This is a hugely widely-prescribed drug, generally considered extraordinarily well tolerated, so whatever impact gabapentin has on dementia, the effect would have to be pretty small --- in particular: there's no spike that tracks the point at which it started become so widely prescribed.
This wouldn't necessarily be expected for the same reason that if one looked at new smokers after 10 years, there'd be no significant spike in lung cancer. This is what makes long terms effects of things so difficult to prove. Even tylenol/paracetomol is still having some interesting new discoveries made. This is the main reason I tend to strongly adhere to the precautionary principle when it comes to any sort of "new" drug.
But we are? The article describes an extremely significant effect because dementia rates are already very high at, for instance, ~10% in the 70+ age group. So twice as likely to develop dementia is an extreme effect, as opposed to e.g. twice as likely for something that occurs at a rate of 1 in 10,000 or whatever.
The bigger question would be causality. Observational studies are generally trash, especially with dementia, because it correlates with practically everything in one way or the other. So is it the drug, or is there a common confounding variable among people who use the drug?
That's the problem that makes proving causality so hard for many drugs. Long-term effects are subject to practically endless possible confounders. Like the National Academy of Sciences is rather fond of saying, you end up with endless scenarios where there is neither enough evidence to accept nor reject a possible causality. People that want to spin things one way then claim there's no evidence, which is plainly false - as there is, but its insufficient to confidently claim causality. In the same way that there's insufficient evidence to reject causality.
Search for '[acetaminophen/paracetamol/tylenol] study' every few years and you'll find something new. The latest seems to be strong observational evidence that it drives neurodevelopmental issues, including ADHD/autism, when taken during pregnancy. This is being pushed back against hard because this has led to Johnson & Johnson being sued by hundreds of people claiming they already knew this, setting them up to become the next big tobacco if they lose.
The link is very strong and so big pharam's defense is that it's not not tylenol, but having an issue for where tylenol might be needed, that is causing the issues. A bizarrely excellent and balanced article on the issue is available here. [1]
