es/iode’s Post

📃Scientific paper: PlexinA1-deficient mice exhibit decreased cell density and augmented oxidative stress in parvalbumin-expressing interneurons in the medial prefrontal cortex Abstract: PlexinA1 (PlxnA1) is a transmembrane receptor for semaphorins (Semas), a large family of axonal guidance cues vital during neural development. PlxnA1 is expressed in embryonic interneurons, and PlxnA1 deletion in mice leads to less interneurons in the developing cortex. In addition, PlxnA1 has been identified as a schizophrenia susceptibility gene. In our previous study, PlxnA1 knockout (KO) mice under a BALB/cAJ genetic background exhibited significantly increased self-grooming and reduced prepulse inhibition, a reliable phenotype for investigating the neurobiology of schizophrenia. However, the mechanism underlying the abnormal behavior of PlxnA1 KO mice remains unclear. We first confirmed PlxnA1 mRNA expression in parvalbumin-expressing interneurons (PV cells) in the medial prefrontal cortex (mPFC) of adult mice. Immunohistochemical analysis (IHC) showed significantly decreased densities of both GABAergic neurons and PV cells in the mPFC of PlxnA1 KO mice compared with wild type mice (WT). PV cells were found to express molecule interacting with CasL 1 (MICAL1), an effector involved in Sema-Plxn signaling for axon guidance, suggesting MICAL1 and PlxnA1 co-expression in PV cells. Furthermore, IHC analysis of 8-oxo-dG, an oxidative stress marker, revealed significantly increased oxidative stress in PlxnA1-deficient PV cells compared with WT. Thus, increased oxidative stress and decreased PV cell density in the mPFC may determine the onset of PlxnA1 KO mice’s abnor... Continued on ES/IODE ➡️ https://etcse.fr/oFgQ ------- 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.

𝗨𝘀𝗶𝗻𝗴 𝗔𝗴𝗲𝗱 𝗣𝗮𝘁𝗶𝗲𝗻𝘁 𝗖𝗲𝗹𝗹𝘀 𝗳𝗼𝗿 𝗠𝗼𝗱𝗲𝗹𝗶𝗻𝗴 𝗟𝗮𝘁𝗲-𝗢𝗻𝘀𝗲𝘁 𝗔𝗹𝘇𝗵𝗲𝗶𝗺𝗲𝗿'𝘀 Alzheimer's disease (AD) is marked by the buildup of harmful proteins and the loss of brain cells. Most research has focused on genetic forms of early-onset AD, but the more common late-onset AD (LOAD) is harder to study  because it involves many factors, including aging. Scientists have found that using stem cells to create neurons often results in cells that are too young to show age-related changes. Instead,  they are reprogramming older cells  from patients to keep their age-related traits. Fibroblast samples from  individuals with LOAD are directly  reprogrammed into cortical neurons  in a 3D environment that better mimics the characteristics of LOAD. This new strategy may help  study and understand the disease more effectively. Hopeful! #alzheimer #neuropathology #modeling #RNA #neurodegenerativedisease #biology #aging #ageing #neurology

This editorial discusses the use of neurogenomics techniques to decode brain function and understand the mechanisms underlying brain diseases and disorders. The key points are: 1. Neurogenomics offers comprehensive perspectives on the impact of genomic alterations on brain function and helps understand the complex interactions between genetics and the environment in the pathogenesis of brain disorders like neurodevelopmental disorders (NDDs) and psychiatric disorders. 2. The research topic covered a range of insights, including functional assessments of genetic polymorphisms, epigenetic studies using patient genome data or polygenic risk scores (PRSs), and comprehensive transcriptome studies using brain disease-related mouse models. 3. The studies discussed identified genetic factors associated with brain dysfunction, such as single nucleotide polymorphisms (SNPs), short tandem repeats (STRs), and PRSs, as well as epigenetic alterations related to disease onset. 4. Future studies combining the latest single-cell transcriptome and epigenomics data will provide more in-depth knowledge on the molecular and cellular mechanisms of brain diseases and dysfunction. 5. While decoding brain function through genetic analysis is in its nascent stages, the diversity of the papers suggests that genetics has great potential to enhance our understanding of brain function, despite the current gap between genomic observations and actual brain function. #genomicanalysis #epigenetics #polygenicriskscores #transcriptomics #singlecellanalysis #neurogenetics #neurogenomics #neurology

Researchers have been exploring various players involved in neurodevelopmental disorders, with focus on a key gene called 𝘚𝘠𝘕𝘎𝘈𝘗1. This gene produces the protein SynGAP1, which is essential for brain development and the plasticity of neuronal connectivity. Changes in how this protein works have been studied in animal models, showing links to developmental delays, intellectual disabilities, motor impairments, and epilepsy. 🤔 But what are the exact functional features of neurons with 𝘚𝘠𝘕𝘎𝘈𝘗1 abnormalities that lead to these outcomes? A recent publication in Translational Psychiatry from Nature Portfolio highlights, for the first time, specific functional patterns in neurons from a 𝘚𝘠𝘕𝘎𝘈𝘗1 mouse model by applying both in vivo and in vitro electrophysiological techniques. 👏 Congratulations to Timothy Fenton and all the authors, under the supervision of Jill Silverman, Roy Ben-Shalom, and Alex S. Nord, from the UC Davis MIND Institute, University of California, Davis, USA, for this exciting work! This study is the first of its kind to report the use of high-density microelectrode arrays (HD-MEAs) in an animal model lacking 𝘚𝘠𝘕𝘎𝘈𝘗1 in neurons. The authors cultured primary neurons from this model, which were plated on the MaxOne HD-MEA system, and analyzed the recorded data using MaxLab Live Software. Adding to their findings with in vivo electrophysiology using electroencephalography (EEG), the authors took advantage of the in vitro HD-MEA to discover that these neurons had increased network firing, with more bursts and shorter gaps between them compared to neurons from control mice. Overall, this study brings a unique combination of in vitro and in vivo tools, paving the way for identifying cellular biomarkers with great potential for the development of targeted therapies. ✨ We look forward to more advances in this field with the help of HD-MEAs! 🗞️ Read the full publication here: https://lnkd.in/dFqNukZa #MaxOne #MEAs #neurodevelopment #therapies #electrophysiology

🧬 Groundbreaking Research Alert! 🚀 UCLA and the University of Pennsylvania have uncovered over 214,516 new gene transcripts in the developing human brain. This extensive catalog could reshape our understanding and treatment of neurodevelopmental disorders. The unique expression of these transcripts during brain maturation could pave the way for precision therapies and enhance genetic diagnoses. This could have a significant impact on the future of neurology and psychiatry. Find out more about how this groundbreaking research could shape the future of medicine in our latest publication in Science. Let's explore the intricate dance of genes that shapes our brain's development and dive deep into the future of medicine! #Neuroscience #Genomics #BrainResearch

☑️ *READ DESCRIPTION BELOW:* PTEN germline mutations account for ~0.2-1% of all autism spectrum disorder (ASD) cases, as well as ~17% of ASD patients with macrocephaly, making it one of the top ASD-associated risk genes. Individuals with germline PTEN mutations receive the molecular diagnosis of PTEN Hamartoma Tumor Syndrome (PHTS), an inherited cancer predisposition syndrome, about 20-23% of whom are diagnosed with ASD. We generated forebrain organoid cultures from gene-edited isogenic human induced pluripotent stem cells (hiPSCs) harboring a PTENG132D (ASD) or PTENM134R (cancer) mutant allele to model how these mutations interrupt neurodevelopmental processes. Here, we show that the PTENG132D allele disrupts early neuroectoderm formation during the first several days of organoid generation, and results in deficient electrophysiology. While organoids generated from PTENM134R hiPSCs remained morphologically similar to wild-type organoids during this early stage in development, we observed disrupted neuronal differentiation, radial glia positioning, and cortical layering in both PTEN-mutant organoids at the later stage of 72+ days of development. Perifosine, an AKT inhibitor, reduced over-activated AKT and partially corrected the abnormalities in cellular organization observed in PTENG132D organoids. Single cell RNAseq analyses on early-stage organoids revealed that genes related to neural cell fate were decreased in PTENG132D mutant organoids, and AKT inhibition was capable of upregulating gene signatures related to neuronal cell fate and CNS maturation pathways. These findings demonstrate that different PTEN missense mutations can have a profound impact on neurodevelopment at diverse stages which in turn may predispose PHTS individuals to ASD. Further study will shed light on ways to mitigate pathological impact of PTEN mutants on neurodevelopment by stage-specific manipulation of downstream PTEN signaling components. Kang SC, Mol Psychiatry. 2023 Nov 29. doi: 10.1038/s41380-023-02325-3. Epub ahead of print. PMID: 38030818 #Gesundheit #Bildung #Fuehrung #Coaching #Mindset #Motivation #Gehirn #Neuroscience #Psychologie #Persoenlichkeitsentwicklung #Kindheit #KeyNoteSpeaker #Humangenetik #Biochemie #Neuroleadership #Ernaehrung #Transformation #Stress #Demografie #Gender #Age #interkulturelleKompetenz #Epigenetik #Veraenderung #EmotionaleIntelligenz #Change #Gesellschaft #Organisationsentwicklung #Philosophie #Beratung # Quantum

I am thrilled to share that our latest review article, titled "miRNA-124 Loaded Extracellular Vesicles Encapsulated Within Hydrogel Matrices for Combating Chemotherapy-Induced Neurodegeneration", has been published in Biochemical and Biophysical Research Communications (BBRC)! In this comprehensive review, we explore the innovative potential of miR-124-loaded extracellular vesicles (EVs) and hydrogel-based delivery systems in addressing the critical issue of chemotherapy-induced neurodegeneration. With the growing number of cancer survivors facing long-term cognitive and neurological side effects from chemotherapy, this research offers insights into how cutting-edge technologies can drive neuroprotection and neuroregeneration. We discuss: 🔬 The role of miR-124 in promoting neural repair and regeneration. 💊 How extracellular vesicles (EVs) can serve as effective delivery vehicles. 🧠 The use of hydrogel matrices for sustained release and enhanced targeting. ⚕️ Potential applications for treating chemotherapy-induced neurotoxicity. I’m incredibly proud of this collaborative work, and I hope it provides valuable insights for those working in neuroregeneration, cancer therapy, and drug delivery systems. A big thank you to my co-authors and collaborators, as well as the editorial team at BBRC! https://lnkd.in/gtKbBa5J #Research #Neuroregeneration #miRNA #ExtracellularVesicles #Hydrogels #CancerTherapy #Neuroscience #BBRC #AcademicPublishing

Exciting news in the field of genetics and neurology! A newly discovered genetic variant has been found to significantly reduce the odds of developing Alzheimer's disease. This discovery opens up new avenues for research and potential treatments. Understanding the genetic factors that influence Alzheimer's could lead to more targeted therapies and improved prevention strategies. A promising development in the fight against this devastating disease! #Alzheimers #Genetics #Neurology #Research #Healthcare #SMO #SCLAManagement Read more about this research development: https://lnkd.in/eZxX3BvQ

We are very pleased to announce that the final article of Mia Langbøl Hjerrilds PhD has been published in Cellular and Molecular Neurobiology as a part of the special issue “Proteomics in Neurodegeneration”.   The article is titled "Proteomic and Cytokine Profiling in Plasma from Patients with Normal-Tension Glaucoma and Ocular Hypertension" and indicates the involvement of the immune system in normal-tension glaucoma and ocular hypertension. Patients with ocular hypertension seem able to withstand inflammation through the anti-inflammatory effect of apolipoproteins.    You can access the article via this link:  https://lnkd.in/dysF8mni A special thanks to Øjenforeningen (Fight for Sight Denmark), Jørgen Bagenkop Nielsens Myopi-Fond, Synoptik-Fonden and Deutsche Forschungsgemeinschaft (DFG) - German Research Foundation for their support of the project.   #EyeTRU #Glaucoma #Proteomics #Springer #CEMN