🆕 New cellular models of myotonic dystrophy type 1 reflect the clinical diversity of the disease Cellular models used to search for new therapies for myotonic dystrophy type 1 do not usually take into account the diversity of subtypes presented by patients. In a study published in the journal iScience, researchers from Germans Trias i Pujol Research Institute (IGTP), in collaboration with University of Belgrade, Biogipuzkoa and Institut de Myologie, have developed three new models that represent this heterogeneity. Read more: https://lnkd.in/dXYzgyPV #DM1 #MyotonicDystrophyType1 #Research #CellularModels
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📃Scientific paper: Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration Abstract: Novel targets to arrest neurodegeneration in several dementing conditions involving misfolded protein accumulations may be found in the diverse signaling pathways of the Mammalian/mechanistic target of rapamycin (mTOR). As a nutrient sensor, mTOR has important homeostatic functions to regulate energy metabolism and support neuronal growth and plasticity. However, in Alzheimer’s disease (AD), mTOR alternately plays important pathogenic roles by inhibiting both insulin signaling and autophagic removal of β-amyloid (Aβ) and phospho-tau (ptau) aggregates. It also plays a role in the cerebrovascular dysfunction of AD. mTOR is a serine/threonine kinase residing at the core in either of two multiprotein complexes termed mTORC1 and mTORC2. Recent data suggest that their balanced actions also have implications for Parkinson's disease (PD) and Huntington's disease (HD), Frontotemporal dementia (FTD) and Amyotrophic Lateral Sclerosis (ALS). Beyond rapamycin; an mTOR inhibitor, there are rapalogs having greater tolerability and micro delivery modes, that hold promise in arresting these age dependent conditions. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/il2r
Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration
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This is BIG 👉 New research by Per Andrén and İbrahim Kaya at Uppsala University and Per Svenningsson at Karolinska Institutet identify #prosaposin as a possible target for drugs & treatment against #parkinsonsdisease ✔ "These results open the doors to an exciting future for research in our field," states Per Andrén, Professor of #Mass #Spectrometry #Imaging 💪 The results are published in #Nature #Communications 👉
Research breakthrough opens doors for Parkinson's Disease Treatment
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📃Scientific paper: Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration Abstract: Novel targets to arrest neurodegeneration in several dementing conditions involving misfolded protein accumulations may be found in the diverse signaling pathways of the Mammalian/mechanistic target of rapamycin (mTOR). As a nutrient sensor, mTOR has important homeostatic functions to regulate energy metabolism and support neuronal growth and plasticity. However, in Alzheimer’s disease (AD), mTOR alternately plays important pathogenic roles by inhibiting both insulin signaling and autophagic removal of β-amyloid (Aβ) and phospho-tau (ptau) aggregates. It also plays a role in the cerebrovascular dysfunction of AD. mTOR is a serine/threonine kinase residing at the core in either of two multiprotein complexes termed mTORC1 and mTORC2. Recent data suggest that their balanced actions also have implications for Parkinson's disease (PD) and Huntington's disease (HD), Frontotemporal dementia (FTD) and Amyotrophic Lateral Sclerosis (ALS). Beyond rapamycin; an mTOR inhibitor, there are rapalogs having greater tolerability and micro delivery modes, that hold promise in arresting these age dependent conditions. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/il2r
Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration
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𝗔𝗰𝗰𝗲𝗹𝗲𝗿𝗮𝘁𝗶𝗻𝗴 𝗗𝗿𝘂𝗴 𝗗𝗲𝘃𝗲𝗹𝗼𝗽𝗺𝗲𝗻𝘁 𝗳𝗼𝗿 𝗟𝘂𝗻𝗴 𝗗𝗶𝘀𝗲𝗮𝘀𝗲𝘀 Scientists around Prof. Dr. Herbert Schiller and Dr. Gerald Burgstaller at #HelmholtzMunich performed an in-depth analysis of human precision-cut lung slices. To mechanistically understand the root causes of lung disease, and identify drugs that target specific pathways, the scientists are collecting deep molecular insights from patient samples and combining these with experimental interventions in the laboratory. A new combination of methods now enabled them to study mechanisms directly in human lung tissue, thereby accelerating drug development for novel therapies. This groundbreaking work is now published in Science Translational Medicine. Read more about the study: https://lnkd.in/eAd4QBHi 💡 AI allows to compare disease states to the Human Lung Cell Atlas. Read more about the HLCA in our research highlight: https://lnkd.in/dvGQ4YKz #AI #ArtificialIntelligence #HLCA #hPCLS #lung Video by Lin Yang
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Happy New Year! The first issue of Trends in Molecular Medicine for 2024 is available online. Before we delve into the content, I would like to express my gratitude to all the authors for their contributions! I hope you enjoy it! As always, I am happy to receive your feedback and ideas for topics and articles so please get in touch! 😀 https://lnkd.in/eaA4Z_W3 In this issue I wrote my first ever editorial ( 😅 ) to introduce myself to the readers of TMM and also to introduce the new TrendsTalk article series "Science around the world", highlighted in the cover! In the TrendsTalk we embark on a journey to learn about the scientific background and expertise of the authors and the geographic landscape that has shaped their ground-breaking work. You can read for free both the editorial and the TrendsTalk article using the links below: https://lnkd.in/d_UJwPB7 (editorial) https://lnkd.in/d6PPTRk9 (TrendsTalk) In this issue, we also have very exciting articles in the field of molecular medicine! The opinion article by Guo et al. discusses the three challenges for #siRNA #drug #development, while the other opinion article by Cecilia Hidalgo and Andrea Paula-Lima focuses on #RyR mediated #calcium release in #hippocampal #health and #disease. The feature review by Lazennec et al. provides an overview on the #CXCR2 chemokine #receptor in #cancer and #physiology. The rest of the reviews cover several topics. Lissah Johnson and Krisopher Sarosiek talk about #apoptosis and #environmental #exposures linked to #disease, Ankit Pandeya and Thirumala-Devi Kanneganti discuss the #theraupeutic potential of #PANoptosis and Ina Yoon and colleagues look at the role of aminoacyl-tRNA #synthases in disease. The scientific life article by Navika Gangrade and Marcus Lambert discuss reform of #postdoctoral #mentorship, while the spotlight of Hemmer et al. highlight a recent study on #PF4 and #brain #aging.
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Dr. Yeran Bai and colleagues have recently published a groundbreaking paper titled "Single-cell mapping of lipid metabolites using an infrared probe in human-derived model systems" in Nature Communications, addressing the pressing need for advanced techniques in metabolic imaging, particularly at the single-cell level. The study introduces a novel approach by employing an azide-tagged infrared probe combined with Optical Photothermal Infrared Spectroscopy (O-PTIR) to enhance the understanding of lipid metabolism in cells. This innovative method offers improved specificity and efficiency in lipid detection compared to traditional methods. The study highlights the unique advantages of O-PTIR over other vibrational spectroscopy techniques, such as its immunity to fluorescence background and cost-effectiveness. The findings deepen our understanding of lipid-related metabolic diseases and pave the way for new therapeutic strategies. Bai et al.'s research marks a significant advancement in metabolic imaging, offering detailed, cell-type-specific insights into lipid metabolism and its role in health and disease. #OPTIR #azide #lipiddetection #naturecommunications
Read more about Bai’s research using O-PTIR
nature.com
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New research: Scientists at Uniformed Services University's Surgical Critical Care Initiative (SC2i) examine the role of microbial colonization and subsequent infections on healing outcomes for blast-related wounds. This research lays “a foundation for precision medicine tools to improve clinical outcomes in traumatic wound care.” This is the first of its kind transcriptomics analysis of combat extremity wound healing, and will point the way toward more targeted predictive tools and more effective treatments. Seth Schobel, PhD, Felipe Lisboa, Desireé Unselt, Ph.D., Meenu Upadhyay, Clifton Dalgard, Matthew D. Wilkerson, Ruben Zamora, Yoram Vodovotz, Benjamin Potter https://lnkd.in/egUqF98M
The influence of microbial colonization on inflammatory versus pro-healing trajectories in combat extremity wounds - PubMed
pubmed.ncbi.nlm.nih.gov
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Scientists at the Max Delbrueck Center for Molecular Medicine in Berlin have found that the Arl8b protein is overexpressed in brain models of Alzheimer's disease, making it a potential therapeutic target. Amyloid beta plaques and tau tangles are the two best-known indicators of Alzheimer's disease. These proteins form in the brain as a result of genetic abnormalities that lead to the formation of aggregates and eventual death of neurons. Although treatments for these targets already exist, they have varying degrees of success in delaying cognitive aging. For this reason, researchers are actively searching for new disease markers. Read on. https://lnkd.in/dKeVFCGc Advance Your Research with #Spectrus 👩🏽🔬 spectruscorp.com #AnalyticalChemistry #MassSpectrometry #LiquidChromatography #Proteomics #Metabolomics #Glycomics #Lipidomics #Epigenetics #FragmentScreening #PolymerAnalysis
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🧬 Welcome to our journey to revolutionize brain regeneration with REGENERAR! Our project is tackling the challenge of limited self-repair capacity in the central nervous system by developing innovative technologies for brain regeneration. At the same time, national and European health organizations and patient associations will also be involved in the project to create a strategy to translate this innovative technology into clinical practice. 🧠 The need: After an injury like a stroke or in neurodegenerative diseases, the loss of neurons is a critical issue. That's where REGENERAR steps in. 🔬 Our approach: We're working to develop a non-viral delivery formulation up to TRL4 for epigenetic reprogramming of glial cells into neurons. This involves rigorous testing of safety and targeting against glial cells and organotypic cortical slice cultures, exploring various administration routes to optimize brain accumulation, and evaluating in vivo safety, elimination, targeting, and epigenetic reprogramming. Additionally, toxicological studies in GLP conditions will assess the formulation's systemic and local effects. 🌱 Collaboration is key: Six academic and industrial entities as partners in this project: the Helmholtz Munich Center in Munich (Germany), the Fraunhofer ITEM (Germany), Single Technologies (Sweden), the pharmaceutical company Hovione (Portugal) and SPI - Sociedade Portuguesa de Inovação (Portugal). 👉 Discover more on our website: regenerar.eu 🔑 Keywords: Cell differentiation, Regenerative medicine, Nanotechnology, Gene editing, Epigenetic reprogramming, Non-viral delivery systems, Spatial transcriptomics. #REGENERAR #BrainRegeneration #Innovation #Research #RegenerativeMedicine #Nanotechnology #GeneEditing #Epigenetics #SpatialTranscriptomics
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📃Scientific paper: CaMKIIβ knockdown decreases store-operated calcium entry in hippocampal dendritic spines Abstract: Calcium/calmodulin-dependent protein kinase II (CaMKII) and neuronal store-operated calcium entry (nSOCE) have been implicated in the development of Alzheimer's disease (AD). nSOCE is involved in regulation of dendritic spine shape, particularly in stability of mushroom spines that play role in formation of strong synapses. CaMKII is involved in regulation of induction of long-term potentiation, that is needed for shaping of memory. In the present study, we demonstrated that inhibition of kinase activity of CaMKII by KN-62 decreases nSOCE amplitude in soma of primary hippocampal neurons. We have shown that knockdown of CaMKIIβ leads to the downregulation of nSOCE in dendritic spines. In agreement with previously published data, we have also observed that CaMKIIβ knockdown causes mushroom spine loss in primary hippocampal culture. The effect of CaMKIIβ knockdown on the nSOCE may be associated with a decrease of dendritic spine head size. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/f1NIn
CaMKIIβ knockdown decreases store-operated calcium entry in hippocampal dendritic spines
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