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ElaKiri Talk!
An approach to remove amyloid plaques in Alzheimer's.
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<blockquote data-quote="imhotep" data-source="post: 29713637" data-attributes="member: 562115"><p>Alzheimer's disease starts with a sticky protein called amyloid beta that builds up into plaques in the brain, setting off a chain of events that results in brain atrophy and cognitive decline. The new generation of Alzheimer's drugs -; the first proven to change the course of the disease -; work by tagging amyloid for clearance by the brain's immune cells.</p><p></p><p>Now, researchers at Washington University School of Medicine in St. Louis have found a different and promising way to remove the noxious plaques: by directly mobilizing immune cells to consume them.</p><p>The approach could have implications beyond Alzheimer's. Toxic clumps of brain proteins are features of many neurodegenerative conditions, including Parkinson's disease, amyotrophic lateral sclerosis (ALS) and Huntington's disease. Encouraged by the study results, researchers are exploring other potential immunotherapies – drugs that harness the immune system – to remove junk proteins from the brain that are believed to advance other diseases.</p><p></p><p>Tests carried out on Mice has shown that this method works.</p><p></p><p>"Lecanemab, as the first therapeutic antibody that has been able to modify the course of the disease, confirmed the importance of amyloid beta protein in Alzheimer's disease progression. And it opened new opportunities for developing other immunotherapies that use different methods of removing damaging proteins from the brain."</p><p></p><p>- David Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology.</p></blockquote><p></p>
[QUOTE="imhotep, post: 29713637, member: 562115"] Alzheimer's disease starts with a sticky protein called amyloid beta that builds up into plaques in the brain, setting off a chain of events that results in brain atrophy and cognitive decline. The new generation of Alzheimer's drugs -; the first proven to change the course of the disease -; work by tagging amyloid for clearance by the brain's immune cells. Now, researchers at Washington University School of Medicine in St. Louis have found a different and promising way to remove the noxious plaques: by directly mobilizing immune cells to consume them. The approach could have implications beyond Alzheimer's. Toxic clumps of brain proteins are features of many neurodegenerative conditions, including Parkinson's disease, amyotrophic lateral sclerosis (ALS) and Huntington's disease. Encouraged by the study results, researchers are exploring other potential immunotherapies – drugs that harness the immune system – to remove junk proteins from the brain that are believed to advance other diseases. Tests carried out on Mice has shown that this method works. "Lecanemab, as the first therapeutic antibody that has been able to modify the course of the disease, confirmed the importance of amyloid beta protein in Alzheimer's disease progression. And it opened new opportunities for developing other immunotherapies that use different methods of removing damaging proteins from the brain." - David Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology. [/QUOTE]
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