November 7, 2026

@michaelokun

What resonates most with me about this important paper by Jhodi Webster and Ashley Harms is that it challenges one of the assumptions that may be holding back progress in Parkinson’s disease: that we can treat a complex brain disease by targeting a single abnormal protein. The authors remind us that more than half of Parkinson’s brains examined after death harbor overlapping pathologies, including alpha-synuclein, tau, and amyloid-beta, and that these proteins may interact with one another and with the immune system to accelerate neurodegeneration and cognitive decline. I have long believed that Parkinson’s is not one disease, but many biological processes converging in the same person. What particularly caught my attention was the discussion of microglia, T cells, and chronic neuroinflammation, which may help explain why therapies targeting alpha-synuclein alone have repeatedly disappointed us. The lesson from cancer treatment is especially compelling: sometimes we need to attack several biological pathways simultaneously to meaningfully change the course of a disease. This does not mean combination therapies are proven to work in Parkinson’s, but it does suggest that our next generation of clinical trials should be smarter, more personalized, and designed around the biology of each person. We need to stop expecting one magic bullet to solve Parkinson’s. Our people (persons w/ disease) deserve treatments that recognize the full complexity of their disease. https://www.nature.com/articles/s41531-026-01502-9