Yet, this drug was approved solely on it's ability to reduce amyloid plaque, without any cognitive effects.

Already 20 years ago there were serious discussions whether the fibrils were actually responsible, or maybe instead some toxic intermediates might be the cause. As far as I understand the case against fibrils as the main cause only got stronger, and the mainstream view among scientists is that it is quite likely that there is more going on there and the fibrils alone are not the full explanation.

I wonder how the amyloid plaques not being thought to be the cause of Alzheimers will affect the research of CTE (one of the many other tauopathies.)

For what it is worth, there seems to be a lot of internal debate around the causes, symptoms, and treatments of CTE. In fact, there are debates as to whether CTE is a distinct tauopathy or even exists at all (at least in the form the public understands it).

I think few people believe amyloid plaques are the sole cause but there is still quite a bit of evidence that amyloid is heavily involved in Alzheimer's. Genetically almost all of the genes associated with Alzheimers have to do with the productions or cleaning up of amyloid beta.