VIVEbiotech’s Post

📣 We welcome the addition of our new consortium partner, the Instituto de Medicina Molecular (iMM), for officially joining the MAGIC Horizon project. It is inspiring to see such strong cross-functional collaboration accelerating the development of gene therapies for muscular dystrophies. What’s the consortium’s goal? Accurate, humanized skeletal muscle disease models for advanced gene therapies and genome editing. ReiThera is involved in setting up both Upstream Process (USP) and Downstream Process (DSP) conditions for GMP-compatible manufacturing of an AAV candidate specifically retargeted to muscle cells with an innovative technological approach to produce batches for NHP studies. 💡 Follow us and keep updated. #biotech #genetherapy #biotechnology #gmp #cellandgenetherapy #healthcare #healthtech

📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health

📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health

📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health

📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health

📃Scientific paper: Exploring the role of CHRFAM7A in the early stages of Alzheimer's disease : in vitro studies and development of a novel humanized mouse model;Implication du gène CHRFAM7A dans la phase précoce de la maladie d'Alzheimer : études in vitro et développement d'un nouveau modèle de souris humanisée Abstract: CHRFAM7A is a human-specific gene that encodes the nicotinic acetylcholine receptor (nAChR) subunit dupα7. This gene originated after a fusion between a partial duplication of the CHRNA7 α7-nAChR gene and ULK4 200.000 years ago. The ancestral CHRNA7 gene has been linked to several neurological disorders such as Alzheimer's disease (AD). In particular, α7-nAChR can directly bind to the Amyloid ß peptide (Aβ), one of the primary molecular hallmarks of the disease, and facilitate its intracellular toxic accumulation. Although extensive research has been carried out to dissect the role of α7-nAChR in AD, no clinical trials have been successful. This translational gap could be attributed to the lack of dupα7 subunit in classical pre-clinical models. Importantly, dupα7 can incorporate into pentamers of α7-nAChRs and negatively regulate its function by reducing its number of ligand binding domains and retaining the receptor in the endoplasmic reticulum (ER). In the context of AD, dupα7 reduces Aß uptake when expressed in neuronal cultures and is associated to the activation of Aβ-induced pro-inflammatory responses. In the first part of the thesis, the role of the human subunit in mediating Aβ-induced toxicity in human induced pluripotent stem cells (hiPSC)-derived interneurons was studied in-vitro. Prior to neuronal differentiation, hiPSC carrying 0 copies of the gene were transduced with a CHRFAM7A lentiviral construction. To assess Aβ-induced toxicity, oxidative stress... Continued on ES/IODE ➡️ https://etcse.fr/IoMU9 ------- 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: Exploring the role of CHRFAM7A in the early stages of Alzheimer's disease : in vitro studies and development of a novel humanized mouse model;Implication du gène CHRFAM7A dans la phase précoce de la maladie d'Alzheimer : études in vitro et développement d'un nouveau modèle de souris humanisée Abstract: CHRFAM7A is a human-specific gene that encodes the nicotinic acetylcholine receptor (nAChR) subunit dupα7. This gene originated after a fusion between a partial duplication of the CHRNA7 α7-nAChR gene and ULK4 200.000 years ago. The ancestral CHRNA7 gene has been linked to several neurological disorders such as Alzheimer's disease (AD). In particular, α7-nAChR can directly bind to the Amyloid ß peptide (Aβ), one of the primary molecular hallmarks of the disease, and facilitate its intracellular toxic accumulation. Although extensive research has been carried out to dissect the role of α7-nAChR in AD, no clinical trials have been successful. This translational gap could be attributed to the lack of dupα7 subunit in classical pre-clinical models. Importantly, dupα7 can incorporate into pentamers of α7-nAChRs and negatively regulate its function by reducing its number of ligand binding domains and retaining the receptor in the endoplasmic reticulum (ER). In the context of AD, dupα7 reduces Aß uptake when expressed in neuronal cultures and is associated to the activation of Aβ-induced pro-inflammatory responses. In the first part of the thesis, the role of the human subunit in mediating Aβ-induced toxicity in human induced pluripotent stem cells (hiPSC)-derived interneurons was studied in-vitro. Prior to neuronal differentiation, hiPSC carrying 0 copies of the gene were transduced with a CHRFAM7A lentiviral construction. To assess Aβ-induced toxicity, oxidative stress... Continued on ES/IODE ➡️ https://etcse.fr/IoMU9 ------- 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: Exploring the role of CHRFAM7A in the early stages of Alzheimer's disease : in vitro studies and development of a novel humanized mouse model;Implication du gène CHRFAM7A dans la phase précoce de la maladie d'Alzheimer : études in vitro et développement d'un nouveau modèle de souris humanisée Abstract: CHRFAM7A is a human-specific gene that encodes the nicotinic acetylcholine receptor (nAChR) subunit dupα7. This gene originated after a fusion between a partial duplication of the CHRNA7 α7-nAChR gene and ULK4 200.000 years ago. The ancestral CHRNA7 gene has been linked to several neurological disorders such as Alzheimer's disease (AD). In particular, α7-nAChR can directly bind to the Amyloid ß peptide (Aβ), one of the primary molecular hallmarks of the disease, and facilitate its intracellular toxic accumulation. Although extensive research has been carried out to dissect the role of α7-nAChR in AD, no clinical trials have been successful. This translational gap could be attributed to the lack of dupα7 subunit in classical pre-clinical models. Importantly, dupα7 can incorporate into pentamers of α7-nAChRs and negatively regulate its function by reducing its number of ligand binding domains and retaining the receptor in the endoplasmic reticulum (ER). In the context of AD, dupα7 reduces Aß uptake when expressed in neuronal cultures and is associated to the activation of Aβ-induced pro-inflammatory responses. In the first part of the thesis, the role of the human subunit in mediating Aβ-induced toxicity in human induced pluripotent stem cells (hiPSC)-derived interneurons was studied in-vitro. Prior to neuronal differentiation, hiPSC carrying 0 copies of the gene were transduced with a CHRFAM7A lentiviral construction. To assess Aβ-induced toxicity, oxidative stress... Continued on ES/IODE ➡️ https://etcse.fr/IoMU9 ------- 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: Exploring the role of CHRFAM7A in the early stages of Alzheimer's disease : in vitro studies and development of a novel humanized mouse model;Implication du gène CHRFAM7A dans la phase précoce de la maladie d'Alzheimer : études in vitro et développement d'un nouveau modèle de souris humanisée Abstract: CHRFAM7A is a human-specific gene that encodes the nicotinic acetylcholine receptor (nAChR) subunit dupα7. This gene originated after a fusion between a partial duplication of the CHRNA7 α7-nAChR gene and ULK4 200.000 years ago. The ancestral CHRNA7 gene has been linked to several neurological disorders such as Alzheimer's disease (AD). In particular, α7-nAChR can directly bind to the Amyloid ß peptide (Aβ), one of the primary molecular hallmarks of the disease, and facilitate its intracellular toxic accumulation. Although extensive research has been carried out to dissect the role of α7-nAChR in AD, no clinical trials have been successful. This translational gap could be attributed to the lack of dupα7 subunit in classical pre-clinical models. Importantly, dupα7 can incorporate into pentamers of α7-nAChRs and negatively regulate its function by reducing its number of ligand binding domains and retaining the receptor in the endoplasmic reticulum (ER). In the context of AD, dupα7 reduces Aß uptake when expressed in neuronal cultures and is associated to the activation of Aβ-induced pro-inflammatory responses. In the first part of the thesis, the role of the human subunit in mediating Aβ-induced toxicity in human induced pluripotent stem cells (hiPSC)-derived interneurons was studied in-vitro. Prior to neuronal differentiation, hiPSC carrying 0 copies of the gene were transduced with a CHRFAM7A lentiviral construction. To assess Aβ-induced toxicity, oxidative stress... Continued on ES/IODE ➡️ https://etcse.fr/IoMU9 ------- 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