Brilliant breakdown of the Septin-2 study. The link between cytoskeletal mutations and AIS disruption makes sense mechanistically, but I wonder if it opens up intervention points beyond just structural restoration. In my experiance working with protein localization assays, the challenge is always whetherthe compensatory mechanisms mask early deficits. Could tracking Septin-2 homodimerization efficiency serve as an earlier biomarker before cognitive symptoms manifest?
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Brilliant breakdown of the Septin-2 study. The link between cytoskeletal mutations and AIS disruption makes sense mechanistically, but I wonder if it opens up intervention points beyond just structural restoration. In my experiance working with protein localization assays, the challenge is always whetherthe compensatory mechanisms mask early deficits. Could tracking Septin-2 homodimerization efficiency serve as an earlier biomarker before cognitive symptoms manifest?
thanks for the comment. to receive personalized newsletters like this. Consider signing up for sciencebriefing.com where you can receive only neurology related briefings.