Alpha-synuclein as a therapeutic target for Parkinson’s disease: challenges and opportunities

Stanford's APDA Information & Referral Center and Stanford Parkinson's Community Outreach coordinate a local Parkinson's Disease (PD) support group in Palo Alto. Pre-pandemic, we met at a senior housing community and, prior to that, at a senior center. During the pandemic, as of March 2021, we are now meeting virtually. Our meetings will highlight local resources.
At the regular Wednesday, November 10th virtual support group meeting, the topic was cutting edge, basic science research into PD going on at Stanford. The guest speaker was:
Birgitt Schüle, MD, researcher with Stanford Pathology.
She spoke on “Alpha-synuclein as a therapeutic target for Parkinson’s disease: challenges and opportunities.” Dr. Schüle focuses on medical genetics and stem cell modeling to unlock disease mechanisms and pathways leading to neurodegeneration in Parkinson’s disease and related disorders, and to develop new therapeutic strategies to advance precision medicine. The line of research she is pursuing runs counter to current scientific concepts. She is investigating whether common genes and pathways underlie both neurodegeneration and neurodevelopment. This knowledge could help guide future therapeutic strategies of lowering alpha-synuclein in Parkinson’s disease and could provide insights into early, potentially reversible disease mechanisms critical for both neurodevelopment and neurodegeneration.
Visit the Palo Alto Parkinson's Support Group med.stanford.edu/parkinsons/n...

[@zhuzhou]

BTW Ambroxol, while OTC in Europe, is not FDA approved in the united states.

[@robertbernard651]

What can we do to help this process?

[@douglaswatt1582]

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.

[@ottoavila9895]

Can ll-37 inhibit alpha-synuclein?

[@supremoluminary]

“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.