I recall Turnbuckle saying at one point that TERT allows epigenetically old cells to become epigenetically older. This is the main criticism which has been levelled at this particular approach (apart from the cancer-permissive nature of TERT, which seems to be statistically overridden by improved organ function that reduces cancer risk). But I think the results of this study (which involves on the order of a hundred cognitive score data points despite having just 5 subjects) demonstrate that there's more to it than that. If lengthening telomeres merely extended cell lifespan without affecting their competency, then we would expect to see dementia scores stabilizing for a protracted length of time. But if you look at the graph, they quite clearly improved, and did so over several months. So this isn't a story about arrested aging in senescent neurons. It's a story about senescent neurons becoming less senescent. Given that, and the extended improvement time period involved, it seems quite clear that TERT (and probably KLOTHO, to a lesser extent) sets off a long cascade of remediation that either reverses some deterimental epigenetic changes or otherwise compensates for them.
Nevertheless, I would certainly endorse a rigorous senolytic regime prior to gene therapy (sodium/potassium butyrate, fasting, sulforaphane, dasatinib plus quercetin, or etc.). My point is only that, in its absence, one is still probably better off lengthening telomeres regardless of cell competency, than not.
And finally... if the results are to be believed, this is the most significant therapeutic result in the history of human Alzheimer's research. It deserves more scrutiny.