That's the rub. Even if this non-traditional brain model is to be taken at face value, there is a missing variable somewhere, arguably more important; HSV-1, at best, would be a contributing factor.
That's the rub. Even if this non-traditional brain model is to be taken at face value, there is a missing variable somewhere, arguably more important; HSV-1, at best, would be a contributing factor.
That is mixing up necessary versus sufficient. If all people who develop Alzheimer’s contracted HSV-1 prior to developing Alzheimer’s and all people who did not contract HSV-1 do not develop Alzheimer’s (technically implied by my first statement), then you can make a good case for causality. Obviously you can do better, but that is a good start.
Did you completely miss the point of the article and even of the quote you copied. "the latest work addresses [this very criticism you have]"?
The article tells us what the missing link is (according to their hypothesis). That's the whole point of it. It's even in the title.
That'd be the suggested missing link, physical impact disturbing dormant virions in the brain or allowing a temporary passage to a part of the brain they're normally unable to reach.
https://www.science.org/doi/pdf/10.1126/science.abj8222?src=... [PDF]