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.