I believe that the current theory holds that it's likely a result of a lot of different things. One big mechanism we're learning about is dysregulated TDP-43, which is an RNA-binding protein that regulates tau and is involved in ribosome metabolism. Abnormal TDP-43 pathology has been found in a ton of cases of CTE, including cytoplasmic neuronal inclusions, neurites, and glial inclusions. In mouse models, TBI has resulted in upregulation of TDP-43, and in diseases associated with odd TDP-43 metabolism, tau metabolism is often altered too.

That being said, there are probably tons of other factors, and how p-tau is able to make more p-tau after neurons die and spill it out (or after it's transported out of neurons like trash) is still under investigation