This is a very good topic to start discussing. I look forward to see much discussion ahead in this topic. There are several hypothesis to discuss one I would like to discuss here is, Amyloid beta induces hyperphosphorylation of tau via different mechanisms either by signal transduction or by induction of oxidative stress or by receptor activation on the neuronal membrane. Abeta can also directly interact with acetylchoiline receptors leading to activation of PI3K/Akt and inducing events leading hyperphosphorylation of tau. (Journal of Alzheimer’s Disease 16 (2009) 15–27)
I agree its time to move beyond Ab, Your review has added an important addition to these new perspectives. However, many basic questions still remain about Ab function. At this point I am excited about understanding parallel processes of Ab and tau pathophysiology that contribute to AD.
The review by Krstic is quite excellent. I am also in agreement his perspective that shows an indirect link between AB and tau pathophysiology which appears mediated by inflammatory factors.
Let's not be too quick to say the link between Abeta pathology and tauopathy is indirect... several groups, including ours, are in the process of generating data that show a direct link. More to come...
Hi dears, I recently got familiar with Alzheimer by Pin1, a prolyl isomerase, which can affect both A beta and fibrilary tangle production that you haven't written anything about.
anyway your points of view made me think about other aspects. thank you.