Liam Taylor’s Post

We've had a fantastic response to our newest product! Make sure to check out the fastest and most affordable human iPSC-derived astrocytes on the market! We recently announced our new axoCells™ Astrocytes line (ax0704) designed to fuel robust in vitro models for neurodegenerative disease research and drug discovery. With labs around the world increasingly moving to in vitro models, drug discovery researchers are embracing human iPSC-derived cells to build more human, more functional models for neuroscience. But with many labs still using rat astrocytes for their work (with very long protocols, some even >100 days), we're "supporting the switch" to human iPSCs with this new axoCells Astrocytes product that can drive faster, cheaper in vitro workflows. Key highlights of our new axoCells Astrocytes product include: • Best price on the market • Derived from fibroblasts taken from a healthy 40-50-year-old male donor • Assay ready in just 48 hours • Express seven key markers of primary human astrocytes including GFAP, AQP4 and S100B and astrocyte-associated markers (EAAT1 and ALDH1L1) with low levels of neuronal progenitor markers including Nestin • Specifically developed for use in powerful in vitro monoculture models and complex co-culture systems for drug discovery Bolstered by our world-leading ISO 9001-accredited manufacturing processes, we are delighted to pass on further cost savings to you. Our new ax0704 astrocytes are cheaper than previous astrocytes and are priced at just £660 / $830 / €770 per vial (1 million cells)- the best price on the market! Click here to read more about this new product line and how you can use axoCells Astrocytes to power robust, physiologically relevant models of Alzheimer’s Disease, Parkinson’s Disease and ALS: https://hubs.la/Q02BjVV50 Want to explore the details and get a quote? Click here: https://hubs.la/Q02BjL-Q0 #iPSCs #Astrocytes #AlzheimersDisease #ParkinsonsDisease #ALS #DrugDiscovery

We've had a fantastic response to our newest product! Make sure to check out the fastest and most affordable human iPSC-derived astrocytes on the market! We recently announced our new axoCells™ Astrocytes line (ax0704) designed to fuel robust in vitro models for neurodegenerative disease research and drug discovery. With labs around the world increasingly moving to in vitro models, drug discovery researchers are embracing human iPSC-derived cells to build more human, more functional models for neuroscience. But with many labs still using rat astrocytes for their work (with very long protocols, some even >100 days), we're "supporting the switch" to human iPSCs with this new axoCells Astrocytes product that can drive faster, cheaper in vitro workflows. Key highlights of our new axoCells Astrocytes product include: • Best price on the market • Derived from fibroblasts taken from a healthy 40-50-year-old male donor • Assay ready in just 48 hours • Express seven key markers of primary human astrocytes including GFAP, AQP4 and S100B and astrocyte-associated markers (EAAT1 and ALDH1L1) with low levels of neuronal progenitor markers including Nestin • Specifically developed for use in powerful in vitro monoculture models and complex co-culture systems for drug discovery Bolstered by our world-leading ISO 9001-accredited manufacturing processes, we are delighted to pass on further cost savings to you. Our new ax0704 astrocytes are cheaper than previous astrocytes and are priced at just £660 / $830 / €770 per vial (1 million cells)- the best price on the market! Click here to read more about this new product line and how you can use axoCells Astrocytes to power robust, physiologically relevant models of Alzheimer’s Disease, Parkinson’s Disease and ALS: https://hubs.la/Q02BjWkX0 Want to explore the details and get a quote? Click here: https://hubs.la/Q02BjWpy0 #iPSCs #Astrocytes #AlzheimersDisease #ParkinsonsDisease #ALS #DrugDiscovery

Transcriptional Profiling of iPSC-Derived Microglia for Neurodegenerative Therapy In the seminal study, "Transcriptional Characterization of iPSC-Derived Microglia as a Model for Therapeutic Development in Neurodegeneration," featured in Scientific Reports, authors Gokul Ramaswami, Yeliz Yuva-Aydemir, Brynn Akerberg, Bryan Matthews, Jenna Williams, Gabriel Golczer, Jiaqi Huang, Ali AlAbdullatif, Dann Huh, Linda C. Burkly, Sandra J. Engle, Iris Grossman, Alfca Sehgal, Alla A. Sigova, Robert T. Fremeau Jr., Yuting Liu, and David Bumcrot deliver a masterful exploration of the potential of iPSC-derived microglia for developing therapies against neurodegenerative diseases. This comprehensive analysis offers groundbreaking insights into the utility of these cells in translational research. Unveiling the Potential of iPSC-Derived Microglia The authors begin by meticulously characterizing iPSC-derived microglia (iMGL) cells, demonstrating their remarkable similarity to primary human microglia. They highlight how iMGL cells express key microglial transcription factors and functional genes, positioning them as a robust in vitro model for neurodegenerative research. This feature singularly positions iMGL cells as a universal tool for studying microglial behavior and therapeutic responses in neurodegeneration. iPSC Microglia: A Paradigm Shift in Neurodegenerative Therapy The study delves deep into the transcriptional profiling of iMGL cells, both at the bulk and single-cell levels. It sheds light on pivotal findings that show iMGL cells exhibit distinct transcriptional subpopulations, representing both homeostatic and activated states similar to those in vivo. The authors meticulously dissect the transcriptional responses of iMGL cells to Liver X Receptor (LXR) pathway agonists, emphasizing their potential in modeling disease states and evaluating therapeutic interventions. Navigating the Therapeutic Landscape Perhaps most compelling is the study's exploration of the clinical relevance of iMGL cells. The authors provide a critical analysis of the cells' transcriptional responsiveness to LXR pathway agonists, demonstrating robust changes in lipid metabolism and cell cycle processes. They advocate for the integration of iMGL cells in drug development pipelines, highlighting their utility in preclinical testing and the potential to uncover novel therapeutic targets. #Neurodegeneration #iPSCCells #Microglia #TherapeuticDevelopment #TranslationalResearch #BiomedicalInnovation #Neurology #CellularTherapy #MedicalResearch #SingleCellSequencing #RNASeq #DiseaseModeling #HealthcareInnovation #Neuroscience #Neuroinflammation #DrugDevelopment #StemCellResearch #GenomicProfiling #LXRPathway #ScientificReports

#Alzheimer #neuron #signaling #cell Signaling interactions among neurons impact cell fitness and death in Alzheimer’s disease https://lnkd.in/grvTt483 Amit Singh University of Dayton The pathology of Alzheimer’s disease involves a long preclinical period, where the characteristic clinical symptoms of the changes in the brain are undetectable. During the preclinical period, homeostatic mechanisms may help prevent widespread cell death. Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role. As the disease progresses, dysregulation of signaling pathways that govern cell death contributes to neurodegeneration. Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42- or tau-mediated neurodegeneration. Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells. This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons. Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells. Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration. Generating genetic mosaics with labeled clones of amyloid-beta 42- or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease. These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.

Revolutionizing High-Grade Glioma Treatment: Our Research Published in ACS Pharmacology and Translational Science   Exciting Announcement We are proud to announce the publication of our latest study, "Differential Expression of SRY-Related HMG-Box Transcription Factor 2, Oligodendrocyte Lineage Transcription Factor 2, and Zinc Finger E-Box Binding Homeobox 1 in Serum-Derived Extracellular Vesicles: Implications for Mithramycin Sensitivity and Targeted Therapy in High-Grade Glioma," in ACS Pharmacology and Translational Science. Check out the study here: https://lnkd.in/gYfHW_22 This research, a collaborative endeavor involving the Apollo Hospitals Educational and Research Foundation team with Forcast Bioscience, Apollo Hospitals (Neurosurgery) and IIT Hyderabad represents a significant advancement in treating high-grade glioma. Our focus has been on harnessing the potential of Mithramycin (Mit-A) in glioma therapy, an approach previously limited by toxicity issues. Key Findings: The study employed an ex vivo tumor sensitivity assay to predict how patients respond to Mit-A, proposing its application in treating Glioblastoma Multiforme (GBM). We developed a pioneering EV-derived mRNA transcript assay gene panel (including Sox2, Olig2, and Zeb1), offering a potential biomarker for selecting optimal Mit-A treatments in high-grade gliomas. Impact: These breakthroughs pave the way for personalized medicine in glioma treatment, underscoring the critical role of precision in therapy selection. Acknowledgments: A heartfelt thank you to our dedicated team of scientists, clinicians, and collaborators. This study is part of Patnam Sreekanth's doctoral research. We extend our gratitude to Biswanath Majumder, Parth Joshi, Balakrishna Nagalla, Anula Singh, Ph.D., Dilli Kumar, Manjusha Biswas, Alok Ranjan, Pradip K. Majumder, Ajith Kamath, Amitava Ray, and others for their invaluable contribution. Special thanks to Venkata Sasidhar Manda and Dr. Aravind Kumar Rengan, who served as industrial and academic mentors for this study. Stay tuned for more updates on our journey and future breakthroughs in medical research. #GliomaTreatment #MedicalResearch #Innovation #Collaboration #Healthcare #BrainCancer #Mithramycin #ACSJournals #apollohospitals #aherf

Earliest-yet Alzheimer's biomarker found in mouse model could point to new targets . A surge of a neural-specific protein in the brain is the earliest-yet biomarker for Alzheimer's disease, report researchers studying a mouse model of the disease. Furthermore, the increased protein activity leads to the seizures associated with the earliest stages of neurodegeneration, and inhibiting the protein in the mice slowed the onset and progression of seizure activity. The neural-specific protein, PSD-95, could pose a new target for Alzheimer's research, early diagnosis and treatment. #ScienceDailynews #InnovativeResearch #NextGenScience #ExploringFrontiers

📃Scientific paper: Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in the 5XFAD Alzheimer's Disease Model Abstract: The mechanistic target of rapamycin (mTOR) signaling pathway plays a major role in key cellular processes including metabolism and differentiation; however, the role of mTOR in microglia and its importance in Alzheimer's disease (AD) have remained largely uncharacterized. We report that selective loss of Tsc1, a negative regulator of mTOR, in microglia in mice of both sexes, caused mTOR activation and upregulation of Trem2 with enhanced β-Amyloid (Aβ) clearance, reduced spine loss, and improved cognitive function in the 5XFAD AD mouse model. Combined loss of Tsc1 and Trem2 in microglia led to reduced Aβ clearance and increased Aβ plaque burden revealing that Trem2 functions downstream of mTOR. Tsc1 mutant microglia showed increased phagocytosis with upregulation of CD68 and Lamp1 lysosomal proteins. In vitro studies using Tsc1-deficient microglia revealed enhanced endocytosis of the lysosomal tracker indicator Green DND-26 suggesting increased lysosomal activity. Incubation of Tsc1-deficient microglia with fluorescent-labeled Aβ revealed enhanced Aβ uptake and clearance, which was blunted by rapamycin, an mTOR inhibitor. In vivo treatment of mice of relevant genotypes in the 5XFAD background with rapamycin, affected microglial activity, decreased Trem2 expression and reduced Aβ clearance causing an increase in Aβ plaque burden. Prolonged treatment with rapamycin caused even further reduction of mTOR activity, reduction in Trem2 expression, and increase in Aβ levels. ... Continued on ES/IODE ➡️ https://etcse.fr/nSf ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you. #alzheimer #science #health

📃Scientific paper: Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in the 5XFAD Alzheimer's Disease Model Abstract: The mechanistic target of rapamycin (mTOR) signaling pathway plays a major role in key cellular processes including metabolism and differentiation; however, the role of mTOR in microglia and its importance in Alzheimer's disease (AD) have remained largely uncharacterized. We report that selective loss of Tsc1, a negative regulator of mTOR, in microglia in mice of both sexes, caused mTOR activation and upregulation of Trem2 with enhanced β-Amyloid (Aβ) clearance, reduced spine loss, and improved cognitive function in the 5XFAD AD mouse model. Combined loss of Tsc1 and Trem2 in microglia led to reduced Aβ clearance and increased Aβ plaque burden revealing that Trem2 functions downstream of mTOR. Tsc1 mutant microglia showed increased phagocytosis with upregulation of CD68 and Lamp1 lysosomal proteins. In vitro studies using Tsc1-deficient microglia revealed enhanced endocytosis of the lysosomal tracker indicator Green DND-26 suggesting increased lysosomal activity. Incubation of Tsc1-deficient microglia with fluorescent-labeled Aβ revealed enhanced Aβ uptake and clearance, which was blunted by rapamycin, an mTOR inhibitor. In vivo treatment of mice of relevant genotypes in the 5XFAD background with rapamycin, affected microglial activity, decreased Trem2 expression and reduced Aβ clearance causing an increase in Aβ plaque burden. Prolonged treatment with rapamycin caused even further reduction of mTOR activity, reduction in Trem2 expression, and increase in Aβ levels. ... Continued on ES/IODE ➡️ https://etcse.fr/nSf ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you. #alzheimer #science #health

📃Scientific paper: Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in the 5XFAD Alzheimer's Disease Model Abstract: The mechanistic target of rapamycin (mTOR) signaling pathway plays a major role in key cellular processes including metabolism and differentiation; however, the role of mTOR in microglia and its importance in Alzheimer's disease (AD) have remained largely uncharacterized. We report that selective loss of Tsc1, a negative regulator of mTOR, in microglia in mice of both sexes, caused mTOR activation and upregulation of Trem2 with enhanced β-Amyloid (Aβ) clearance, reduced spine loss, and improved cognitive function in the 5XFAD AD mouse model. Combined loss of Tsc1 and Trem2 in microglia led to reduced Aβ clearance and increased Aβ plaque burden revealing that Trem2 functions downstream of mTOR. Tsc1 mutant microglia showed increased phagocytosis with upregulation of CD68 and Lamp1 lysosomal proteins. In vitro studies using Tsc1-deficient microglia revealed enhanced endocytosis of the lysosomal tracker indicator Green DND-26 suggesting increased lysosomal activity. Incubation of Tsc1-deficient microglia with fluorescent-labeled Aβ revealed enhanced Aβ uptake and clearance, which was blunted by rapamycin, an mTOR inhibitor. In vivo treatment of mice of relevant genotypes in the 5XFAD background with rapamycin, affected microglial activity, decreased Trem2 expression and reduced Aβ clearance causing an increase in Aβ plaque burden. Prolonged treatment with rapamycin caused even further reduction of mTOR activity, reduction in Trem2 expression, and increase in Aβ levels. ... Continued on ES/IODE ➡️ https://etcse.fr/nSf ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you. #alzheimer #science #health

📃Scientific paper: Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in the 5XFAD Alzheimer's Disease Model Abstract: The mechanistic target of rapamycin (mTOR) signaling pathway plays a major role in key cellular processes including metabolism and differentiation; however, the role of mTOR in microglia and its importance in Alzheimer's disease (AD) have remained largely uncharacterized. We report that selective loss of Tsc1, a negative regulator of mTOR, in microglia in mice of both sexes, caused mTOR activation and upregulation of Trem2 with enhanced β-Amyloid (Aβ) clearance, reduced spine loss, and improved cognitive function in the 5XFAD AD mouse model. Combined loss of Tsc1 and Trem2 in microglia led to reduced Aβ clearance and increased Aβ plaque burden revealing that Trem2 functions downstream of mTOR. Tsc1 mutant microglia showed increased phagocytosis with upregulation of CD68 and Lamp1 lysosomal proteins. In vitro studies using Tsc1-deficient microglia revealed enhanced endocytosis of the lysosomal tracker indicator Green DND-26 suggesting increased lysosomal activity. Incubation of Tsc1-deficient microglia with fluorescent-labeled Aβ revealed enhanced Aβ uptake and clearance, which was blunted by rapamycin, an mTOR inhibitor. In vivo treatment of mice of relevant genotypes in the 5XFAD background with rapamycin, affected microglial activity, decreased Trem2 expression and reduced Aβ clearance causing an increase in Aβ plaque burden. Prolonged treatment with rapamycin caused even further reduction of mTOR activity, reduction in Trem2 expression, and increase in Aβ levels. ... Continued on ES/IODE ➡️ https://etcse.fr/nSf ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you. #alzheimer #science #health