One hypothesis is that in neurodegenerative diseases, tau function is disrupted through phosphorylation or through the binding of effector molecules which leads to its polymerization. The accumulation of these filaments then leads to neurodegeneration and neuronal loss. This is called the "tau hypothesis".
In the brains of Alzheimer's disease patients, these accumulations of filaments appear as neuropil threads, neurofibrillary tangles, and neuritic plaques.
Our laboratory uses two main techniques to try to understand how and why tau filaments form. We use immunohistochemistry to try to map the changes in tau that lead to neurodegneration. Secondly, we use in vitro molecular modeling to try to dissect the mechanisms that result in the polymerization of tau filaments.