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Lien Nguyen 0111

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Last Updated: 02 July 2021

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New preclinical research shows promise for potential treatment pathway aimed at slowing the disease process and extending survival in patients with ALS, often called Lou Gehrigs disease, insidious neurological condition. Research by University of Florida neurogeneticist Laura Ranum, ph. D., And Lien Nguyen, ph. D; Neurimmune; Biogen; and collaborators at Johns Hopkins University show that targeting specific mutant protein in the brain with human-derive antibody can lower neuroinflammation, slow neurodegeneration and lengthen survival in the most common genetic form of amyotrophic lateral sclerosis, or ALS, and frontotemporal dementia, or FTD. The Mouse-model study, published online today in the journal Neuron, offers first evidence that a novel type of immunotherapy could be a viable treatment approach for genetic types of ALS and FTD involving repetitive DNA that produces repeat associate non-ATG proteins. Study demonstrate that antibodies delivered by injection can cross the blood-brain barrier, enter cells and target run proteins that build up in the brain. The study, carried out by the UF College of Medicines Center for NeuroGenetics team in collaboration with investigators at biopharmaceutical companies Neurimmune and Biogen as well as Johns Hopkins University, opens a prospective new path to treating diseases by targeting particular pathological protein produced by the mutant C9orf72 gene. These proteins, which are unexpectedly produce without normal signals for protein production, accumulate in the brains of affected individuals, said Ranum, director of the Center for NeuroGenetics and Kitzman Family Professor of Molecular Genetics and Microbiology. We have test idea that we can use human antibodies derived from healthy elderly people to target protein that is made from genetic mutation. We find that by targeting one mutant protein, there is a collateral beneficial effect that results in reduction of multiple related mutant proteins. In other words, treatment antibody lead to activation of garbage disposal-like system in cells that get rid of multiple types of proteins produced by disease mutation. Study offer evidence that run proteins trigger motor neuron loss and other characteristics of ALS and FTD, and show how antibodies enter cells, bind to these proteins and then haul bad proteins away to other parts of the cell that can process and get rid of them. We have identified an important protein that can be targeted in disease and found a way to attack that mutant protein to slow down and lessen the impact of disease, Nguyen say. This can be developed further to create drug candidates for human clinical trials. A similar antibody-base approach may be applicable to other neurologic diseases. Jan Grimm, managing director and chief scientific officer of Neurimmune, say: We are excited about the rapid progress of this collaborative project to develop human antibodies addressing the most common genetic cause of ALS and FTD. Discovery of antibodies with therapeutic potential in preclinical models is an important milestone in our quest to develop urgently needed novel therapies for these devastating diseases.

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* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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