4.3.2 Effect of rapamycin on AD
In addition to extending lifespan and boosting the immune system, rapamycin has been shown to be efficacious in attenuating one of the most common neurodegenerative disease, AD, in animals. Specifically, in 2010, researcher found that rapamycin administered to AD mice in early life protected against cognitive deficits and resulted in a reduction of amyloid-β and tau 156, 157. However, there has been varied evidence regarding the effect of rapamycin on AD. For example, Oddo et al. reported that when starting treatment of rapamycin AD mice at 2 months, a significant reduction of tau and plaques were observed, whereas treating with rapamycin at 15 months had no such effect. This indicated that rapamycin can only accelerate autophagy before the formation of tau and plaques in AD.
Although tau tangles and plaques are considered hallmarks of AD, cerebrovascular pathological alterations are also commonly found in AD patients. Rapamycin appears to alter cerebrovascular circulation. For example, administering rapamycin to APOE4 mutant carrier mice, a transgenic AD mice model, can result in a restored cerebral blood flow and maintenance of blood-brain barrier integrity, suggesting that rapamycin may have a putative role in reducing vascular progression in AD mice 158.