Rapamycin is known to extend life in mice, so researchers are looking into the mechanisms and possible uses as a therapy for age-related diseases. "Previous studies have shown that inducing autophagy ameliorates early cognitive deficits associated with the build-up of soluble amyloid-β (Aβ). However, the effects of inducing autophagy on plaques and tangles are yet to be determined. While soluble Aβ and tau represent toxic species in Alzheimer's disease (AD) pathogenesis, there is well documented evidence that plaques and tangles also are detrimental to normal brain function. Thus, it is critical to assess the effects of inducing autophagy in an animal model with established plaques and tangles. Here we show that rapamycin, when given prophylactically to 2-month-old 3xTg-AD mice throughout their life, induces autophagy and significantly reduces plaques, tangles and cognitive deficits. In contrast, inducing autophagy in 15-month-old 3xTg-AD mice, which have established plaques and tangles, has no effects on AD-like pathology and cognitive deficits. In conclusion, we show that autophagy induction via rapamycin may represent a valid therapeutic strategy in AD when administered early in the disease progression." This research is actually fairly indicative of the field as a whole: mechanisms that are potentially modestly useful as ways to slow aging across life are forced into consideration as late-stage therapies only. This happens because regulators will not permit commercialization of ways to treat aging in otherwise healthy people - they only permit treatments for named diseases. So progress is necessarily sub-optimal where it is permitted at all.