ProMIS Biotech Hopes to Prove Amyloid Theory in Alzheimer’s with New Targeted Therapies

ProMIS Biotech Hopes to Prove Amyloid Theory in Alzheimer’s with New Targeted Therapies
In the wake of the failure of the investigational drug solanezumab, which stirred the debate over whether the prevailing amyloid theory of Alzheimer’s disease is still a viable working hypothesis, ProMIS Neurosciences announced their contribution to Alzheimer’s amyloid-related drug development. The announcement was accompanied by a commentary interpreting the failure of certain drugs — and offering an explanation of how ProMIS's drug development efforts differ from others targeting amyloid-beta to slow or prevent Alzheimer’s disease. According to the company, the earlier drug candidates failed to work because they targeted single soluble amyloid-molecules — so-called monomers — or large aggregates known as plaque. Amyloid-beta is produced as a single molecule, but is prone to attached itself to other amyloid molecules. In recent years, research has shown that it is not the monomers nor the plaques that are toxic to neurons. Instead, it is an intermediate between the two that causes harm, consisting of aggregates holding only a few amyloid-molecules. Research has also shown that these smaller aggregates, known as oligomers, are also capable of triggering amyloid-beta aggregation in nearby areas. For this reason, ProMIS refers to them as prions, and they are not alone in interpreting Alzheimer’s
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