Interesting animal model research from earlier this month I managed to miss, via ScienceDaily: "Tau is made normally by brain cells and regulates the stability of their internal skeleton. In [Alzheimer's disease (AD)], tau is altered in a way that makes it aggregate into clumps, called tangles. A lot of effort has been devoted to finding ways to specifically eliminate these abnormal forms of tau, but this has been difficult. ... Many investigational therapies for AD aim to reduce levels of amyloid-beta proteins (AB) because Amyloid-beta builds up to abnormally high levels in the brains of people with AD and is widely suspected to cause the disease. ... We wanted to pursue a complementary strategy and try to make the brain more resistant to A-Beta without having to change the levels of A-Beta itself. Amazingly, even partial reduction of tau prevented memory problems and premature deaths in our Alzheimer mice, even though their brains were full of amyloid beta." This looks to be related to Buck Institute research from last year, which also demonstrated healthy mice full of amyloid beta.