It's still amazes me when senior people who should know better talk about aggregated proteins in neurodegenerative disorders as simple causes instead of markers or as causes in interaction. Contrary to the overconfident protein-centric view of neurodegenerative disorders, we actually don't understand what's causing them. And to describe aggregated protein is the cause obscures the simple fact that we don't know where these protein aggregates really come from or how they get started or how they escaped protein quality control, in other words the failure of proteostasis has to be antecedent to these aggregates spreading. In addition, the aggregates aren't simply a cause of inflammation they are often times spread via inflammation and changes in the glial system, famously the Tauopathy in Alzheimer's disease. Additionally there are over two dozen monoclonal antibody therapies that have failed to show disease modification or that show only very minimal slowing of degeneration despite the success that these oftentimes have in removing the protein villain. So this whole proteinopathic theory of neurodegeneration has serious challenges and even more serious holes in it. This is not to suggest the ridiculous notion that protein aggregates are not contributing to neurodegeneration, because that's also ridiculous. But it is not by any conceivable stretch a complete theory of neurodegeneration and far from a guide to treating clinical stage disease.
“She received her medical training in Germany and umm uhh later on umm a umm study genetics..” If you can’t speak, don’t. People come to the Internet to get information. We are not captive audience submissively held captive to kiss up to the professor in order to get a grade. As a teacher, as a speaker, you fail.
BTW Ambroxol, while OTC in Europe, is not FDA approved in the united states.
Can ll-37 inhibit alpha-synuclein?
What can we do to help this process?
It's still amazes me when senior people who should know better talk about aggregated proteins in neurodegenerative disorders as simple causes instead of markers or as causes in interaction. Contrary to the overconfident protein-centric view of neurodegenerative disorders, we actually don't understand what's causing them. And to describe aggregated protein is the cause obscures the simple fact that we don't know where these protein aggregates really come from or how they get started or how they escaped protein quality control, in other words the failure of proteostasis has to be antecedent to these aggregates spreading. In addition, the aggregates aren't simply a cause of inflammation they are often times spread via inflammation and changes in the glial system, famously the Tauopathy in Alzheimer's disease. Additionally there are over two dozen monoclonal antibody therapies that have failed to show disease modification or that show only very minimal slowing of degeneration despite the success that these oftentimes have in removing the protein villain. So this whole proteinopathic theory of neurodegeneration has serious challenges and even more serious holes in it. This is not to suggest the ridiculous notion that protein aggregates are not contributing to neurodegeneration, because that's also ridiculous. But it is not by any conceivable stretch a complete theory of neurodegeneration and far from a guide to treating clinical stage disease.
“She received her medical training in Germany and umm uhh later on umm a umm study genetics..”
If you can’t speak, don’t. People come to the Internet to get information. We are not captive audience submissively held captive to kiss up to the professor in order to get a grade.
As a teacher, as a speaker, you fail.
The talk is very good. Its a pity that you are unable to focus on the content.