Maybe. Maybe not. To know that for sure, you'd want two large studies to be done. One showing correlation between having cold sores and AD. And then, one where

Maybe. Maybe not. To know that for sure, you'd want two large studies to be done. One showing correlation between having cold sores and AD. And then, one where some people are cured of HSV (I don't think we really have a cure yet...) and where others are given a placebo, with long term tracking to see if intervention reduces AD. That sort of work is how the link between cholesterol levels and heart failures was demonstrated. This paper isn't even really about the Alzheimers-herpes link, it's more about demoing how you can use HSV-1 with their brain structure to get what looks like a good model of Alzheimers disease. What they gave the model might not even be "real" Alzheimers. Their goal was to develop a really good research tool[0], not necessarily to show an AD/HSV link, and the cells in their model, as induced neuronal stem cells redifferentiated into brain-like tissue on a scaffold, might not be truly reacting like cells in your brain. [0] from the discussion in the paper, here's the first line emphasizing the takeaway: "Generating in vitro human models of sporadic AD poses a considerable challenge because of the complex, undefined etiology and slow disease progression that naturally occurs in patients. Here, we describe a multidisciplinary approach to address this critical need by generating robust and physiologically relevant 3D human tissues for studying sporadic AD through the use of hiNSC technology and HSV-1 in combination with a bioengineered brain tissue model." The herpes-AD link is somewhat supported by this since clearly adding HSV to this brain model caused these AD-like developments, but that could be a factor of how the cells used to make these models react and their physiology might be different as differentiated induced stem cells.