoamine oxidase type A. Mutations in SCN9A, SCN3, SCN8A (encoding voltage-gated sodium channels Nav1.7, Nav1.3, Nav1.6), and TRPM8 and TRPM7 (encoding transient receptor potential channels) have been linked to TN. Structural changes from compression lead to important downstream effects, including imbalances in Nav channels, which contribute to enhanced sensitivity and ectopic impulse generation in the trigeminal nerve. Also, hyperexcitability of trigeminal neurons, altered resting potential mediated by voltage-gated potassium channels, apoptosis, and downregulation of myelin-associated glycoprotein in Schwann cells are involved in TN. Ectopic impulse and ephaptic crosstalk can lead to central sensitization involving NMDA receptor activation. Elevated levels of substance P, CGRP, and inflammatory cytokines like TNF and IL-6 further contribute to TN's pathophysiology. This illustrates the complexity and the need for continued research to improve diagnosis and treatment strategies. #TrigeminalNeuralgia #Neurology #Neurosurgery #Dentistry #FacialPain #MedicalResearch #PainManagement #Pain #Genetics #IonChannels #Cytokines #Neuroinflammation #Molecular #Inflammation #CGRP #Neuroscience 👉 https://lnkd.in/gJqsthzq
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Did you miss our presentation on the diagnosis of Alzheimer’s disease pathology using a novel blood-based assay? Watch an on-demand presentation from Henrik Zetterberg, PhD, and Kaj Blennow, PhD, for a deep dive into how the ALZpath novel plasma pTau217 immunoassay identifies abnormal amyloid-ß and tau pathologies at various clinical stages from plasma samples. Topics they covered include: • The results obtained from Wisconsin’s Registry for Alzheimer's Prevention (WRAP) in relation to pTau217 and the practical aspects of high-throughput sample analysis • pTau217’s superior solo performance compared to pTau217/non-pTau212-221 ratio • The advancements in developing an easy-to-use, highly accurate blood-based AD test Watch on-demand today: https://hubs.li/Q02nqBJd0 #pTau217 #Alzheimers #neuroscience #ClinicalResearch #AlzheimersDisease #AlzheimersResearch #AlzheimersAssociation #AlzheimersSociety #diagnostics #biomarkers
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I will be presenting our "Synthetic" DSC Perfusion methodology at the European Society of Neuroradiology annual meeting in Paris. DSC Perfusion MRI is highly dependent on the acquisition protocol (flip angle, preload, echo time, ...). CBV-optimized protocols (with low T1-sensitivity) differ from PSR-optimized protocols (with high T1-sensitivity), and the heterogeneity of protocols across institutions limits the universalizability of this technique. Using multi-echo perfusion datasets, it is possible to apply the Bloch equations (with a few assumptions/approximations) for a synthetic adjustment of the acquisition parameters. Synthetic DSC can be used to obtain simultaneous CBV-optimized and PSR-optimized datasets (as in the figure), and possibly to achieve post-hoc harmonization in multicenter studies. ESNR presentation: Scientific Session 1 - Oral Presentations - Neuro-oncology: Thursday, September 19th 2024, 2 pm – Room 3 Benjamin Ellingson Jingwen Yao Nicholas Cho Catalina Raymond Donatello Telesca Noriko Salamon Timothy Cloughesy BTIL UCLA UCLA #uclabtil #glioblastoma #glioma #neuroradiology #neuroimaging #neurooncology #DSC #Perfusion #MRI #braintumors
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🔎 DYK: You can gain first-hand experience on The National Institutes of Health grant application evaluations within CSR's Early Career Reviewer program: https://go.nih.gov/ECRmain The program aims to help early career scientists become more competitive as grant applicants through first-hand experience with peer review and to enrich and diversify CSR’s pool of trained reviewers. #biochemistry #biology #biophysics #cancer #cellbiology #chemistry #drugdiscovery #genomics #hematology #HIV #infectiousdiseases #neuroscience #vascular #virology
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Would like to share this inseideful Information from EMBO Journal: "Regulation of directed axon guidance and branching during development is essential for the generation of neuronal networks. However, the molecular mechanisms that underlie interstitial (or collateral) axon branching in the mammalian brain remain unresolved. Here, we investigate interstitial axon branching in vivo using an approach for precise labeling of layer 2/3 callosal projection neurons (CPNs). This method allows for quantitative analysis of axonal morphology at high acuity and also manipulation of gene expression in well-defined temporal windows. We find that the GSK3β serine/threonine kinase promotes interstitial axon branching in layer 2/3 CPNs by releasing MAP1B-mediated inhibition of axon branching. Further, we find that the tubulin tyrosination cycle is a key downstream component of GSK3β/MAP1B signaling. These data suggest a cell-autonomous molecular regulation of cortical neuron axon morphology, in which GSK3β can release a MAP1B-mediated brake on interstitial axon branching upstream of the posttranslational tubulin code." https://lnkd.in/epiFiyiV #cognition #cognitive #cognitivefunction #brain #neuroscience #neuroscienceresearch #neurobiology #neurons #sciencenews #scienceandtechnology #scienceinnovation #biology #researchanddevelopment #research #researchers #molecularbiology #neurodevelopment
Microtubule-binding protein MAP1B regulates interstitial axon branching of cortical neurons via the tubulin tyrosination cycle | The EMBO Journal
embopress.org
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Don't forget to register for our webinar tomorrow to learn what multiplex cell phenotyping tells us about malignant brain tumors! 🧠 Attendees will also learn: - How to build a robust phenotyping panel informed by single-cell RNA-seq data - How to choose and establish essential biomarkers for the investigation of cellular hierarchies in complex brain tumor tissues - Factors to consider in evaluating multiplex platforms and technologies to optimize your research needs Register at your preferred time on April 25, 2024: ✔️ Europe: 7 AM EDT, 12 PM BST, 1 PM CEST, 7 PM CST https://bit.ly/4avdSuk ✔️ North America: 9 AM PDT, 12 PM EDT, 5 PM BST, 6 PM CEST https://bit.ly/3PY4MOc #glioma #gliomas #neuroscience #spatialbiology #multiplex
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Doctoral researcher at DZNE │ Translational Neuroscientist │ Member of the Elite Network of Bavaria (ENB) │ Bringing new insights on Alzheimer's disease mechanisms and etiologies
🧠Excited to Share Our New Publication!💪 I am thrilled to announce that I am a co-author on a recently published paper in Nature Neuroscience! Our study, titled “T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis”, explores the role of CD8+ T cells in neuroinflammation and myelin damage associated with Alzheimer’s disease. 🔬 Key Findings: • We discovered that CD8+ T cells contribute significantly to oligodendrocyte and myelin pathology in Alzheimer’s mouse models. • The depletion of CD8+ T cells improved cognitive functions and partially reduced anxiety-related behaviors in these models. • Our research highlights potential therapeutic targets for treating neuroinflammation in Alzheimer’s disease. This work would not have been possible without the incredible support and collaboration of all co-authors and the broader research team. 📖 You can read the full article here: https://lnkd.in/eKHKm8ae #Neuroscience #Research #AlzheimersDisease #Neuroinflammation #Science #Tcells #Nature #Immunity #Neurodegeneration
T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis - Nature Neuroscience
nature.com
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