Microbial theories of Alzheimer's don't change the amyloid cascade hypothesis picture - that the disease begins with high levels of amyloid aggregates, then proceeds to high levels of tau aggregates enabled by the amyloid, and it is the tau that causes the real harm. That persistent infections raise amyloid production - because that amyloid is a feature of the innate immune system - is a way to try to answer the question of why only some people have raised levels of amyloid. If you can point to chronic infections that are present in 10% or 20% or 30% of the population (but not much more than that), such as some herpesviruses, this sounds plausible.

The other problem is that there are people with high levels of of amyloid who don't get Alzheimer's, so you need other factors as well. That may be obesity / metabolic dysfunction, hence the view of Alzheimer's informed by metabolic syndrome, diabetes, insulin.

The further challenge is that chronic inflammation in immune aging is clearly an important factor, as is vascular aging. A third of Alzheimer's patients also have some degree of vascular dementia, and the decline in blood flow and capillary networks are clearly significant in neurodegeneration considered as a whole.

Another point to consider is that a competing hypothesis for the microbial increase in amyloid levels is the progressive age-related failure of cerebrospinal fluid drainage to remove buildup of aggregates as it does in youth. This has just as compelling a set of supporting evidence at the present time.

Alzheimer's is a condition with many significant contributing causes. The amyloid cascade (with the various reasons as to why there might be more amyloid), immune aging, vascular aging. All the causes may be real, and about as important as one another. It is a condition that results from many discrete items, most of which may have to be addressed to produce significant gains in the patient population.