The woman’s mutation is in an area of the APOE gene that binds with a sugar-protein compound called heparan sulfate proteoglycans (HSPG), which is involved in spreading tau in Alzheimer’s disease.
She has lots of AB plaque, but little Tau, and no signs of AD - could lead to drug treatment at some point.
Very interesting. I just read the article in NY Times too. High accumulation of plaque with no cognitive problems. Lots of potential for progress In the area of treatment with this info on the benefits of having the Christchurch mutation.